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Copyright ©The Author(s) 2024. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Radiol. Jun 28, 2024; 16(6): 168-183
Published online Jun 28, 2024. doi: 10.4329/wjr.v16.i6.168
Navigating nephrotoxic waters: A comprehensive overview of contrast-induced acute kidney injury prevention
Panagiotis Theofilis, Rigas Kalaitzidis, Center for Nephrology "G Papadakis", General Hospital of Nikaia-Piraeus "Agios Panteleimon", Nikaia-Piraeus 18454, Greece
ORCID number: Panagiotis Theofilis (0000-0001-9260-6306); Rigas Kalaitzidis (0000-0002-7773-7575).
Author contributions: Theofilis P performed the literature review and drafted the original manuscript; Kalaitzidis R supervised the study and performed revisions on the original draft.
Conflict-of-interest statement: All the authors report no relevant conflicts of interest for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: Https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Panagiotis Theofilis, MD, PhD, Doctor, Researcher, Center for Nephrology "G Papadakis", General Hospital of Nikaia-Piraeus "Agios Panteleimon", Mantouvalou 3, Nikaia-Piraeus 18454, Greece. panos.theofilis@hotmail.com
Received: April 27, 2024
Revised: May 19, 2024
Accepted: June 17, 2024
Published online: June 28, 2024
Processing time: 59 Days and 20 Hours

Abstract

Contrast-induced acute kidney injury (CI-AKI) is the third leading cause of acute kidney injury deriving from the intravascular administration of contrast media in diagnostic and therapeutic procedures and leading to longer in-hospital stay and increased short and long-term mortality. Its pathophysiology, although not well-established, revolves around medullary hypoxia paired with the direct toxicity of the substance to the kidney. Critically ill patients, as well as those with pre-existing renal disease and cardiovascular comorbidities, are more susceptible to CI-AKI. Despite the continuous research in the field of CI-AKI prevention, clinical practice is based mostly on periprocedural hydration. In this review, all the investigated methods of prevention are presented, with an emphasis on the latest evidence regarding the potential of RenalGuard and contrast removal systems for CI-AKI prevention in high-risk individuals.

Key Words: Contrast-induced acute kidney injury, Contrast media, Prevention, Hydration, RenalGuard, Dyevert

Core Tip: Although periprocedural hydration is a fundamental preventive measure for contrast-induced acute kidney injury (CI-AKI), recent research suggests exploring emerging strategies such as RenalGuard and contrast removal systems. These innovative approaches show promise, particularly in high-risk individuals with critical illness or pre-existing renal and cardiovascular conditions. By staying updated on the latest evidence and incorporating these advancements into clinical practice, healthcare professionals can enhance CI-AKI prevention efforts and improve patient outcomes.



INTRODUCTION

Contrast media (CM), administered intravascularly during radiodiagnostic procedures to improve the visibility of blood vessels, can lead to a complication known as acute kidney injury shortly after their use[1]. This condition, termed contrast-induced acute kidney injury (CI-AKI), is the third most common cause of acute kidney injury, following reduced renal perfusion and the use of nephrotoxic drugs[2]. CI-AKI is characterized by an increase in serum creatinine levels within 48-72 hours after CM injection, after ruling out other causes of kidney impairment. Typically, serum creatinine levels return to baseline within 1-3 weeks[1]. The first 24 hours following CM exposure are critical, as 80% of cases show a rise in serum creatinine within this period, and nearly all patients who develop severe renal dysfunction exhibit increased serum creatinine within the same timeframe[3].

CI-AKI is linked to serious adverse outcomes, including chronic kidney disease (CKD), heart attacks, strokes, and death, with patients who develop CI-AKI experiencing higher mortality rates within one month[4,5]. The one-year mortality rate varies depending on the severity of pre-existing renal impairment before the CM procedure, ranging from 8%-23%, and can reach up to 55% in patients who require dialysis due to CI-AKI[6,7]. This review discusses the latest evidence on CI-AKI, covering the different prevention strategies and exploring new approaches currently under investigation..

EPIDEMIOLOGY AND OUTCOMES
Incidence and risk factors

The incidence of CI-AKI ranges from 0.6% to 2.3% in the general population but may increase in the presence of risk factors[8]. With over a million CM procedures performed annually in the USA, the incidence of CI-AKI is approximately 150000 cases per year[9]. Acute kidney injury following the intravascular injection of contrast agents for diagnostic or therapeutic purposes primarily occurs in patients with underlying risk factors that heighten the kidney's vulnerability to the CM. Pre-existing renal disease with elevated serum creatinine is a significant risk factor for CI-AKI development (Table 1). According to Mehran and Nikolsky[8], the incidence of CI-AKI in patients with underlying CKD ranges from 14.8% to 55%. The risk of CI-AKI increases with higher baseline creatinine values. For plasma creatinine levels ≤ 1.4 mg/dL, 1.4-1.9 mg/dL, and ≥ 2.0 mg/dL, the risk of CI-AKI is 2%, 10.4%, and 62%, respectively[8]. The need for dialysis is 10%, compared to less than 1% in CI-AKI requiring dialysis in patients without preexisting renal disease[10-12]. Renal function in patients with preexisting renal disease and elevated serum creatinine should be evaluated before exposure to CM for CI-AKI risk assessment[13]. Patients with renal transplants are at an increased risk for CI-AKI due to the high prevalence of diabetes, renal insufficiency, and the use of nephrotoxic drugs (e.g., cyclosporine and nephrotoxic antibiotics)[14]. The incidence of CI-AKI in such patients is approximately 21.2%[14].

Table 1 Clinical pearls for contrast-induced acute kidney injury in every day clinical practice.
Risk factors-complications
    Serum creatinine elevation occurs within 48-72 hours after the injection of the CM, with the first 24 hours post-exposure are crucial to the development of CI-AKI
    Patients with preexisting CKD, elderly, and renal transplant recipients are at increased risk for CI-AKI development
    Renal function via serum creatinine and eGFR calculation should be evaluated in high-risk patients before exposure to CM for CI-AKI risk assessment
    Other notable complications of CM exposure: Myocardial infarction, shock, stroke, death, longer in-hospital stays
Prevention
    CM considerations: Apply non-ionic, hypo-osmolar CM at lowest dose, prewarm at 37 °C
    Discontinue nephrotoxic drugs: Non-steroidal anti-inflammatory drugs, aminoglycosides, metformin
    Periprocedural hydration with normal saline in patients at risk:
        Three mL/kg/hour 1 hour before to 4 hours after the procedure
        One mL/kg/hour 12 hours before to 12 hours after the procedure
    Individualized use of specialized systems (RenalGuard/DyeVert) in coronary procedures

Diabetes is a risk factor in the case of underlying renal impairment[15]. Morabito et al[16] detected a comparable incidence of CI-AKI in non-diabetic and diabetic patients with preserved renal function and without other risk factors who underwent coronary angiography or Percutaneous Coronary Intervention (PCI)[16]. The incidence of CI-AKI depends on the value of serum creatinine. For serum creatinine levels ≤ 2 mg/dL, 2-4 mg/dL, and ≥ 4 mg/dL, the incidence of CI-AKI was 5.7%, 29.4%, and 81%, respectively[16]. Moreover, pre-diabetes (fasting serum glucose between 100 and 125 mg/dL) increases the incidence of CI-AKI through the enhanced synthesis of reactive oxygen species (ROS) and activated renin-angiotensin–aldosterone system[17]. Toprak et al[17] in a study of 421 patients (137 with diabetes, 140 with prediabetes, 140 normoglycemic) who underwent coronary angiography found that CI-AKI occurred in 20% of diabetic patients, 11.4% of pre-diabetic patients, and 5.5% of normoglycemic patients. The increase in serum creatinine was significantly higher in diabetic patients (absolute increase in serum creatinine 0.33 ± 0.08 mg/dL) and pre-diabetic patients (absolute increase in serum creatinine 0.22 ± 0.32 mg/dL) than in normoglycemic patients (absolute increase in serum creatinine 0.11 ± 0.06 mg/dL)[17]. Hemodialysis was required in 3.6% of diabetic patients, 0.7% of pre-diabetic patients, and none of the normoglycemic patients[17].

Patients older than 75 years have a 2-5-fold increased risk of CI-AKI[18]. Every one-year increment after 75 years increases the risk of the occurrence of CI-AKI by 2%[18]. The etiology is multifactorial, including age-related alterations in renal function [diminished glomerular filtration rate (GFR), tubular secretion, and concentrating ability][18]. The elderly also have an increased propensity for vasoconstriction from excessive angiotensin II and endothelin and higher levels of oxidatively modified biomarkers[18]. Renal function in the elderly should be evaluated before intravascular exposure to CM[18].

Outcomes

Patients who underwent CM procedures and developed CI-AKI experienced longer in-hospital stays than patients who did not develop CI-AKI. In a study of 1111 Israeli hospitalized patients in 2006, the average in-hospital length of stay was almost twice as long among patients with CI-AKI compared to patients without CI-AKI[19]. Turan et al[20] reported a mean in-hospital stay of 9 (7-16) days in 30 NSTEMI patients who underwent a CM procedure and developed CI-AKI compared to 7 (5-9) days in 282 NSTEMI patients who did not develop CI-AKI.

Patients developing CI-AKI more frequently exhibit procedural cardiac complications, including myocardial infarction (even requiring emergency coronary artery bypass grafting), hypotension, shock, use of intra-aortic balloon pump, and cardiac arrest[21]. Furthermore, procedural complications occurred more frequently in patients who developed CI-AKI and included femoral bleeding, hematoma, pseudoaneurysm, stroke, acute respiratory distress syndrome, pulmonary embolism, and gastrointestinal bleeding[21].

Patients who develop CI-AKI also have a higher in-hospital mortality rate when compared with those who do not. McCullough et al[10] in a study of 1826 patients undergoing coronary interventions, reported a 7.1% in-hospital mortality rate in patients with CI-AKI vs 1.1% in patients without CI-AKI. The in-hospital mortality rate for patients with CI-AKI requiring dialysis was 35.7%[10]. Nearly one-third of patients who require in-hospital dialysis because of CI-AKI die before discharge[10]. The increased in-hospital mortality rate was additionally reported by Rihal et al[21] in a large randomized clinical trial (RCT) of 7586 PCI patients (22% in patients who developed CI-AKI vs 1.4% in patients who did not, respectively). In-hospital mortality rates are low (approximately 0.7%) for patients with CI-AKI without preexisting renal disease and diabetes mellitus[21].

Patients with CI-AKI also experience diminished long-term survival. According to Sadeghi et al[22], the one-year mortality rate in CI-AKI patients is 23.3%, compared to 3.2% in those who do not develop CI-AKI. CI-AKI significantly impacts long-term survival, particularly in patients with pre-existing renal disease. Gruberg et al[7], in a study involving 439 patients with pre-existing renal disease undergoing coronary interventions, reported a 37.7% one-year mortality rate for patients with preexisting renal disease who developed CI-AKI, compared to 19.4% for patients who did not have pre-existing chronic renal disease and developed CI-AKI. Additionally, diabetes mellitus contributes to increased long-term mortality rates, with a one-year mortality rate of 25.9% in diabetic patients who developed CI-AKI[23]. Last but not least, the analysis of 7287 patients (476 with CI-AKI) included in a prospective multicenter registry showed that 2-year net adverse clinical events occurred at a greater frequency in those affected by CI-AKI compared to those who did not (adjusted hazard ratio: 1.88)[24]. CKD was an additional aggravating factor (CI-AKI + CKD hazard ratio 3.29 with reference no CI-AKI + no CKD)[24].

PATHOPHYSIOLOGY OF CI-AKI

CI-AKI is thought to stem from renal medulla hypoxia, culminating in acute tubular necrosis, as opposed to direct toxic damage to renal tubules[25,26]. The renal tubule toxicity induced by CM directly promoting apoptosis is attributed to the suppression of mitochondrial enzyme activity[26]. Hypoxia in the renal medulla is the result of a reduction in vasa recta perfusion, heightened oxygen consumption by epithelial tubular cells, and alterations in medullary vasculature, further diminishing blood flow in the outer renal medulla[26]. This outer region is already poorly perfused under normal circumstances, as it is located distantly from the descending vasa recta[26]. Osmosis caused by CM contributes to heightened pressure in the interstitium and enhanced mobilization of sodium due to the entrainment of water in the renal tubule[26]. Ultimately, compressed vasa recta and peritubular capillaries are noted, as well as elevated blood viscosity, which together decrease vasa recta perfusion and exacerbate the hypoxic injury in the renal medulla[27]. Additionally, water is reabsorbed to a lesser extent in the presence of CM in the renal tubule, resulting in greater intraluminal pressure and diminished filtration from glomerular capillaries. This enhances sodium transport[28], raising oxygen consumption from the epithelial cells in the renal tubule, thus aggravating the hypoxic insult in the renal medulla[27]. Adenosine also has constrictive effects, thereby decreasing the GFR. This results in lower sodium delivery, further contributing to decreased oxygen use[29]. Medullary vasoconstriction due to CM is also evident due to the action of released endothelin and prostanoids by endothelial cells through the activation of prostaglandin E2 receptors 1 and 3 and endothelin receptor A[30]. Endothelin-induced vasoconstriction is more pronounced in subjects with preexisting renal disease[26]. The combination of adenosine catabolism and hypoxic renal medulla generates free radicals that scour nitric oxide (NO), resulting in weakened vasodilatory response[29]. Furthermore, impaired NO bioavailability boosts sodium reabsorption, leading to greater oxygen spending and hypoxia in the renal medulla[31].

PREVENTION OF CI-AKI
CI-AKI risk stratification

Mehran et al[32] devised a straightforward risk score to predict CI-AKI and the need for dialysis following PCI based on their study of 8357 patients. Each risk factor is assigned a weighted integer score, and the cumulative score has a predictive power for the incidence of CI-AKI, as well as the requirement for renal replacement therapy[32]. Recently, there have been emerging prognosticators of CI-AKI, particularly in patients undergoing coronary interventions in the setting of an acute coronary syndrome, namely the Athens Score or the PRECISE-DAPT[33,34]. Nevertheless, considering that renal function significantly influences CI-AKI incidence, estimating GFR remains the most practical method for risk stratification. This is especially pertinent in patients with certain characteristics such as the elderly, and those with diabetes mellitus, arterial hypertension, and CKD[35,36].

CM considerations

Concerning CM, it is recommended that a non-ionic and hypo-osmolar or iso-osmolar CM is administered at the lowest dose possible, especially for individuals at risk of CI-AKI[37]. Notably, CI-AKI requiring dialysis after PCI did not occur with CM doses below 100 mL[38]. Additionally, the concept of zero-contrast PCI, facilitated by Intravascular Ultrasound or Optical Coherence Tomography, may emerge as a viable alternative for patients with CKD undergoing coronary procedures[39,40]. However, even doses below 100 mL of CM can potentially induce CI-AKI in patients with both CKD and diabetes mellitus, particularly when the iodine concentration of CM ranges from 140-400 mg/mL[41,42]. Safety predictors for CI-AKI extend beyond contrast volume alone. Ratios such as the volume of CM to baseline creatinine clearance less than 3, the volume of CM to baseline estimated GFR (eGFR) less than 5.1, or the grams of iodine of CM to baseline eGFR less than 1 are considered more reliable indicators[43,44]. While automated contrast injector systems reduce the administered CM volume, there is no significant difference in the incidence of CI-AKI or the need for dialysis[45]. In a recent analysis of 182196 consecutive patients who underwent PCI over a 7-year period (2010-2016) to document the trends in CM volume use, Gurm et al[46] noted a decline in mean CM volume from 197 to 168 mL, as well as in the mean ratio of CM volume to GFR (from 2.91 to 2.51). The percentage of patients with a ratio of CM/GFR ≥ 3 was also significantly diminished (from 36% to 25%)[46].

Optimal CM administration is based on prewarming to 37 °C, as well as adequate dilution to lower its viscosity[47]. In patients with circulatory collapse or severe congestive heart failure, CM administration should be postponed until an improvement in hemodynamic parameters is achieved[37,48]. Repeated doses of CM ought to be postponed for 48 hours in patients at low risk for CI-AKI, extended to 72 hours for high-risk patients, in cases of CI-AKI, subsequent CM administration must be avoided until resolution of the acute event[37]. If procedural delays are feasible, an interval of 2-3 weeks is deemed reasonable in such cases[49].

Discontinuation of nephrotoxic drugs

In managing the risk of CI-AKI, the cessation of concurrent nephrotoxic drugs, particularly non-steroidal anti-inflammatory drugs, aminoglycosides, amphotericin-B, high-dose loop diuretics, and antivirals, could be considered prior to and following the procedure[50]. If feasible, the examination should be postponed to mitigate the cumulative impact of nephrotoxic drugs and CM[37]. Additionally, metformin discontinuation is advised 48 hours before the procedure and can be reinstated after assessing renal function in diabetic patients with severely impaired renal function (eGFR < 30 mL/min/1.73 m2)[50]. While metformin is not considered a direct risk factor for CI-AKI, caution is exercised due to its kidney excretion and stimulation of intestinal lactic acid production, which could lead to lactic acidosis in the event of CI-AKI[51].

There is ongoing debate regarding the discontinuation of renin-angiotensin system-blocking drugs. While some argue that there is no need to interrupt angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs) before CM exposure[52], the CAPTAIN study reported a higher incidence of CI-AKI in patients who continued these medications compared to those who withheld them[53]. A meta-analysis also indicated an increased CI-AKI risk, especially in elderly patients and those with CKD[54]. Considering the controversial findings, discontinuation of ACE inhibitors or ARBs could be contemplated, particularly in these subpopulations, 48 hours before the procedure, with reinstitution post-evaluation for CI-AKI[36].

Ischemic conditioning

Another technique that has been used for CI-AKI prevention is remote Ischemic Conditioning (RIC). Walsh et al[55] were among the first to document its effectiveness in 40 patients in whom endovascular aortic aneurysm repair was performed. Additional RCTs have since been performed, highlighting a benefit from RIC, irrespective of timing (pre or post-ischemic)[56,57]. A recent meta-analysis of 16 RCTs proved that RIC led to lower CI-AKI rates, along with fewer major adverse cardiovascular events based on a follow-up of 6 months, with hydration defined as an important contributor[58]. Despite those encouraging preliminary findings, RIC is not considered a standard of care for CI-AKI prevention, with additional studies being awaited.

Hydration

Periprocedural hydration has long been considered a fundamental approach for preventing CI-AKI in both renal-impaired and non-impaired patients[59,60]. The positive impact of hydration was initially elucidated in a study involving 78 CKD patients who underwent angiography[61]. The underlying mechanism involves volume expansion-induced inhibition of the renin-angiotensin-aldosterone system (RAAS), leading to the attenuation of renal vasoconstriction and hypoperfusion. Simultaneously, the increased concentration of renal prostaglandins is associated with vasodilatory actions. Furthermore, the dilution of intratubular CM and increased diuresis restrict the interaction of CM with renal tubular cells, lowering the risk of direct renal tubular toxicity[62].

The optimal route of hydration, whether enteral or parenteral, for preventing CI-AKI lacks clear evidence. A meta-analysis of eight studies involving 1754 participants demonstrated the noninferiority of oral hydration compared to IV hydration in preventing CI-AKI during coronary angiography[63]. Mueller et al[64] concluded that prophylactic hydration with isotonic saline 0.9% (809 patients, CI-AKI incidence 0.7%) was superior to saline 0.45% (811 patients, CI-AKI incidence 2%), especially in women, patients with diabetes mellitus, or those receiving equal or more than 250 mL of CM. Standard clinical practice typically involves IV isotonic saline administration at a rate of 1 mL/kg/h, initiated 3-4 hours before and continued for 4-6 hours after the procedure[50].

The groundbreaking AMACING trial introduced controversy, suggesting that no intervention was non-inferior to IV infusion of 0.9% saline, as recommended by current guidelines for CI-AKI prevention[65]. This approach was not only cost-effective but also demonstrated no subgroup differences based on eGFR, diabetes mellitus status, or the type of procedure. However, complications arised in a significant proportion of saline hydrated patients, such as symptomatic heart failure, emphasizing the need for cautious administration[65]. Long-term results showed no differences in mortality or renal function metrics during a 1-year follow-up[66]. The CI-AKIART study, following these results, advocated for a more restricted prophylactic hydration approach, recommending its administration only in patients with eGFR < 30 mL/min/1.73 m²[67]. Recently, in a multicenter, open-label, randomized controlled study involving 1002 patients with CKD (eGFR 15-60 mL/min/1.73 m2) undergoing coronary angiography, Liu et al[68] showed that a simplified hydration protocol of normal saline from 1 hours before to 4 hours after CAG at a rate of 3 mL/kg/hour was non-inferior to the standard hydration protocol (12 hours before and 12 hours after) in terms of CI-AKI occurrence, acute heart failure, or major adverse cardiovascular events at 1 year. The analysis of subgroups revealed a similar magnitude of effect irrespective of age, sex, eGFR, contrast volume administered, contrast volume/eGFR, or the presence of congestive heart failure[68]. The rate of the CI-AKI was also lower with the simplified hydration protocol in those undergoing PCI[68].

Methods assessing intravascular volume, including left ventricular end-diastolic pressure (LVEDP) or Central Venous Pressure, may reduce CI-AKI risk in CKD or heart failure patients by guiding the degree of IV hydration[69-73]. In the randomized study of 469 patients with ST-elevation myocardial infarction undergoing primary PCI, CI-AKI rates were lower in the LVEDP-guided aggressive hydration group, without an increase in acute heart failure incidence when compared to standard hydration (0.9% saline at 1 mL/kg/hour for 6 hours after randomization)[74]. However, another recent RCT with 114 patients undergoing coronary angiography failed to demonstrate the superiority of LVEDP-guided hydration over routine hydration for preventing CI-AKI[75]. Aggressive hydration guided by the Vigileo/FloTrac system has also been attempted in a randomized controlled study of 344 patients with acute myocardial infarction undergoing urgent PCI[76]. The investigators found a remarkably lower CI-AKI incidence in the intervention group compared to control (12.1% vs 22.2%) associated with a significantly greater mean volume received (1910 vs 440 mL), without increased rates of acute heart failure[76].

A balanced hydration strategy, involving temporary forced diuresis with furosemide with matched hydration via the RenalGuard System, has been proposed (Table 2). Dorval et al[77] studied high-risk patients undergoing a CM procedure and reported lower than predicted CI-AKI rates (9.5% vs 14.5%-55%) with RenalGuard balanced hydration. Moreover, in patients undergoing transcatheter aortic valve implantation (TAVI), RenalGuard hydration demonstrated significant CI-AKI protection[78]. Briguori et al[79] proved the advantage of RenalGuard compared to LVEDP-guided hydration, demonstrating noteworthy reductions in CI-AKI occurrence and one-month major adverse events in patients undergoing vascular procedures. It should be noted that RenalGuard-guided group exhibited a higher rate of hypokalemia[79]. There have also been studies with neutral outcomes, such as the REDUCE-AKI randomized, sham-controlled clinical trial that failed to detect a benefit of RenalGuard in patients undergoing TAVI, with indications of an increased long-term mortality in the treatment group[80]. In the STRENGTH trial of patients with CKD undergoing complex coronary, structural, or peripheral procedures, RenalGuard did not offer additional protection against CI-AKI and other adverse outcomes compared to standard hydration[81]. Similarly, patients with CKD undergoing TAVI did not gain any benefit from RenalGuard in the study of Voigtländer-Buschmann et al[82]. According to the meta-analysis of Wang et al[83], the RenalGuard system can reduce the risk of CI-AKI in patients undergoing PCI but not in those undergoing TAVI. Considering the existing evidence, RenalGuard’s routine use is not advised, especially in TAVI procedures, but it could be employed on a case-by-case basis (Table 2)[84-90].

Table 2 Clinical evidence on the role of RenalGuard for the prevention of contrast-induced acute kidney injury in patients at risk.
Ref.
Patients
Study design
Preventive strategy
Outcome
Briguori et al[79]702RCTRenalGuardLess CI-AKI, PE and 1-month MAE
LVEDP-guided hydration
Katoh et al[84]60 (Japanese)ObservationalRenalGuardHigh UFR associated with less CI-AKI
Chorin et al[85]300ObservationalRenalGuardNet decrease in eGFR and CI-AKI incidence
Isotonic saline
Visconti et al[78]48Non-randomizedRenalGuardProtective against CI-AKI (OR 0.71)
SB
Briguori et al[86]400ObservationalRenalGuardEffective in reaching the target UFR (≥ 450 mL/h)
Barbanti et al[87]112RCTRenalGuardReduced incidence of CI-AKI
Isotonic saline
Briguori et al[88]292RCTRenalGuard (NAC + SB)Lower CI-AKI and in-hospital dialysis incidence
NAC + SB
Arbel et al[80]136RCTRenalGuard-activeSimilar CI-AKI incidence
RenalGuard-shamIncreased long-term mortality in active group
Mauler-Wittwer et al[81]259RCTRenalGuardSimilar CI-AKI incidence at day 3
Isotonic salineNo difference in secondary outcomes
Voigtländer-Buschmann et al[82]100RCTRenalGuardSimilar CI-AKI incidence
Isotonic salineSimilar 30-day and 12-month mortality rates
Ben-Haim et al[89]58Non-randomizedRenalGuardRenalGuard was an independent predictor of lower Renal CM accumulation score
Isotonic saline
None
Mirza et al[90]1205RCTRenalGuard (non-automated)Significantly lower incidence of CI-AKI with RenalGuard
Isotonic saline
Sodium bicarbonate

Bicarbonate serves to mitigate the acidification of renal tubular fluid, diminishing pH-dependent ROS formation, and enhancing ROS neutralization. According to a CI-AKI Consensus Working Panel of KDIGO, a potential but inconsistent advantage of isotonic bicarbonate over saline solutions in preventing CI-AKI was suggested[91]. This arises from the controversy in RCTs comparing the renoprotective effects of sodium bicarbonate and sodium chloride infusions[91]. However, Brar et al[92], in a study involving 353 patients undergoing coronary angiography with either sodium chloride or sodium bicarbonate, explored outcomes beyond CI-AKI (death, dialysis, myocardial infarction, stroke) and found no significant benefit with sodium bicarbonate infusion.

In a meta-analysis by Jang et al[93], the preventive effects of saline vs sodium bicarbonate for CI-AKI were compared, revealing beneficial results with sodium bicarbonate administration. Notably, there was no difference in the need for renal replacement therapy and mortality, while side effects consisted of serum bicarbonate and potassium abnormalities[93]. Conversely, a meta-analysis of 14 RCTs by Zoungas et al[94] showed no significant difference in efficacy between sodium bicarbonate and sodium chloride. The PRESERVE trial, involving 5177 high-risk patients undergoing angiography, failed to document a benefit of sodium bicarbonate over IV saline in preventing CI-AKI, the requirement of renal replacement therapy, or death[95]. The recently reported TEATE trial showed that even though IV or oral sodium bicarbonate administration led to more frequent urine alkalization (pH > 6), the difference in the rates of CI-AKI was not significant compared to standard saline hydration[96]. Nonetheless, sodium bicarbonate is considered more convenient for emergent procedures and cost-efficient compared to saline. Thus, the decision to use it should be based on an individualized approach[91,97].

N-acetylcysteine

N-acetylcysteine (NAC) possesses antioxidant and vasodilatory properties, acting by scavenging ROS, increasing NO synthase expression, competing with superoxide radicals for NO, forming S-nitrosothiol with vasodilatory effects, inhibiting vascular cell adhesion molecule-1 expression in glomerular mesangial cells who are in charge of inflammatory cell recruitment, and promoting glutathione production[98-100]. However, a CI-AKI-protective effect remains controversial, and no evidence suggesting a reduction in the need for dialysis in patients developing CI-AKI after receiving NAC. Marenzi et al[101] reported an effect of NAC which was dose-dependent, but this finding has not been consistently confirmed. Moreover, Hoffmann et al[102] concluded showed that creatinine metabolism might be influenced by NAC administration, rather than renal function, based on a study involving 50 healthy subjects not receiving CM but administered NAC.

A meta-analysis by Adabag et al[103], covering RCTs with oral or IV NAC administration (10 RCTs, 1163 patients), found no significant impact of NAC against CI-AKI (NAC group: 35%, Control group: 37%). In another meta-analysis of 10 RCTs (1163 patients), the CI-AKI rates were lower in the NAC group compared to the control group (7.9% vs 14.3%)[104].Considering the overall evidence, however, the use of NAC is currently not recommended.

Statins

Beyond their hypolipidemic effects, statins exhibit antioxidative and anti-inflammatory actions[105], potentially conferring renoprotection. They reduce ROS formation by enhancing heme oxygenase-1 protein production, an antioxidant protein that interferes with NADPH oxidase activity[106]. Studies on the efficacy of statins in preventing CI-AKI have yielded debatable outcomes. While most studies demonstrated a benefit, others showed minimal or no protective effect against CI-AKI. It's important to note that the majority of these studies focused on patients undergoing coronary procedures, limiting the generalizability of conclusions to this specific study population.

A meta-analysis by Zhang et al[107] suggested that a high dose of statins could reduce the incidence of CI-AKI. Zhou et al[108] found that statin administration was efficient primarily in patients with significant renal dysfunction. On the contrary, Zhang et al[109] showed that statins had a negligible impact in CI-AKI prevention. Additionally, Liu et al[110] meta-analyzed 9 RCTs (2560 statin-treated patients, 2583 control), observed a 53% decreased risk of CI-AKI and a reduced need for dialysis in the statin group. In another meta-analysis of 9 RCTs, Liu et al[111], reported that administering high doses of atorvastatin before coronary angiography significantly lowered CI-AKI incidence compared to low-dose statins or placebo. Lastly, Li et al[112], in their meta-analysis of 21 RCTs involving 7746 patients undergoing coronary angiography/PCI, confirmed the efficacy of short-term statin administration for preventing CI-AKI, despite the heterogeneity of the study group.

Despite these positive findings, questions remain unanswered regarding the optimal statin choice, timing, and dosage. However, their use is permitted, especially in patients undergoing coronary procedures. Giacoppo et al[113], in a Bayesian meta-analysis spanning two decades (124 trials, 28240 patients, 10 different preventive regimens), established that statins were the only preventive approach consistently and significantly preventing CI-AKI compared to saline.

Other antioxidants

Ascorbic acid, with its antioxidant properties scavenging ROS and vasodilatory effects[114], has been investigated for its potential in preventing CI-AKI. However, the limited number of studies and inconsistent data currently do not support its use in this setting[115-119].

Tocopherols, specifically vitamin E, act as ROS inhibitors, enhance NO activity, and improve mitochondrial membrane function[120]. Despite positive results in some studies, the limited number of investigations assessing the efficacy of vitamin E (α or γ tocopherol) for CI-AKI prevention does not warrant its current recommendation for prophylaxis[121-123].

Allopurinol, a xanthine oxidase inhibitor, restricts ROS formation following CM exposure[124]. While some studies demonstrate its beneficial action, others do not consistently support its efficacy for preventing CI-AKI[125-128]. In a meta-analysis of 5 RCTs involving 754 patients, allopurinol showed efficacy in high-risk CI-AKI patients undergoing PCI[129]. However, further investigation through large-scale RCTs is necessary to establish allopurinol as a recommended preventive agent for CI-AKI.

Calcium channel blockers

Calcium overload contributes to the pathogenesis of CI-AKI, as the sodium/calcium exchanger system plays a role in intracellular calcium overload, especially in hypoxic conditions induced by CM injection[130]. In this context, the reversal of transport leads to intracellular Ca2+ overload, contributing to tubular epithelial cell apoptosis. Calcium channel blockers (CCBs) may exert a renoprotective effect by inhibiting intracellular calcium overload, as initially demonstrated by Yang et al[131] and Neumayer et al[132] in a study of 35 patients who received intravascular CM along with oral nitrendipine, resulting in significant preservation of GFR. Russo et al[133] further supported the efficacy of CCBs in CI-AKI prophylaxis in a study of 30 patients without risk factors during intravenous pyelography, where nifedipine administration showed positive effects. Additionally, Yin et al[134] documented the effectiveness of amlodipine administration prior to CM administration in a cohort of 2666 hypertensive patients, by reducing the incidence of CI-AKI as well as the long-term survival.

Conversely, Khoury et al[135], in a study of 85 patients undergoing radiologic examinations involving CM infusion, found no statistically significant difference in serum creatinine increase between the control and nifedipine groups. The positive effect of nitrendipine was not established by Carraro et al[136] in a RCT with 121 patients who underwent arteriography after its administration for CI-AKI prevention. Moreover, Arici et al[137] failed to demonstrate a protective effect of amlodipine in an RCT with 29 patients undergoing coronary angiography, as it had no impact on serum creatinine levels. In conclusion, due to controversial data, the use of CCBs in the prophylaxis of CI-AKI is not recommended.

Other vasoactive agents

Atrial natriuretic peptide (ANP), an endogenous natriuretic compound produced by cardiac myocytes in atria, demonstrates increased levels following CM injection, particularly in patients with underlying diabetes or preexisting renal disease[138,139]. ANP's actions include attenuating the reduction of GFR by increasing sodium delivery to the distal nephron through tubuloglomerular feedback[138,139]. Studies evaluating ANP's protective effect in CI-AKI prophylaxis yield controversial results, necessitating further research[140,141]. Similarly, recombinant brain natriuretic peptide is being studied for CI-AKI prevention[142,143], with its actions encompassing vasodilation, reduction of preload and afterload, inhibition of cardiac remodeling, the RAAS, sympathetic nervous system, as well as adenosine and endothelin release. However, conclusive data confirming its efficacy are awaited.

Trimetazidine, a drug used in stable coronary artery disease, inhibits β-oxidation of fatty acids, leading to glucose oxidation, thereby requiring less oxygen and ensuring adequate energy utilization in ischemic conditions[144]. Despite a notable reduction in CI-AKI incidence in high-risk patients, limited RCTs hinder its current recommendation[145,146].

Prostaglandin E1 and prostacyclin (PGI2) promote vasodilation, enhancing kidney perfusion and alleviating CM-induced hypoxic injury to the medulla[147]. Earlier studies have already pointed towards their potential in CI-AKI prevention[148-152]. In a recently reported RCT of 1146 individuals undergoing PCI, alprostadil was an independent protective factor towards CI-AKI in patients at moderate and high risk according to the Mehran risk score when compared to placebo, potentially driven by an anti-inflammatory action[153]. Moreover, according to a systematic review and meta-analysis by Xu et al[154], alprostadil use on top of hydration was related to a lower risk of CI-AKI as well as ameliorated renal function biomarkers (serum creatinine, blood urea nitrogen, serum cystatin, neutrophil gelatinase-associated lipocalin, urine macroglobulin). Despite the available evidence, the lack of a large-scale RCT testing alprostadil’s efficacy in this setting is a deterring factor in its routine use. Ongoing is a RCT assessing the effectiveness of alprostadil liposome injection for CI-AKI prevention in patients with CKD and an additional risk factor for CI-AKI undergoing PCI (NCT05475717).

Theophylline, acting as an adenosine antagonist with vasodilatory and antioxidative effects, inhibits adenosine production stimulated by CM. A meta-analysis by Dai et al[155] suggested a significant beneficial effect of theophylline infusion for CI-AKI prevention. However, inconsistent findings in studies by Bagshaw and Ghali[156], and Kelly et al[157] warrant cautious consideration, and, as of now, theophylline use is not recommended for CI-AKI prophylaxis[155-157].

Hemodialysis-hemofiltration

The removal of CM from the bloodstream can be achieved through renal replacement therapy following the CM-requiring procedure. A single hemodialysis session can eliminate 60%-90% of the administered CM, while peritoneal dialysis can also achieve similar results but requires a longer duration than hemodialysis[158]. Despite several RCTs investigating the potential protective effect of hemodialysis on CI-AKI prophylaxis, a significant reduction in the incidence of CI-AKI was not consistently demonstrated[159-163]. The reasons for the lack of benefit from hemodialysis are not fully understood, with possibilities including rapid onset of renal injury post-CM administration or potential nephrotoxicity of hemodialysis[159].

In a notable RCT of 114 patients undergoing coronary interventions, Marenzi et al[164] demonstrated the potential of hemofiltration in comparison to hydration. Conversely, in a small-sized trial, hemodialysis was proven superior to hemofiltration regarding CM removal[165]. A pilot study highlighted the positive impact of high-flow intermittent hemodiafiltration both prior to and following angiography of coronary and peripheral arteries, against hydration, in individuals at risk of CI-AKI[166]. The study reported no such incidents, along with a steeper renal function decline at 1 year[166]. Although hemofiltration may reduce the risk of CI-AKI, its cost, the need for intensive care unit admission, and associated risks necessitate further studies to establish its benefit and cost-effectiveness.

Contrast removal-reduction systems

A novel approach involves removing the majority of injected CM from the coronary sinuses before it enters the systemic circulation during coronary angiography. This is achieved by inserting a catheter into the coronary sinus through the right femoral vein and transferring blood into an extracorporeal contrast-absorbing column. While effective in reducing CI-AKI incidence, this technique faces challenges with a high failure rate (57%), limiting its clinical applicability[165,167]. a new contrast reduction system known as DyeVert was utilized to prevent CI-AKI by minimizing residual CM administration and aortic reflux. A study involving 96 patients undergoing coronary angiography assessed its effectiveness, demonstrating reduced CM exposure without compromising image quality[168]. In 451 patients with acute coronary syndromes that ultimately underwent diagnostic and therapeutic coronary interventions, DyeVert resulted in a lower incidence of CI-AKI (DyeVert: 8% vs control: 19%)[169]. In a recent study of 136 patients undergoing PCI for stable coronary artery disease, DyeVert emerged superior to LVEDP-guided hydration in terms of creatinine increase and CI-AKI occurrence[170]. DyeVert may be extremely useful in cases of chronic total occlusion revascularizations, where large volumes of CM are usually required. Tajti et al[171] showed that its use is feasible in this setting, significantly reducing the amount of administered CM. Notably, a UK-based cost-utility analysis revealed significant cost savings and improved quality of life with the use of DyeVert[172]. Such findings were replicated in a hypothetical cohort of 1000 patients with stage 3b-4 CKD undergoing PCI, with DyeVert being more effective and less costly compared to standard of care[173]. Last but not least, we should mention the results of the latest RCT of 550 patients with acute MI (74.5% with STEMI) undergoing PCI, who were randomized to either CM volume reduction through the DyeVert system or manual/automatic CM injection syringe[174]. A lower CM volume was recorded in the DyeVert group (95 ± 30 mL vs 160 ± 23 mL) and fewer CI-AKI events (16% vs 24.3%, absolute risk difference: -8.3%)[174].

CONCLUSION

CI-AKI, an iatrogenic complication of procedures requiring CM administration, has an overall low incidence in the general population which increases in the presence of risk factors, namely pre-existing renal disease. Managing CI-AKI is largely dependent on its prevention. This is achieved by precise risk stratification, appropriate choice and handling of CM, and interruption of agents that are potentially associated with nephrotoxicity. Prevention is the cornerstone of CI-AKI management starting with risk assessment, application of CM-related measures, and withholding of nephrotoxic drugs. Despite the plethora of clinical trials that have been conducted in this setting, no measure appears to have an unequivocal effect in preventing CI-AKI, with hydration being the most well-characterized. Modern approaches such as the RenalGuard balanced hydration and contrast manipulation systems may be of use in certain clinical scenarios but are not widely available in everyday practice.

Footnotes

Provenance and peer review: Invited article; Externally peer reviewed.

Peer-review model: Single blind

Specialty type: Radiology, nuclear medicine and medical imaging

Country of origin: Greece

Peer-review report’s classification

Scientific Quality: Grade B

Novelty: Grade A

Creativity or Innovation: Grade B

Scientific Significance: Grade B

P-Reviewer: Kotlyarov S S-Editor: Li L L-Editor: A P-Editor: Che XX

References
1.  van der Molen AJ, Reimer P, Dekkers IA, Bongartz G, Bellin MF, Bertolotto M, Clement O, Heinz-Peer G, Stacul F, Webb JAW, Thomsen HS. Post-contrast acute kidney injury - Part 1: Definition, clinical features, incidence, role of contrast medium and risk factors: Recommendations for updated ESUR Contrast Medium Safety Committee guidelines. Eur Radiol. 2018;28:2845-2855.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 207]  [Cited by in F6Publishing: 272]  [Article Influence: 45.3]  [Reference Citation Analysis (0)]
2.  Nash K, Hafeez A, Hou S. Hospital-acquired renal insufficiency. Am J Kidney Dis. 2002;39:930-936.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1317]  [Cited by in F6Publishing: 1248]  [Article Influence: 56.7]  [Reference Citation Analysis (0)]
3.  Solomon R. Contrast-medium-induced acute renal failure. Kidney Int. 1998;53:230-242.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 162]  [Cited by in F6Publishing: 166]  [Article Influence: 6.4]  [Reference Citation Analysis (0)]
4.  Solomon RJ, Mehran R, Natarajan MK, Doucet S, Katholi RE, Staniloae CS, Sharma SK, Labinaz M, Gelormini JL, Barrett BJ. Contrast-induced nephropathy and long-term adverse events: cause and effect? Clin J Am Soc Nephrol. 2009;4:1162-1169.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 199]  [Cited by in F6Publishing: 213]  [Article Influence: 14.2]  [Reference Citation Analysis (0)]
5.  Chong E, Poh KK, Liang S, Tan HC. Risk factors and clinical outcomes for contrast-induced nephropathy after percutaneous coronary intervention in patients with normal serum creatinine. Ann Acad Med Singap. 2010;39:374-380.  [PubMed]  [DOI]  [Cited in This Article: ]
6.  Dangas G, Iakovou I, Nikolsky E, Aymong ED, Mintz GS, Kipshidze NN, Lansky AJ, Moussa I, Stone GW, Moses JW, Leon MB, Mehran R. Contrast-induced nephropathy after percutaneous coronary interventions in relation to chronic kidney disease and hemodynamic variables. Am J Cardiol. 2005;95:13-19.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 408]  [Cited by in F6Publishing: 415]  [Article Influence: 21.8]  [Reference Citation Analysis (0)]
7.  Gruberg L, Mintz GS, Mehran R, Gangas G, Lansky AJ, Kent KM, Pichard AD, Satler LF, Leon MB. The prognostic implications of further renal function deterioration within 48 h of interventional coronary procedures in patients with pre-existent chronic renal insufficiency. J Am Coll Cardiol. 2000;36:1542-1548.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 535]  [Cited by in F6Publishing: 502]  [Article Influence: 20.9]  [Reference Citation Analysis (0)]
8.  Mehran R, Nikolsky E. Contrast-induced nephropathy: definition, epidemiology, and patients at risk. Kidney Int Suppl. 2006;S11-S15.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 494]  [Cited by in F6Publishing: 541]  [Article Influence: 30.1]  [Reference Citation Analysis (0)]
9.  McCullough PA, Sandberg KR. Epidemiology of contrast-induced nephropathy. Rev Cardiovasc Med. 2003;4 Suppl 5:S3-S9.  [PubMed]  [DOI]  [Cited in This Article: ]
10.  McCullough PA, Wolyn R, Rocher LL, Levin RN, O'Neill WW. Acute renal failure after coronary intervention: incidence, risk factors, and relationship to mortality. Am J Med. 1997;103:368-375.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1214]  [Cited by in F6Publishing: 1146]  [Article Influence: 42.4]  [Reference Citation Analysis (0)]
11.  Scanlon PJ, Faxon DP, Audet AM, Carabello B, Dehmer GJ, Eagle KA, Legako RD, Leon DF, Murray JA, Nissen SE, Pepine CJ, Watson RM, Ritchie JL, Gibbons RJ, Cheitlin MD, Gardner TJ, Garson A Jr, Russell RO Jr, Ryan TJ, Smith SC Jr. ACC/AHA guidelines for coronary angiography. A report of the American College of Cardiology/American Heart Association Task Force on practice guidelines (Committee on Coronary Angiography). Developed in collaboration with the Society for Cardiac Angiography and Interventions. J Am Coll Cardiol. 1999;33:1756-1824.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 679]  [Cited by in F6Publishing: 659]  [Article Influence: 26.4]  [Reference Citation Analysis (0)]
12.  Hall KA, Wong RW, Hunter GC, Camazine BM, Rappaport WA, Smyth SH, Bull DA, McIntyre KE, Bernhard VM, Misiorowski RL. Contrast-induced nephrotoxicity: the effects of vasodilator therapy. J Surg Res. 1992;53:317-320.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 80]  [Cited by in F6Publishing: 85]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
13.  Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med. 1999;130:461-470.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11183]  [Cited by in F6Publishing: 11575]  [Article Influence: 463.0]  [Reference Citation Analysis (0)]
14.  Ahuja TS, Niaz N, Agraharkar M. Contrast-induced nephrotoxicity in renal allograft recipients. Clin Nephrol. 2000;54:11-14.  [PubMed]  [DOI]  [Cited in This Article: ]
15.  Parfrey PS, Griffiths SM, Barrett BJ, Paul MD, Genge M, Withers J, Farid N, McManamon PJ. Contrast material-induced renal failure in patients with diabetes mellitus, renal insufficiency, or both. A prospective controlled study. N Engl J Med. 1989;320:143-149.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 726]  [Cited by in F6Publishing: 652]  [Article Influence: 18.6]  [Reference Citation Analysis (0)]
16.  Morabito S, Pistolesi V, Benedetti G, Di Roma A, Colantonio R, Mancone M, Sardella G, Cibelli L, Ambrosino M, Polistena F, Pierucci A. Incidence of contrast-induced acute kidney injury associated with diagnostic or interventional coronary angiography. J Nephrol. 2012;25:1098-1107.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 31]  [Article Influence: 2.6]  [Reference Citation Analysis (0)]
17.  Toprak O, Cirit M, Yesil M, Bayata S, Tanrisev M, Varol U, Ersoy R, Esi E. Impact of diabetic and pre-diabetic state on development of contrast-induced nephropathy in patients with chronic kidney disease. Nephrol Dial Transplant. 2007;22:819-826.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 62]  [Cited by in F6Publishing: 62]  [Article Influence: 3.6]  [Reference Citation Analysis (0)]
18.  Bouzas-Mosquera A, Vázquez-Rodríguez JM, Calviño-Santos R, Peteiro-Vázquez J, Flores-Ríos X, Marzoa-Rivas R, Piñón-Esteban P, Aldama-López G, Salgado-Fernández J, Vázquez-González N, Castro-Beiras A. [Contrast-induced nephropathy and acute renal failure following emergent cardiac catheterization: incidence, risk factors and prognosis]. Rev Esp Cardiol. 2007;60:1026-1034.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 40]  [Cited by in F6Publishing: 44]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
19.  Shema L, Ore L, Geron R, Kristal B. Contrast-induced nephropathy among Israeli hospitalized patients: incidence, risk factors, length of stay and mortality. Isr Med Assoc J. 2009;11:460-464.  [PubMed]  [DOI]  [Cited in This Article: ]
20.  Turan B, Erkol A, Gül M, Fındıkçıoğlu U, Erden İ. Effect of Contrast-Induced Nephropathy on the Long-Term Outcome of Patients with Non-ST Segment Elevation Myocardial Infarction. Cardiorenal Med. 2015;5:116-124.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 13]  [Cited by in F6Publishing: 14]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
21.  Rihal CS, Textor SC, Grill DE, Berger PB, Ting HH, Best PJ, Singh M, Bell MR, Barsness GW, Mathew V, Garratt KN, Holmes DR Jr. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation. 2002;105:2259-2264.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1212]  [Cited by in F6Publishing: 1187]  [Article Influence: 54.0]  [Reference Citation Analysis (0)]
22.  Sadeghi HM, Stone GW, Grines CL, Mehran R, Dixon SR, Lansky AJ, Fahy M, Cox DA, Garcia E, Tcheng JE, Griffin JJ, Stuckey TD, Turco M, Carroll JD. Impact of renal insufficiency in patients undergoing primary angioplasty for acute myocardial infarction. Circulation. 2003;108:2769-2775.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 291]  [Cited by in F6Publishing: 300]  [Article Influence: 14.3]  [Reference Citation Analysis (0)]
23.  Nikolsky E, Mehran R. Understanding the consequences of contrast-induced nephropathy. Rev Cardiovasc Med. 2003;4 Suppl 5:S10-S18.  [PubMed]  [DOI]  [Cited in This Article: ]
24.  Mohebi R, Karimi Galougahi K, Garcia JJ, Horst J, Ben-Yehuda O, Radhakrishnan J, Chertow GM, Jeremias A, Cohen DJ, Cohen DJ, Maehara A, Mintz GS, Chen S, Redfors B, Leon MB, Stuckey TD, Rinaldi MJ, Weisz G, Witzenbichler B, Kirtane AJ, Mehran R, Dangas GD, Stone GW, Ali ZA. Long-Term Clinical Impact of Contrast-Associated Acute Kidney Injury Following PCI: An ADAPT-DES Substudy. JACC Cardiovasc Interv. 2022;15:753-766.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 29]  [Article Influence: 14.5]  [Reference Citation Analysis (0)]
25.  Heyman SN, Rosen S, Rosenberger C. Renal parenchymal hypoxia, hypoxia adaptation, and the pathogenesis of radiocontrast nephropathy. Clin J Am Soc Nephrol. 2008;3:288-296.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 158]  [Cited by in F6Publishing: 154]  [Article Influence: 9.1]  [Reference Citation Analysis (0)]
26.  Wong PC, Li Z, Guo J, Zhang A. Pathophysiology of contrast-induced nephropathy. Int J Cardiol. 2012;158:186-192.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 116]  [Cited by in F6Publishing: 129]  [Article Influence: 10.8]  [Reference Citation Analysis (0)]
27.  Ueda J, Nygren A, Hansell P, Ulfendahl HR. Effect of intravenous contrast media on proximal and distal tubular hydrostatic pressure in the rat kidney. Acta Radiol. 1993;34:83-87.  [PubMed]  [DOI]  [Cited in This Article: ]
28.  Tumlin J, Stacul F, Adam A, Becker CR, Davidson C, Lameire N, McCullough PA; CIN Consensus Working Panel. Pathophysiology of contrast-induced nephropathy. Am J Cardiol. 2006;98:14K-20K.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 253]  [Cited by in F6Publishing: 272]  [Article Influence: 15.1]  [Reference Citation Analysis (0)]
29.  Vallon V. Tubuloglomerular feedback and the control of glomerular filtration rate. News Physiol Sci. 2003;18:169-174.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 52]  [Article Influence: 2.5]  [Reference Citation Analysis (0)]
30.  Cantley LG, Spokes K, Clark B, McMahon EG, Carter J, Epstein FH. Role of endothelin and prostaglandins in radiocontrast-induced renal artery constriction. Kidney Int. 1993;44:1217-1223.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 116]  [Cited by in F6Publishing: 124]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
31.  Emans TW, Janssen BJ, Joles JA, Krediet CTP. Nitric Oxide Synthase Inhibition Induces Renal Medullary Hypoxia in Conscious Rats. J Am Heart Assoc. 2018;7:e009501.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 11]  [Cited by in F6Publishing: 9]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
32.  Mehran R, Aymong ED, Nikolsky E, Lasic Z, Iakovou I, Fahy M, Mintz GS, Lansky AJ, Moses JW, Stone GW, Leon MB, Dangas G. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol. 2004;44:1393-1399.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 246]  [Cited by in F6Publishing: 662]  [Article Influence: 33.1]  [Reference Citation Analysis (0)]
33.  Çınar T, Tanık VO, Aruğaslan E, Karabağ Y, Çağdaş M, Rencüzoğulları İ, Keskin M. The association of PRECISE-DAPT score with development of contrast-induced nephropathy in patients with ST-elevation myocardial infarction undergoing primary percutaneous coronary intervention. Cardiovasc Interv Ther. 2019;34:207-215.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 19]  [Article Influence: 3.2]  [Reference Citation Analysis (2)]
34.  Lazaros G, Zografos T, Oikonomou E, Siasos G, Georgiopoulos G, Vavuranakis M, Antonopoulos A, Kalogeras K, Tsalamandris S, Tousoulis D. Usefulness of C-Reactive Protein as a Predictor of Contrast-Induced Nephropathy After Percutaneous Coronary Interventions in Patients With Acute Myocardial Infarction and Presentation of a New Risk Score (Athens CIN Score). Am J Cardiol. 2016;118:1329-1333.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 7]  [Article Influence: 0.9]  [Reference Citation Analysis (0)]
35.  Davenport MS, Khalatbari S, Cohan RH, Ellis JH. Contrast medium-induced nephrotoxicity risk assessment in adult inpatients: a comparison of serum creatinine level- and estimated glomerular filtration rate-based screening methods. Radiology. 2013;269:92-100.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 36]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
36.  Davenport MS, Perazella MA, Yee J, Dillman JR, Fine D, McDonald RJ, Rodby RA, Wang CL, Weinreb JC. Use of Intravenous Iodinated Contrast Media in Patients with Kidney Disease: Consensus Statements from the American College of Radiology and the National Kidney Foundation. Radiology. 2020;294:660-668.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 190]  [Cited by in F6Publishing: 235]  [Article Influence: 58.8]  [Reference Citation Analysis (0)]
37.  Liss P, Nygren A, Erikson U, Ulfendahl HR. Injection of low and iso-osmolar contrast medium decreases oxygen tension in the renal medulla. Kidney Int. 1998;53:698-702.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 109]  [Cited by in F6Publishing: 97]  [Article Influence: 3.7]  [Reference Citation Analysis (0)]
38.  Manske CL, Sprafka JM, Strony JT, Wang Y. Contrast nephropathy in azotemic diabetic patients undergoing coronary angiography. Am J Med. 1990;89:615-620.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 352]  [Cited by in F6Publishing: 314]  [Article Influence: 9.2]  [Reference Citation Analysis (0)]
39.  Ali ZA, Karimi Galougahi K, Nazif T, Maehara A, Hardy MA, Cohen DJ, Ratner LE, Collins MB, Moses JW, Kirtane AJ, Stone GW, Karmpaliotis D, Leon MB. Imaging- and physiology-guided percutaneous coronary intervention without contrast administration in advanced renal failure: a feasibility, safety, and outcome study. Eur Heart J. 2016;37:3090-3095.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 122]  [Cited by in F6Publishing: 126]  [Article Influence: 15.8]  [Reference Citation Analysis (0)]
40.  Azzalini L, Mitomo S, Hachinohe D, Regazzoli D, Colombo A. Zero-Contrast Percutaneous Coronary Intervention Guided by Dextran-Based Optical Coherence Tomography. Can J Cardiol. 2018;34:342.e1-342.e3.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 17]  [Cited by in F6Publishing: 18]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
41.  Toprak O. Is acquired immunodeficiency syndrome a risk for development of contrast-induced nephropathy? Can Assoc Radiol J. 2008;59:100.  [PubMed]  [DOI]  [Cited in This Article: ]
42.  Keaney JJ, Hannon CM, Murray PT. Contrast-induced acute kidney injury: how much contrast is safe? Nephrol Dial Transplant. 2013;28:1376-1383.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 47]  [Cited by in F6Publishing: 50]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
43.  Gurm HS, Dixon SR, Smith DE, Share D, Lalonde T, Greenbaum A, Moscucci M; BMC2 (Blue Cross Blue Shield of Michigan Cardiovascular Consortium) Registry. Renal function-based contrast dosing to define safe limits of radiographic contrast media in patients undergoing percutaneous coronary interventions. J Am Coll Cardiol. 2011;58:907-914.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 221]  [Cited by in F6Publishing: 230]  [Article Influence: 17.7]  [Reference Citation Analysis (0)]
44.  Laskey WK, Jenkins C, Selzer F, Marroquin OC, Wilensky RL, Glaser R, Cohen HA, Holmes DR Jr; NHLBI Dynamic Registry Investigators. Volume-to-creatinine clearance ratio: a pharmacokinetically based risk factor for prediction of early creatinine increase after percutaneous coronary intervention. J Am Coll Cardiol. 2007;50:584-590.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 268]  [Cited by in F6Publishing: 282]  [Article Influence: 16.6]  [Reference Citation Analysis (0)]
45.  Gurm HS, Smith D, Share D, Wohns D, Collins J, Madala M, Koneru S, Menees D, Chetcuti S. Impact of automated contrast injector systems on contrast use and contrast-associated complications in patients undergoing percutaneous coronary interventions. JACC Cardiovasc Interv. 2013;6:399-405.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 25]  [Cited by in F6Publishing: 25]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
46.  Gurm HS, Seth M, Dixon S, Kraft P, Jensen A. Trends in Contrast Volume Use and Incidence of Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Intervention: Insights From Blue Cross Blue Shield of Michigan Cardiovascular Collaborative (BMC2). JACC Cardiovasc Interv. 2018;11:509-511.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 17]  [Cited by in F6Publishing: 17]  [Article Influence: 3.4]  [Reference Citation Analysis (0)]
47.  Cho E, Ko GJ. The Pathophysiology and the Management of Radiocontrast-Induced Nephropathy. Diagnostics (Basel). 2022;12.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 13]  [Article Influence: 6.5]  [Reference Citation Analysis (0)]
48.  Fader MI. Preheated contrast media: the advantage of intravenous injection. Radiol Technol. 1986;58:117-119.  [PubMed]  [DOI]  [Cited in This Article: ]
49.  Marenzi G, Assanelli E, Campodonico J, Lauri G, Marana I, De Metrio M, Moltrasio M, Grazi M, Rubino M, Veglia F, Fabbiocchi F, Bartorelli AL. Contrast volume during primary percutaneous coronary intervention and subsequent contrast-induced nephropathy and mortality. Ann Intern Med. 2009;150:170-177.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 248]  [Cited by in F6Publishing: 246]  [Article Influence: 16.4]  [Reference Citation Analysis (0)]
50.  van der Molen AJ, Reimer P, Dekkers IA, Bongartz G, Bellin MF, Bertolotto M, Clement O, Heinz-Peer G, Stacul F, Webb JAW, Thomsen HS. Post-contrast acute kidney injury. Part 2: risk stratification, role of hydration and other prophylactic measures, patients taking metformin and chronic dialysis patients : Recommendations for updated ESUR Contrast Medium Safety Committee guidelines. Eur Radiol. 2018;28:2856-2869.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 182]  [Cited by in F6Publishing: 159]  [Article Influence: 26.5]  [Reference Citation Analysis (0)]
51.  McCullough PA. Contrast-induced acute kidney injury. J Am Coll Cardiol. 2008;51:1419-1428.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 672]  [Cited by in F6Publishing: 672]  [Article Influence: 42.0]  [Reference Citation Analysis (0)]
52.  Rosenstock JL, Bruno R, Kim JK, Lubarsky L, Schaller R, Panagopoulos G, DeVita MV, Michelis MF. The effect of withdrawal of ACE inhibitors or angiotensin receptor blockers prior to coronary angiography on the incidence of contrast-induced nephropathy. Int Urol Nephrol. 2008;40:749-755.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 67]  [Cited by in F6Publishing: 51]  [Article Influence: 3.2]  [Reference Citation Analysis (0)]
53.  Bainey KR, Rahim S, Etherington K, Rokoss ML, Natarajan MK, Velianou JL, Brons S, Mehta SR; CAPTAIN Investigators. Effects of withdrawing vs continuing renin-angiotensin blockers on incidence of acute kidney injury in patients with renal insufficiency undergoing cardiac catheterization: Results from the Angiotensin Converting Enzyme Inhibitor/Angiotensin Receptor Blocker and Contrast Induced Nephropathy in Patients Receiving Cardiac Catheterization (CAPTAIN) trial. Am Heart J. 2015;170:110-116.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 55]  [Cited by in F6Publishing: 56]  [Article Influence: 6.2]  [Reference Citation Analysis (0)]
54.  Jo SH, Lee JM, Park J, Kim HS. The impact of renin-angiotensin-aldosterone system blockade on contrast-induced nephropathy: a meta-analysis of 12 studies with 4,493 patients. Cardiology. 2015;130:4-14.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 22]  [Article Influence: 2.2]  [Reference Citation Analysis (0)]
55.  Walsh SR, Boyle JR, Tang TY, Sadat U, Cooper DG, Lapsley M, Norden AG, Varty K, Hayes PD, Gaunt ME. Remote ischemic preconditioning for renal and cardiac protection during endovascular aneurysm repair: a randomized controlled trial. J Endovasc Ther. 2009;16:680-689.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 95]  [Cited by in F6Publishing: 86]  [Article Influence: 6.1]  [Reference Citation Analysis (0)]
56.  Deftereos S, Giannopoulos G, Tzalamouras V, Raisakis K, Kossyvakis C, Kaoukis A, Panagopoulou V, Karageorgiou S, Avramides D, Toutouzas K, Hahalis G, Pyrgakis V, Manolis AS, Alexopoulos D, Stefanadis C, Cleman MW. Renoprotective effect of remote ischemic post-conditioning by intermittent balloon inflations in patients undergoing percutaneous coronary intervention. J Am Coll Cardiol. 2013;61:1949-1955.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 69]  [Cited by in F6Publishing: 75]  [Article Influence: 6.8]  [Reference Citation Analysis (0)]
57.  Er F, Nia AM, Dopp H, Hellmich M, Dahlem KM, Caglayan E, Kubacki T, Benzing T, Erdmann E, Burst V, Gassanov N. Ischemic preconditioning for prevention of contrast medium-induced nephropathy: randomized pilot RenPro Trial (Renal Protection Trial). Circulation. 2012;126:296-303.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 189]  [Cited by in F6Publishing: 189]  [Article Influence: 15.8]  [Reference Citation Analysis (0)]
58.  Zhou CC, Yao WT, Ge YZ, Xu LW, Wu R, Gao XF, Song KW, Jiang XM, Wang M, Huang WJ, Zhu YP, Li LP, Zhou LH, Xu ZL, Zhang SL, Zhu JG, Li WC, Jia RP. Remote ischemic conditioning for the prevention of contrast-induced acute kidney injury in patients undergoing intravascular contrast administration: a meta-analysis and trial sequential analysis of 16 randomized controlled trials. Oncotarget. 2017;8:79323-79336.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 13]  [Article Influence: 1.9]  [Reference Citation Analysis (0)]
59.  Levine GN, Bates ER, Blankenship JC, Bailey SR, Bittl JA, Cercek B, Chambers CE, Ellis SG, Guyton RA, Hollenberg SM, Khot UN, Lange RA, Mauri L, Mehran R, Moussa ID, Mukherjee D, Nallamothu BK, Ting HH. 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines and the Society for Cardiovascular Angiography and Interventions. Circulation. 2011;124:e574-e651.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 788]  [Cited by in F6Publishing: 896]  [Article Influence: 68.9]  [Reference Citation Analysis (0)]
60.  Kolh P, Windecker S. ESC/EACTS myocardial revascularization guidelines 2014. Eur Heart J. 2014;35:3235-3236.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 44]  [Article Influence: 4.9]  [Reference Citation Analysis (0)]
61.  Solomon R, Werner C, Mann D, D'Elia J, Silva P. Effects of saline, mannitol, and furosemide on acute decreases in renal function induced by radiocontrast agents. N Engl J Med. 1994;331:1416-1420.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 909]  [Cited by in F6Publishing: 759]  [Article Influence: 25.3]  [Reference Citation Analysis (0)]
62.  Weisbord SD, Palevsky PM. Prevention of contrast-induced nephropathy with volume expansion. Clin J Am Soc Nephrol. 2008;3:273-280.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 129]  [Cited by in F6Publishing: 139]  [Article Influence: 8.2]  [Reference Citation Analysis (0)]
63.  Zhang W, Zhang J, Yang B, Wu K, Lin H, Wang Y, Zhou L, Wang H, Zeng C, Chen X, Wang Z, Zhu J, Songming C. Effectiveness of oral hydration in preventing contrast-induced acute kidney injury in patients undergoing coronary angiography or intervention: a pairwise and network meta-analysis. Coron Artery Dis. 2018;29:286-293.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 16]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
64.  Mueller C, Buerkle G, Buettner HJ, Petersen J, Perruchoud AP, Eriksson U, Marsch S, Roskamm H. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med. 2002;162:329-336.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 582]  [Cited by in F6Publishing: 500]  [Article Influence: 22.7]  [Reference Citation Analysis (0)]
65.  Nijssen EC, Rennenberg RJ, Nelemans PJ, Essers BA, Janssen MM, Vermeeren MA, Ommen VV, Wildberger JE. Prophylactic hydration to protect renal function from intravascular iodinated contrast material in patients at high risk of contrast-induced nephropathy (AMACING): a prospective, randomised, phase 3, controlled, open-label, non-inferiority trial. Lancet. 2017;389:1312-1322.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 284]  [Cited by in F6Publishing: 294]  [Article Influence: 42.0]  [Reference Citation Analysis (0)]
66.  Nijssen EC, Nelemans PJ, Rennenberg RJ, van Ommen V, Wildberger JE. Prophylactic Intravenous Hydration to Protect Renal Function From Intravascular Iodinated Contrast Material (AMACING): Long-term Results of a Prospective, Randomised, Controlled Trial. EClinicalMedicine. 2018;4-5:109-116.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 19]  [Article Influence: 3.2]  [Reference Citation Analysis (0)]
67.  Nijssen EC, Nelemans PJ, Rennenberg RJ, van der Molen AJ, van Ommen GV, Wildberger JE. Impact on clinical practice of updated guidelines on iodinated contrast material: CINART. Eur Radiol. 2020;30:4005-4013.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 10]  [Article Influence: 2.5]  [Reference Citation Analysis (0)]
68.  Liu Y, Tan N, Huo Y, Chen SQ, Liu J, Wang Y, Li L, Tao JH, Su X, Zhang L, Li QX, Zhang JY, Guo YS, Du ZM, Zhou YP, Fang ZF, Xu GM, Liang Y, Tao L, Chen H, Ji Z, Han B, Chen PY, Ge JB, Han YL, Chen JY. Simplified Rapid Hydration Prevents Contrast-Associated Acute Kidney Injury Among CKD Patients Undergoing Coronary Angiography. JACC Cardiovasc Interv. 2023;16:1503-1513.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 5]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
69.  Bader BD, Berger ED, Heede MB, Silberbaur I, Duda S, Risler T, Erley CM. What is the best hydration regimen to prevent contrast media-induced nephrotoxicity? Clin Nephrol. 2004;62:1-7.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 114]  [Cited by in F6Publishing: 124]  [Article Influence: 6.2]  [Reference Citation Analysis (0)]
70.  Brar SS, Aharonian V, Mansukhani P, Moore N, Shen AY, Jorgensen M, Dua A, Short L, Kane K. Haemodynamic-guided fluid administration for the prevention of contrast-induced acute kidney injury: the POSEIDON randomised controlled trial. Lancet. 2014;383:1814-1823.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 269]  [Cited by in F6Publishing: 258]  [Article Influence: 25.8]  [Reference Citation Analysis (0)]
71.  Krasuski RA, Beard BM, Geoghagan JD, Thompson CM, Guidera SA. Optimal timing of hydration to erase contrast-associated nephropathy: the OTHER CAN study. J Invasive Cardiol. 2003;15:699-702.  [PubMed]  [DOI]  [Cited in This Article: ]
72.  Qian G, Fu Z, Guo J, Cao F, Chen Y. Prevention of Contrast-Induced Nephropathy by Central Venous Pressure-Guided Fluid Administration in Chronic Kidney Disease and Congestive Heart Failure Patients. JACC Cardiovasc Interv. 2016;9:89-96.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 70]  [Cited by in F6Publishing: 55]  [Article Influence: 6.9]  [Reference Citation Analysis (0)]
73.  Yan Y, Ye M, Dong X, Chen Q, Hong H, Chen L, Luo Y. Prevention of Contrast-Induced Nephropathy by Inferior Vena Cava Ultrasonography-Guided Hydration in Chronic Heart Failure Patients. Cardiology. 2021;146:187-194.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 1]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
74.  Liu Y, Tan N, Huo Y, Chen S, Liu J, Chen YD, Wu K, Wu G, Chen K, Ye J, Liang Y, Feng X, Dong S, Wu Q, Ye X, Zeng H, Zhang M, Dai M, Duan CY, Sun G, He Y, Song F, Guo Z, Chen PY, Ge J, Xian Y, Chen J. Hydration for prevention of kidney injury after primary coronary intervention for acute myocardial infarction: a randomised clinical trial. Heart. 2022;108:948-955.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 1]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
75.  Marashizadeh A, Sanati HR, Sadeghipour P, Peighambari MM, Moosavi J, Shafe O, Firouzi A, Zahedmehr A, Maadani M, Shakerian F, Kiani R, Mohebbi B, Alemzadeh-Ansari MJ, Tahvili R, Naghavi B. Left ventricular end-diastolic pressure-guided hydration for the prevention of contrast-induced acute kidney injury in patients with stable ischemic heart disease: the LAKESIDE trial. Int Urol Nephrol. 2019;51:1815-1822.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 7]  [Cited by in F6Publishing: 5]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
76.  Ling W, Jiang Z, Liu K, Zhang H, Qian Y, Tian J, Zhang Z, Chen Y, Qian G. Effect of Vigileo/FloTrac System-Guided Aggressive Hydration in Acute Myocardial Infarction Patients to Prevent Contrast-Induced Nephropathy After Urgent Percutaneous Coronary Intervention. Am J Cardiol. 2023;195:77-82.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 1]  [Reference Citation Analysis (0)]
77.  Dorval JF, Dixon SR, Zelman RB, Davidson CJ, Rudko R, Resnic FS. Feasibility study of the RenalGuard™ balanced hydration system: a novel strategy for the prevention of contrast-induced nephropathy in high risk patients. Int J Cardiol. 2013;166:482-486.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 35]  [Cited by in F6Publishing: 35]  [Article Influence: 3.2]  [Reference Citation Analysis (0)]
78.  Visconti G, Focaccio A, Donahue M, Golia B, Marzano A, Donnarumma E, Ricciardelli B, Selvetella L, Marino L, Briguori C. RenalGuard System for the prevention of acute kidney injury in patients undergoing transcatheter aortic valve implantation. EuroIntervention. 2016;11:e1658-e1661.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 24]  [Article Influence: 3.0]  [Reference Citation Analysis (0)]
79.  Briguori C, D'Amore C, De Micco F, Signore N, Esposito G, Visconti G, Airoldi F, Signoriello G, Focaccio A. Left Ventricular End-Diastolic Pressure Versus Urine Flow Rate-Guided Hydration in Preventing Contrast-Associated Acute Kidney Injury. JACC Cardiovasc Interv. 2020;13:2065-2074.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 12]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
80.  Arbel Y, Ben-Assa E, Puzhevsky D, Litmanowicz B, Galli N, Chorin E, Halkin A, Sadeh B, Konigstein M, Bassat OK, Steinvil A, Bazan S, Banai S, Finkelstein A. Forced diuresis with matched hydration during transcatheter aortic valve implantation for Reducing Acute Kidney Injury: a randomized, sham-controlled study (REDUCE-AKI). Eur Heart J. 2019;40:3169-3178.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 20]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
81.  Mauler-Wittwer S, Sievert H, Ioppolo AM, Mahfoud F, Carrié D, Lipiecki J, Nickenig G, Fajadet J, Eckert S, Morice MC, Garot P. Study Evaluating the Use of RenalGuard to Protect Patients at High Risk of AKI. JACC Cardiovasc Interv. 2022;15:1639-1648.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 1]  [Article Influence: 0.5]  [Reference Citation Analysis (0)]
82.  Voigtländer-Buschmann L, Schäfer S, Schmidt-Lauber C, Weimann J, Shenas M, Giraldo Cortes J, Kuta PM, Zeller T, Twerenbold R, Seiffert M, Schofer N, Schneeberger Y, Schäfer A, Schirmer J, Reichenspurner H, Blankenberg S, Conradi L, Schäfer U. Effect of periprocedural furosemide-induced diuresis with matched isotonic intravenous hydration in patients with chronic kidney disease undergoing transcatheter aortic valve implantation. Clin Res Cardiol. 2024;113:801-811.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Reference Citation Analysis (0)]
83.  Wang Y, Guo Y. RenalGuard system and conventional hydration for preventing contrast-associated acute kidney injury in patients undergoing cardiac interventional procedures: A systematic review and meta-analysis. Int J Cardiol. 2021;333:83-89.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 9]  [Cited by in F6Publishing: 7]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
84.  Katoh H, Nozue T, Horie K, Sozu T, Inoue N, Michishita I. RenalGuard system to prevent contrast-induced acute kidney injury in Japanese patients with renal dysfunction; RESPECT KIDNEY study. Cardiovasc Interv Ther. 2019;34:105-112.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 2]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
85.  Chorin E, Ben-Assa E, Konigstein M, Rofe MT, Hochstadt A, Galli N, Schnapper M, Arbel Y, Rabey I, Shoshan JB, Halkin A, Herz I, Finkelstein A, Bazan S, Keren G, Banai S. Prevention of post procedural acute kidney injury in the catheterization laboratory in a real-world population. Int J Cardiol. 2017;226:42-47.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 15]  [Cited by in F6Publishing: 15]  [Article Influence: 2.1]  [Reference Citation Analysis (0)]
86.  Briguori C, Visconti G, Donahue M, De Micco F, Focaccio A, Golia B, Signoriello G, Ciardiello C, Donnarumma E, Condorelli G. RenalGuard system in high-risk patients for contrast-induced acute kidney injury. Am Heart J. 2016;173:67-76.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 31]  [Cited by in F6Publishing: 32]  [Article Influence: 4.0]  [Reference Citation Analysis (0)]
87.  Barbanti M, Gulino S, Capranzano P, Immè S, Sgroi C, Tamburino C, Ohno Y, Attizzani GF, Patanè M, Sicuso R, Pilato G, Di Landro A, Todaro D, Di Simone E, Picci A, Giannetto G, Costa G, Deste W, Giannazzo D, Grasso C, Capodanno D, Tamburino C. Acute Kidney Injury With the RenalGuard System in Patients Undergoing Transcatheter Aortic Valve Replacement: The PROTECT-TAVI Trial (PROphylactic effecT of furosEmide-induCed diuresis with matched isotonic intravenous hydraTion in Transcatheter Aortic Valve Implantation). JACC Cardiovasc Interv. 2015;8:1595-1604.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 89]  [Cited by in F6Publishing: 93]  [Article Influence: 10.3]  [Reference Citation Analysis (0)]
88.  Briguori C, Visconti G, Focaccio A, Airoldi F, Valgimigli M, Sangiorgi GM, Golia B, Ricciardelli B, Condorelli G; REMEDIAL II Investigators. Renal Insufficiency After Contrast Media Administration Trial II (REMEDIAL II): RenalGuard System in high-risk patients for contrast-induced acute kidney injury. Circulation. 2011;124:1260-1269.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 173]  [Cited by in F6Publishing: 165]  [Article Influence: 12.7]  [Reference Citation Analysis (0)]
89.  Ben-Haim Y, Chorin E, Hochstadt A, Ingbir M, Arbel Y, Khoury S, Halkin A, Finkelstein A, Banai S, Konigstein M. Forced Diuresis with Matched Isotonic Intravenous Hydration Prevents Renal Contrast Media Accumulation. J Clin Med. 2022;11.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
90.  Mirza AJ, Ali K, Huwez F, Taha AY, Ahmed FJ, Ezzaddin SA, Abdulrahman ZI, Lang CC. Contrast Induced Nephropathy: Efficacy of matched hydration and forced diuresis for prevention in patients with impaired renal function undergoing coronary procedures-CINEMA trial. Int J Cardiol Heart Vasc. 2022;39:100959.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
91.  Section 4: Contrast-induced AKI. Kidney Int Suppl (2011). 2012;2:69-88.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 40]  [Cited by in F6Publishing: 44]  [Article Influence: 3.7]  [Reference Citation Analysis (0)]
92.  Brar SS, Shen AY, Jorgensen MB, Kotlewski A, Aharonian VJ, Desai N, Ree M, Shah AI, Burchette RJ. Sodium bicarbonate vs sodium chloride for the prevention of contrast medium-induced nephropathy in patients undergoing coronary angiography: a randomized trial. JAMA. 2008;300:1038-1046.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 292]  [Cited by in F6Publishing: 250]  [Article Influence: 15.6]  [Reference Citation Analysis (0)]
93.  Jang JS, Jin HY, Seo JS, Yang TH, Kim DK, Kim TH, Urm SH, Kim DS, Kim DK, Seol SH, Kim DI, Cho KI, Kim BH, Park YH, Je HG, Ahn JM, Kim WJ, Lee JY, Lee SW. Sodium bicarbonate therapy for the prevention of contrast-induced acute kidney injury – a systematic review and meta-analysis –. Circ J. 2012;76:2255-2265.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 69]  [Cited by in F6Publishing: 70]  [Article Influence: 5.8]  [Reference Citation Analysis (0)]
94.  Zoungas S, Ninomiya T, Huxley R, Cass A, Jardine M, Gallagher M, Patel A, Vasheghani-Farahani A, Sadigh G, Perkovic V. Systematic review: sodium bicarbonate treatment regimens for the prevention of contrast-induced nephropathy. Ann Intern Med. 2009;151:631-638.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 130]  [Cited by in F6Publishing: 143]  [Article Influence: 9.5]  [Reference Citation Analysis (0)]
95.  Weisbord SD, Gallagher M, Jneid H, Garcia S, Cass A, Thwin SS, Conner TA, Chertow GM, Bhatt DL, Shunk K, Parikh CR, McFalls EO, Brophy M, Ferguson R, Wu H, Androsenko M, Myles J, Kaufman J, Palevsky PM; PRESERVE Trial Group. Outcomes after Angiography with Sodium Bicarbonate and Acetylcysteine. N Engl J Med. 2018;378:603-614.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 316]  [Cited by in F6Publishing: 305]  [Article Influence: 50.8]  [Reference Citation Analysis (0)]
96.  Lombardi M, Molisana M, Genovesi E, De Innocentiis C, Limbruno U, Misuraca L, Moretti L, Di Vito L, Renda G, Zimarino M, Di Nicola M, De Caterina R. Urine alkalinisation to prevent contrast-induced acute kidney injury: the prospective, randomised, controlled, open-label TEATE trial. EuroIntervention. 2022;18:562-573.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 1]  [Reference Citation Analysis (0)]
97.  Kooiman J, de Vries JPM, Van der Heyden J, Sijpkens YWJ, van Dijkman PRM, Wever JJ, van Overhagen H, Vahl AC, Aarts N, Verberk-Jonkers IJAM, Brulez HFH, Hamming JF, van der Molen AJ, Cannegieter SC, Putter H, van den Hout WB, Kilicsoy I, Rabelink TJ, Huisman MV. Randomized trial of one-hour sodium bicarbonate vs standard periprocedural saline hydration in chronic kidney disease patients undergoing cardiovascular contrast procedures. PLoS One. 2018;13:e0189372.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 8]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
98.  Khachigian LM, Collins T, Fries JW. N-acetyl cysteine blocks mesangial VCAM-1 and NF-kappa B expression in vivo. Am J Pathol. 1997;151:1225-1229.  [PubMed]  [DOI]  [Cited in This Article: ]
99.  Lopez BL, Snyder JW, Birenbaum DS, Ma XI. N-acetylcysteine enhances endothelium-dependent vasorelaxation in the isolated rat mesenteric artery. Ann Emerg Med. 1998;32:405-410.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 24]  [Cited by in F6Publishing: 25]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
100.  Safirstein R, Andrade L, Vieira JM. Acetylcysteine and nephrotoxic effects of radiographic contrast agents--a new use for an old drug. N Engl J Med. 2000;343:210-212.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 95]  [Cited by in F6Publishing: 102]  [Article Influence: 4.3]  [Reference Citation Analysis (0)]
101.  Marenzi G, Assanelli E, Marana I, Lauri G, Campodonico J, Grazi M, De Metrio M, Galli S, Fabbiocchi F, Montorsi P, Veglia F, Bartorelli AL. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med. 2006;354:2773-2782.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 442]  [Cited by in F6Publishing: 394]  [Article Influence: 21.9]  [Reference Citation Analysis (0)]
102.  Hoffmann U, Fischereder M, Krüger B, Drobnik W, Krämer BK. The value of N-acetylcysteine in the prevention of radiocontrast agent-induced nephropathy seems questionable. J Am Soc Nephrol. 2004;15:407-410.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 231]  [Cited by in F6Publishing: 174]  [Article Influence: 8.7]  [Reference Citation Analysis (0)]
103.  Adabag AS, Ishani A, Bloomfield HE, Ngo AK, Wilt TJ. Efficacy of N-acetylcysteine in preventing renal injury after heart surgery: a systematic review of randomized trials. Eur Heart J. 2009;30:1910-1917.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 67]  [Cited by in F6Publishing: 72]  [Article Influence: 4.8]  [Reference Citation Analysis (0)]
104.  Sun Z, Fu Q, Cao L, Jin W, Cheng L, Li Z. Intravenous N-acetylcysteine for prevention of contrast-induced nephropathy: a meta-analysis of randomized, controlled trials. PLoS One. 2013;8:e55124.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 57]  [Cited by in F6Publishing: 63]  [Article Influence: 5.7]  [Reference Citation Analysis (0)]
105.  Mansouri A, Reiner Ž, Ruscica M, Tedeschi-Reiner E, Radbakhsh S, Bagheri Ekta M, Sahebkar A. Antioxidant Effects of Statins by Modulating Nrf2 and Nrf2/HO-1 Signaling in Different Diseases. J Clin Med. 2022;11.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 6]  [Cited by in F6Publishing: 34]  [Article Influence: 17.0]  [Reference Citation Analysis (0)]
106.  Stoll LL, McCormick ML, Denning GM, Weintraub NL. Antioxidant effects of statins. Drugs Today (Barc). 2004;40:975-990.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 96]  [Cited by in F6Publishing: 79]  [Article Influence: 4.2]  [Reference Citation Analysis (0)]
107.  Zhang BC, Li WM, Xu YW. High-dose statin pretreatment for the prevention of contrast-induced nephropathy: a meta-analysis. Can J Cardiol. 2011;27:851-858.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 45]  [Cited by in F6Publishing: 46]  [Article Influence: 3.5]  [Reference Citation Analysis (0)]
108.  Zhou Y, Yuan WJ, Zhu N, Wang L. Short-term, high-dose statins in the prevention of contrast-induced nephropathy: a systematic review and meta-analysis. Clin Nephrol. 2011;76:475-483.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 19]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
109.  Zhang T, Shen LH, Hu LH, He B. Statins for the prevention of contrast-induced nephropathy: a systematic review and meta-analysis. Am J Nephrol. 2011;33:344-351.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 62]  [Cited by in F6Publishing: 66]  [Article Influence: 5.1]  [Reference Citation Analysis (0)]
110.  Liu YH, Liu Y, Duan CY, Tan N, Chen JY, Zhou YL, Li LW, He PC. Statins for the Prevention of Contrast-Induced Nephropathy After Coronary Angiography/Percutaneous Interventions: A Meta-analysis of Randomized Controlled Trials. J Cardiovasc Pharmacol Ther. 2015;20:181-192.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 20]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
111.  Liu LY, Liu Y, Wu MY, Sun YY, Ma FZ. Efficacy of atorvastatin on the prevention of contrast-induced acute kidney injury: a meta-analysis. Drug Des Devel Ther. 2018;12:437-444.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 21]  [Article Influence: 3.5]  [Reference Citation Analysis (0)]
112.  Li H, Wang C, Liu C, Li R, Zou M, Cheng G. Efficacy of Short-Term Statin Treatment for the Prevention of Contrast-Induced Acute Kidney Injury in Patients Undergoing Coronary Angiography/Percutaneous Coronary Intervention: A Meta-Analysis of 21 Randomized Controlled Trials. Am J Cardiovasc Drugs. 2016;16:201-219.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 39]  [Cited by in F6Publishing: 40]  [Article Influence: 5.0]  [Reference Citation Analysis (0)]
113.  Giacoppo D, Gargiulo G, Buccheri S, Aruta P, Byrne RA, Cassese S, Dangas G, Kastrati A, Mehran R, Tamburino C, Capodanno D. Preventive Strategies for Contrast-Induced Acute Kidney Injury in Patients Undergoing Percutaneous Coronary Procedures: Evidence From a Hierarchical Bayesian Network Meta-Analysis of 124 Trials and 28 240 Patients. Circ Cardiovasc Interv. 2017;10.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 47]  [Cited by in F6Publishing: 55]  [Article Influence: 9.2]  [Reference Citation Analysis (0)]
114.  Zheng H, Xu Y, Liehn EA, Rusu M. Vitamin C as Scavenger of Reactive Oxygen Species during Healing after Myocardial Infarction. Int J Mol Sci. 2024;25.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 1]  [Reference Citation Analysis (0)]
115.  Gokce N, Keaney JF Jr, Frei B, Holbrook M, Olesiak M, Zachariah BJ, Leeuwenburgh C, Heinecke JW, Vita JA. Long-term ascorbic acid administration reverses endothelial vasomotor dysfunction in patients with coronary artery disease. Circulation. 1999;99:3234-3240.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 257]  [Cited by in F6Publishing: 265]  [Article Influence: 10.6]  [Reference Citation Analysis (0)]
116.  Spargias K, Alexopoulos E, Kyrzopoulos S, Iokovis P, Greenwood DC, Manginas A, Voudris V, Pavlides G, Buller CE, Kremastinos D, Cokkinos DV. Ascorbic acid prevents contrast-mediated nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. Circulation. 2004;110:2837-2842.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 209]  [Cited by in F6Publishing: 225]  [Article Influence: 11.3]  [Reference Citation Analysis (0)]
117.  Boscheri A, Weinbrenner C, Botzek B, Reynen K, Kuhlisch E, Strasser RH. Failure of ascorbic acid to prevent contrast-media induced nephropathy in patients with renal dysfunction. Clin Nephrol. 2007;68:279-286.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 41]  [Cited by in F6Publishing: 49]  [Article Influence: 2.9]  [Reference Citation Analysis (0)]
118.  Jo SH, Koo BK, Park JS, Kang HJ, Kim YJ, Kim HL, Chae IH, Choi DJ, Sohn DW, Oh BH, Park YB, Choi YS, Kim HS. N-acetylcysteine versus AScorbic acid for preventing contrast-Induced nephropathy in patients with renal insufficiency undergoing coronary angiography NASPI study-a prospective randomized controlled trial. Am Heart J. 2009;157:576-583.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 56]  [Cited by in F6Publishing: 59]  [Article Influence: 3.9]  [Reference Citation Analysis (0)]
119.  Palli E, Makris D, Papanikolaou J, Garoufalis G, Tsilioni I, Zygoulis P, Zakynthinos E. The impact of N-acetylcysteine and ascorbic acid in contrast-induced nephropathy in critical care patients: an open-label randomized controlled study. Crit Care. 2017;21:269.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 26]  [Cited by in F6Publishing: 20]  [Article Influence: 2.9]  [Reference Citation Analysis (0)]
120.  Liu P, Feng Y, Wang Y, Zhou Y, Zhao L. Protective effect of vitamin E against acute kidney injury. Biomed Mater Eng. 2015;26 Suppl 1:S2133-S2144.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 11]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
121.  Tasanarong A, Piyayotai D, Thitiarchakul S. Protection of radiocontrast induced nephropathy by vitamin E (alpha tocopherol): a randomized controlled pilot study. J Med Assoc Thai. 2009;92:1273-1281.  [PubMed]  [DOI]  [Cited in This Article: ]
122.  Tasanarong A, Vohakiat A, Hutayanon P, Piyayotai D. New strategy of α- and γ-tocopherol to prevent contrast-induced acute kidney injury in chronic kidney disease patients undergoing elective coronary procedures. Nephrol Dial Transplant. 2013;28:337-344.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 39]  [Cited by in F6Publishing: 41]  [Article Influence: 3.7]  [Reference Citation Analysis (0)]
123.  Rezaei Y, Khademvatani K, Rahimi B, Khoshfetrat M, Arjmand N, Seyyed-Mohammadzad MH. Short-Term High-Dose Vitamin E to Prevent Contrast Medium-Induced Acute Kidney Injury in Patients With Chronic Kidney Disease Undergoing Elective Coronary Angiography: A Randomized Placebo-Controlled Trial. J Am Heart Assoc. 2016;5:e002919.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 19]  [Cited by in F6Publishing: 22]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
124.  Katholi RE, Woods WT Jr, Taylor GJ, Deitrick CL, Womack KA, Katholi CR, McCann WP. Oxygen free radicals and contrast nephropathy. Am J Kidney Dis. 1998;32:64-71.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 147]  [Cited by in F6Publishing: 159]  [Article Influence: 6.1]  [Reference Citation Analysis (0)]
125.  Iranirad L, Sadeghi MS, Bagheri A, Doostali K, Norouzi S, Hejazi SF, Saghafi H, Roshani-Mobaraki S. Allopurinol prophylactic therapy and the prevention of contrast-induced nephropathy in high-risk patients undergoing coronary angiography: A prospective randomized controlled trial. ARYA Atheroscler. 2017;13:230-235.  [PubMed]  [DOI]  [Cited in This Article: ]
126.  Ghelich Khan Z, Talasaz AH, Pourhosseini H, Hosseini K, Alemzadeh Ansari MJ, Jalali A. Potential Role of Allopurinol in Preventing Contrast-Induced Nephropathy in Patients Undergoing Percutaneous Coronary Intervention: A Randomized Placebo-Controlled Trial. Clin Drug Investig. 2017;37:853-860.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 6]  [Article Influence: 0.9]  [Reference Citation Analysis (0)]
127.  Erol T, Tekin A, Katırcıbaşı MT, Sezgin N, Bilgi M, Tekin G, Zümrütdal A, Sezgin AT, Müderrisoğlu H. Efficacy of allopurinol pretreatment for prevention of contrast-induced nephropathy: a randomized controlled trial. Int J Cardiol. 2013;167:1396-1399.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 33]  [Cited by in F6Publishing: 38]  [Article Influence: 3.2]  [Reference Citation Analysis (0)]
128.  Kumar A, Bhawani G, Kumari N, Murthy KS, Lalwani V, Raju ChN. Comparative study of renal protective effects of allopurinol and N-acetyl-cysteine on contrast induced nephropathy in patients undergoing cardiac catheterization. J Clin Diagn Res. 2014;8:HC03-HC07.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 6]  [Cited by in F6Publishing: 14]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
129.  Xin W, Lin Z, Zhang T, Jia S. Effects of allopurinol pretreatment on the risk of contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention: A meta-analysis of randomized controlled trials . Clin Nephrol. 2020;93:24-33.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 3]  [Cited by in F6Publishing: 3]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
130.  Yang D, Yang D. Role of intracellular Ca2+ and Na+/Ca2+ exchanger in the pathogenesis of contrast-induced acute kidney injury. Biomed Res Int. 2013;2013:678456.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 15]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
131.  Yang D, Yang D, Jia R, Tan J. Na+/Ca2+ exchange inhibitor, KB-R7943, attenuates contrast-induced acute kidney injury. J Nephrol. 2013;26:877-885.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 16]  [Cited by in F6Publishing: 18]  [Article Influence: 1.6]  [Reference Citation Analysis (0)]
132.  Neumayer HH, Junge W, Küfner A, Wenning A. Prevention of radiocontrast-media-induced nephrotoxicity by the calcium channel blocker nitrendipine: a prospective randomised clinical trial. Nephrol Dial Transplant. 1989;4:1030-1036.  [PubMed]  [DOI]  [Cited in This Article: ]
133.  Russo D, Testa A, Della Volpe L, Sansone G. Randomised prospective study on renal effects of two different contrast media in humans: protective role of a calcium channel blocker. Nephron. 1990;55:254-257.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 73]  [Cited by in F6Publishing: 81]  [Article Influence: 2.4]  [Reference Citation Analysis (0)]
134.  Yin WJ, Zhou LY, Li DY, Xie YL, Wang JL, Zuo SR, Liu K, Hu C, Zhou G, Chen LH, Yang HQ, Zuo XC. Protective Effects of Amlodipine Pretreatment on Contrast-Induced Acute Kidney Injury And Overall Survival In Hypertensive Patients. Front Pharmacol. 2020;11:44.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 6]  [Article Influence: 1.5]  [Reference Citation Analysis (0)]
135.  Khoury Z, Schlicht JR, Como J, Karschner JK, Shapiro AP, Mook WJ, Weber RJ. The effect of prophylactic nifedipine on renal function in patients administered contrast media. Pharmacotherapy. 1995;15:59-65.  [PubMed]  [DOI]  [Cited in This Article: ]
136.  Carraro M, Mancini W, Artero M, Stacul F, Grotto M, Cova M, Faccini L. Dose effect of nitrendipine on urinary enzymes and microproteins following non-ionic radiocontrast administration. Nephrol Dial Transplant. 1996;11:444-448.  [PubMed]  [DOI]  [Cited in This Article: ]
137.  Arici M, Usalan C, Altun B, Erdem Y, Yasavul U, Turgan C, Kes S, Cağlar S. Radiocontrast-induced nephrotoxicity and urinary alpha-glutathione S-transferase levels: effect of amlodipine administration. Int Urol Nephrol. 2003;35:255-261.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 14]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
138.  Clark BA, Kim D, Epstein FH. Endothelin and atrial natriuretic peptide levels following radiocontrast exposure in humans. Am J Kidney Dis. 1997;30:82-86.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 50]  [Cited by in F6Publishing: 52]  [Article Influence: 1.9]  [Reference Citation Analysis (0)]
139.  Margulies KB, Burnett JC Jr. Atrial natriuretic factor modulates whole kidney tubuloglomerular feedback. Am J Physiol. 1990;259:R97-101.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 3]  [Article Influence: 0.1]  [Reference Citation Analysis (0)]
140.  Kurnik BR, Allgren RL, Genter FC, Solomon RJ, Bates ER, Weisberg LS. Prospective study of atrial natriuretic peptide for the prevention of radiocontrast-induced nephropathy. Am J Kidney Dis. 1998;31:674-680.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 182]  [Cited by in F6Publishing: 191]  [Article Influence: 7.3]  [Reference Citation Analysis (0)]
141.  Morikawa S, Sone T, Tsuboi H, Mukawa H, Morishima I, Uesugi M, Morita Y, Numaguchi Y, Okumura K, Murohara T. Renal protective effects and the prevention of contrast-induced nephropathy by atrial natriuretic peptide. J Am Coll Cardiol. 2009;53:1040-1046.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 76]  [Cited by in F6Publishing: 83]  [Article Influence: 5.5]  [Reference Citation Analysis (0)]
142.  Liu J, Xie Y, He F, Gao Z, Hao Y, Zu X, Chang L, Li Y. Recombinant Brain Natriuretic Peptide for the Prevention of Contrast-Induced Nephropathy in Patients with Chronic Kidney Disease Undergoing Nonemergent Percutaneous Coronary Intervention or Coronary Angiography: A Randomized Controlled Trial. Biomed Res Int. 2016;2016:5985327.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 10]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
143.  Liu JM, Xie YN, Gao ZH, Zu XG, Li YJ, Hao YM, Chang L. Brain natriuretic peptide for prevention of contrast-induced nephropathy after percutaneous coronary intervention or coronary angiography. Can J Cardiol. 2014;30:1607-1612.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 10]  [Article Influence: 1.0]  [Reference Citation Analysis (0)]
144.  Kallistratos MS, Poulimenos LE, Giannitsi S, Tsinivizov P, Manolis AJ. Trimetazidine in the Prevention of Tissue Ischemic Conditions. Angiology. 2019;70:291-298.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 16]  [Article Influence: 2.7]  [Reference Citation Analysis (0)]
145.  Ye Z, Lu H, Su Q, Xian X, Li L. Effect of trimetazidine on preventing contrast-induced nephropathy in diabetic patients with renal insufficiency. Oncotarget. 2017;8:102521-102530.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 5]  [Article Influence: 0.7]  [Reference Citation Analysis (0)]
146.  Ibrahim TA, El-Mawardy RH, El-Serafy AS, El-Fekky EM. Trimetazidine in the prevention of contrast-induced nephropathy in chronic kidney disease. Cardiovasc Revasc Med. 2017;18:315-319.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 14]  [Cited by in F6Publishing: 16]  [Article Influence: 2.3]  [Reference Citation Analysis (0)]
147.  Kim GH. Renal effects of prostaglandins and cyclooxygenase-2 inhibitors. Electrolyte Blood Press. 2008;6:35-41.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 42]  [Cited by in F6Publishing: 45]  [Article Influence: 2.8]  [Reference Citation Analysis (0)]
148.  Koch JA, Plum J, Grabensee B, Mödder U. Prostaglandin E1: a new agent for the prevention of renal dysfunction in high risk patients caused by radiocontrast media? PGE1 Study Group. Nephrol Dial Transplant. 2000;15:43-49.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 81]  [Cited by in F6Publishing: 91]  [Article Influence: 3.8]  [Reference Citation Analysis (0)]
149.  Gurkowski L, MacDougall M, Wiegmann T. Effects of Misoprostol on Contrast-Induced Renal Dysfunction. Am J Ther. 1995;2:837-842.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 12]  [Cited by in F6Publishing: 13]  [Article Influence: 0.4]  [Reference Citation Analysis (0)]
150.  Spargias K, Adreanides E, Demerouti E, Gkouziouta A, Manginas A, Pavlides G, Voudris V, Cokkinos DV. Iloprost prevents contrast-induced nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. Circulation. 2009;120:1793-1799.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 61]  [Cited by in F6Publishing: 64]  [Article Influence: 4.3]  [Reference Citation Analysis (0)]
151.  Yang SC, Fu NK, Zhang J, Liang M, Cong HL, Lin WH, Tian FS, Lu CZ, Sun TT, Zhang WY, Ma ZH. Preventive Effects of Alprostadil Against Contrast-Induced Nephropathy Inpatients With Renal Insufficiency Undergoing Percutaneous Coronary Intervention. Angiology. 2018;69:393-399.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 10]  [Cited by in F6Publishing: 10]  [Article Influence: 1.4]  [Reference Citation Analysis (0)]
152.  Liu X, Hang Y, Shen L, Yang J, Zhou L, Sha W, Lu G. Prevention of contrast-induced nephropathy with prostaglandin E1 in patients undergoing percutaneous coronary procedures: A meta-analysis of 24 randomized controlled trials . Clin Nephrol. 2018;90:313-324.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 2]  [Cited by in F6Publishing: 2]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
153.  Liu X, Zhang P, Zhang J, Zhang X, Yang S, Fu N. The Preventive Effect of Alprostadil on the Contrast-Induced Nephropathy of Coronary Heart Disease Treated by Percutaneous Coronary Intervention in Moderate and High-Risk Population Stratified by Mehran Score. Angiology. 2022;73:33-41.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 1]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
154.  Xu H, Wang H, Zhang C, Xiao J, Hua N, Tang X, Xie J, Zhang Z. Efficacy of Alprostadil in Preventing Contrast-Induced Nephropathy: A Systematic Review and Meta-Analysis. Angiology. 2021;72:878-888.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Cited by in F6Publishing: 1]  [Article Influence: 0.3]  [Reference Citation Analysis (0)]
155.  Dai B, Liu Y, Fu L, Li Y, Zhang J, Mei C. Effect of theophylline on prevention of contrast-induced acute kidney injury: a meta-analysis of randomized controlled trials. Am J Kidney Dis. 2012;60:360-370.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 43]  [Cited by in F6Publishing: 47]  [Article Influence: 3.9]  [Reference Citation Analysis (0)]
156.  Bagshaw SM, Ghali WA. Theophylline for prevention of contrast-induced nephropathy: a systematic review and meta-analysis. Arch Intern Med. 2005;165:1087-1093.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 95]  [Cited by in F6Publishing: 85]  [Article Influence: 4.5]  [Reference Citation Analysis (0)]
157.  Kelly AM, Dwamena B, Cronin P, Bernstein SJ, Carlos RC. Meta-analysis: effectiveness of drugs for preventing contrast-induced nephropathy. Ann Intern Med. 2008;148:284-294.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 297]  [Cited by in F6Publishing: 313]  [Article Influence: 19.6]  [Reference Citation Analysis (0)]
158.  Deray G. Dialysis and iodinated contrast media. Kidney Int Suppl. 2006;S25-S29.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 58]  [Cited by in F6Publishing: 59]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
159.  Vogt B, Ferrari P, Schönholzer C, Marti HP, Mohaupt M, Wiederkehr M, Cereghetti C, Serra A, Huynh-Do U, Uehlinger D, Frey FJ. Prophylactic hemodialysis after radiocontrast media in patients with renal insufficiency is potentially harmful. Am J Med. 2001;111:692-698.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 197]  [Cited by in F6Publishing: 208]  [Article Influence: 9.0]  [Reference Citation Analysis (0)]
160.  Lehnert T, Keller E, Gondolf K, Schäffner T, Pavenstädt H, Schollmeyer P. Effect of haemodialysis after contrast medium administration in patients with renal insufficiency. Nephrol Dial Transplant. 1998;13:358-362.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 102]  [Cited by in F6Publishing: 108]  [Article Influence: 4.2]  [Reference Citation Analysis (0)]
161.  Reinecke H, Fobker M, Wellmann J, Becke B, Fleiter J, Heitmeyer C, Breithardt G, Hense HW, Schaefer RM. A randomized controlled trial comparing hydration therapy to additional hemodialysis or N-acetylcysteine for the prevention of contrast medium-induced nephropathy: the Dialysis-versus-Diuresis (DVD) Trial. Clin Res Cardiol. 2007;96:130-139.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 64]  [Cited by in F6Publishing: 52]  [Article Influence: 2.9]  [Reference Citation Analysis (0)]
162.  Kawashima S, Takano H, Iino Y, Takayama M, Takano T. Prophylactic hemodialysis does not prevent contrast-induced nephropathy after cardiac catheterization in patients with chronic renal insufficiency. Circ J. 2006;70:553-558.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 21]  [Cited by in F6Publishing: 24]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
163.  Lee PT, Chou KJ, Liu CP, Mar GY, Chen CL, Hsu CY, Fang HC, Chung HM. Renal protection for coronary angiography in advanced renal failure patients by prophylactic hemodialysis. A randomized controlled trial. J Am Coll Cardiol. 2007;50:1015-1020.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 73]  [Cited by in F6Publishing: 78]  [Article Influence: 4.6]  [Reference Citation Analysis (0)]
164.  Marenzi G, Marana I, Lauri G, Assanelli E, Grazi M, Campodonico J, Trabattoni D, Fabbiocchi F, Montorsi P, Bartorelli AL. The prevention of radiocontrast-agent-induced nephropathy by hemofiltration. N Engl J Med. 2003;349:1333-1340.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 364]  [Cited by in F6Publishing: 384]  [Article Influence: 18.3]  [Reference Citation Analysis (0)]
165.  Schindler R, Stahl C, Venz S, Ludat K, Krause W, Frei U. Removal of contrast media by different extracorporeal treatments. Nephrol Dial Transplant. 2001;16:1471-1474.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 41]  [Cited by in F6Publishing: 45]  [Article Influence: 2.0]  [Reference Citation Analysis (0)]
166.  Oyamada N, Hamanaka I, Fujioka A, Iwasaku T, Minami T, Fujie H, Ueda K. Effectiveness of high flow-volume intermittent hemodiafiltration during and after intervention to prevent contrast-induced nephropathy in patients with advanced chronic kidney disease: A pilot study. Catheter Cardiovasc Interv. 2020;96:1174-1181.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 4]  [Cited by in F6Publishing: 4]  [Article Influence: 0.8]  [Reference Citation Analysis (0)]
167.  Danenberg HD, Lotan C, Varshitski B, Rosenheck S, Weiss AT. Removal of contrast medium from the coronary sinus during coronary angiography: feasibility of a simple and available technique for the prevention of nephropathy. Cardiovasc Revasc Med. 2008;9:9-13.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 18]  [Cited by in F6Publishing: 10]  [Article Influence: 0.6]  [Reference Citation Analysis (0)]
168.  Desch S, Fuernau G, Pöss J, Meyer-Saraei R, Saad M, Eitel I, Thiele H, de Waha S. Impact of a novel contrast reduction system on contrast savings in coronary angiography - The DyeVert randomised controlled trial. Int J Cardiol. 2018;257:50-53.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 20]  [Cited by in F6Publishing: 20]  [Article Influence: 3.3]  [Reference Citation Analysis (0)]
169.  Briguori C, Golino M, Porchetta N, Scarpelli M, De Micco F, Rubino C, Focaccio A, Signoriello G. Impact of a contrast media volume control device on acute kidney injury rate in patients with acute coronary syndrome. Catheter Cardiovasc Interv. 2021;98:76-84.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 5]  [Cited by in F6Publishing: 5]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
170.  Paolucci L, De Micco F, Bezzeccheri A, Scarpelli M, Esposito G, Airoldi F, Focaccio A, Briguori C. Contrast media volume reduction with the DyeVert(TM) system to prevent acute kidney injury in stable patients undergoing coronary procedures. Catheter Cardiovasc Interv. 2023;102:655-662.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in F6Publishing: 1]  [Reference Citation Analysis (0)]
171.  Tajti P, Xenogiannis I, Hall A, Burke MN, Chavez I, Garcia S, Gössl M, Mooney M, Poulose A, Sorajja P, Wang Y, Vemmou E, Nikolakopoulos I, Morley P, Rangan BV, Ungi I, Brilakis ES. Use of the DyeVert System in Chronic Total Occlusion Percutaneous Coronary Intervention. J Invasive Cardiol. 2019;31:253-259.  [PubMed]  [DOI]  [Cited in This Article: ]
172.  Javanbakht M, Hemami MR, Mashayekhi A, Branagan-Harris M, Zaman A, Al-Najjar Y, O'Donoghue D, Fath-Ordoubadi F, Wheatcroft S. DyeVert™ PLUS EZ System for Preventing Contrast-Induced Acute Kidney Injury in Patients Undergoing Diagnostic Coronary Angiography and/or Percutaneous Coronary Intervention: A UK-Based Cost-Utility Analysis. Pharmacoecon Open. 2020;4:459-472.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 8]  [Cited by in F6Publishing: 5]  [Article Influence: 1.3]  [Reference Citation Analysis (0)]
173.  López-Mínguez JR, Martín de Francisco AL, Soler MJ, Hernández F, Moreno R, Pinar E, Sampedro A, Mareque M, Oyagüez I. Cost-effectiveness analysis of dyevert™ Power XT in patients with chronic kidney disease undergoing percutaneous coronary intervention procedures in Spain. Catheter Cardiovasc Interv. 2023;102:233-240.  [PubMed]  [DOI]  [Cited in This Article: ]  [Reference Citation Analysis (0)]
174.  Briguori C, Quintavalle C, Mariano E, D'Agostino A, Scarpelli M, Focaccio A, Zoccai GB, Evola S, Esposito G, Sangiorgi GM, Condorelli G. Kidney Injury After Minimal Radiographic Contrast Administration in Patients With Acute Coronary Syndromes. J Am Coll Cardiol. 2024;83:1059-1069.  [PubMed]  [DOI]  [Cited in This Article: ]  [Cited by in Crossref: 1]  [Reference Citation Analysis (0)]