Contrast-induced nephropathy (CIN), also called as contrast associated-acute kidney injury (CA-AKI) is a common complication following cardiac procedures. KDIGO guidelines define CIN as a ≥25% increase in serum creatinine or an absolute increase of at least 0.5 mg/dl 48-72 h post-contrast administration. The single most effective measure in preventing CIN is peri-procedural intravascular hydration typically from 12 h before to 24 h after contrast media exposure but has limitations. Recently, the RenalGuard (RG) system has emerged as a new tool, demonstrating safer and more efficient hydration and reducing the incidence of AKI caused by CIN.

We conducted this meta-analysis on the effectiveness of the RG system in preventing CIN in patients undergoing cardiac interventions.

A comprehensive literature search of PubMed (MEDLINE), Science Direct, and Embase was conducted from its inception until February 2024 for randomized controlled trials (RCTs) including patients aged >18 years undergoing cardiac procedures with underlying chronic kidney disease (CKD), estimated glomerular filtration rate (eGFR) 20-60 ml/min/1.73 m2 and left ventricular ejection fraction (LVEF) >50%. The outcomes of interest were risk of CIN, risk of renal replacement therapy (RRT), in-hospital mortality and 30-day mortality, major adverse cardiovascular events (MACE), changes in serum creatinine (sCr) levels, and incidence of pulmonary edema. A random-effects meta-analysis was performed using Review Manager (RevMan) [Computer Program] Version 5.4 Cochrane Collaboration.

A total of 9 RCTs including 3,215 patients with CKD undergoing cardiac procedures on volume expansion strategies were included with 1,802 patients on the RG system and 1,413 patients using alternate volume expansion techniques. Pooled analysis of 9 RCTs reported a significantly lower risk of CIN in patients using the RG system vs. control [OR 0.51 (0.35, 0.74), P = 0.0004; I2 = 55%]. There was no significant difference in the risks of RRT, in-hospital mortality, 30-day MACE, pulmonary edema, or change in sCr levels.

This meta-analysis indicates the beneficial utilization of the RG system in populations with moderate-to-high risk and underlying CKD undergoing cardiac interventions in preventing CIN. However, it did not demonstrate a notable impact on mortality, RRT, MACE, pulmonary edema, and sCr levels when compared to the control group.

Iodinated contrast material (ICM) is a critical component for many radiologic examinations and procedures. However, ICM has often been withheld in the past out of concern for its potential nephrotoxicity and increased risk of morbidity and mortality, often at the expense of diagnostic accuracy and timely diagnosis. Evidence from controlled studies now suggest that most cases of acute kidney injury (AKI) caused by ICM were instead due to contrast-independent causes of AKI or normal variation in renal function. This study will discuss current knowledge of contrast-induced AKI, including the incidence, sequelae, risk factors, and prevention strategies of this potential complication.

Iodinated contrast material (ICM) has revolutionized the field of diagnostic radiology through improvements in diagnostic performance and the expansion of clinical indications for radiographic and CT examinations. Historically, nephrotoxicity was a feared complication of ICM use, thought to be associated with a significant risk of morbidity and mortality. Such fears often precluded the use of ICM in imaging evaluations, commonly at the expense of diagnostic performance and timely diagnosis. Over the past 20 years, the nephrotoxic risk of ICM has become a topic of debate, as more recent evidence from higher-quality studies now suggests that many cases of what was considered contrast-induced acute kidney injury (CI-AKI) likely were cases of mistaken causal attribution; most of these cases represented either acute kidney injury (AKI) caused by any of myriad other known factors that can adversely affect renal function and were coincidentally present at the time of contrast media exposure (termed "contrast-associated AKI" [CA-AKI]) or a manifestation of the normal variation in renal function that increases with worsening renal function. This Special Series Review discusses the current state of knowledge regarding CI-AKI and CA-AKI, including the incidence, risk factors, outcomes, and prophylactic strategies in the identification and management of these clinical conditions.

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.

Administration of fluid (oral and intravenous) is the cornerstone of prevention of contrast-associated acute kidney injury in the cardiac environment. Intravenous saline is the preferred fluid. The amount, timing, and duration of therapy are discussed. A key determinant of the benefit may be the rate of urine output stimulated by the therapy. Approaches using hemodynamic-guided rates of fluid administration and novel techniques to generate large urine outputs while maintaining fluid balance are highlighted.

Contrast-associated acute kidney injury (CA-AKI) is a potential complication of procedures requiring administration of iodinated contrast medium. RenalGuard, which provides real-time matching of intravenous hydration with furosemide-induced diuresis, is an alternative to standard periprocedural hydration strategies. The evidence on RenalGuard in patients undergoing percutaneous cardiovascular procedures is sparse. We used a Bayesian framework to perform a meta-analysis of RenalGuard as a CA-AKI preventive strategy.

We searched Medline, Cochrane Library and Web of Science for randomized trials of RenalGuard vs standard periprocedural hydration strategies. The primary outcome was CA-AKI. Secondary outcomes were all-cause death, cardiogenic shock, acute pulmonary edema, and renal failure requiring renal replacement therapy. A Bayesian random-effect risk ratio (RR) with corresponding 95% credibility interval (95%CrI) was calculated for each outcome. PROSPERO database number CRD42022378489.

Six studies were included. RenalGuard was associated with a significant relative reduction in CA-AKI (median RR, 0.54; 95%CrI, 0.31-0.86) and acute pulmonary edema (median RR, 0.35; 95%CrI, 0.12-0.87). No significant differences were observed for the other secondary endpoints [all-cause death (RR, 0.49; 95%CrI, 0.13-1.08), cardiogenic shock (RR, 0.06; 95%CrI, 0.00-1.91), and renal replacement therapy (RR, 0.52; 95%CrI, 0.18-1.18)]. The Bayesian analysis also showed that RenalGuard had a high probability of ranking first for all the secondary outcomes. These results were consistent in multiple sensitivity analyses.

In patients undergoing percutaneous cardiovascular procedures, RenalGuard was associated with a reduced risk of CA-AKI and acute pulmonary edema compared with standard periprocedural hydration strategies.

Despite an often favorable risk/benefit ratio, patients with severe chronic kidney disease are sometimes declined for interventional coronary procedures, due to the risk of acute kidney injury post-contrast (AKI-PC). A large preventive supply of intravenous fluid may be problematic in this population. The RenalGuard® system allows hyperhydration by maintaining a stable volemia through an enhanced diuresis.

This work reports the evaluation of the RenalGuard® system in 25 consecutive patients with chronic kidney disease (glomerular filtration rate < 40 mL/min/1.73 m²) requiring an interventional coronary procedure (coronary angiography and/or percutaneous coronary intervention) and at high risk of IRA-PC. An increase in serum creatinine ≥ 26.5 µmol/L at 48-72 hours (AKI-PC definition) was observed in 4 patients (16%). The mean glomerular filtration rate was 26 ± 8 mL/min/1.73 m² at 48-72 hours versus 25 ± 8 mL/min/1.73 m² at baseline. No patient presented with an increase in serum creatinine ≥ 1.5 from baseline, stage 2 or 3 AKI, or acute pulmonary edema. No renal replacement therapy was necessary. One death unrelated to AKI-PC occurred during hospital stay.

This single-center observational study suggests that the RenalGuard® system, allowing diuresis-adjusted hyperhydration, is safe and useful for patients at high risk of AKI-PC after an interventional coronary procedure.

Physiological Closed-Loop Controlled systems continue to take a growing part in clinical practice, offering possibilities of providing more accurate, goal-directed care while reducing clinicians' cognitive and task load. These systems also provide a standardized approach for the clinical management of the patient, leading to a reduction in care variability across multiple dimensions. For fluid management and administration, the advantages of closed-loop technology are clear, especially in conditions that require precise care to improve outcomes, such as peri-operative care, trauma, and acute burn care. Controller design varies from simplistic to complex designs, based on detailed physiological models and adaptive properties that account for inter-patient and intra-patient variability; their maturity level ranges from theoretical models tested in silico to commercially available, FDA-approved products. This comprehensive scoping review was conducted in order to assess the current technological landscape of this field, describe the systems currently available or under development, and suggest further advancements that may unfold in the coming years. Ten distinct systems were identified and discussed.

Acute kidney injury (AKI) is common in hospitalized patients and is a major risk factor for increased length of stay, morbidity, and mortality in postoperative patients. There are multiple barriers to reducing perioperative AKI - the etiology is multi-factorial and the diagnosis is fraught with issues. We review the recent literature on perioperative AKI and some considerations for anesthesiologists that examine the far-reaching effects of AKI on multiple organ systems.

This review will discuss recent literature that addresses the epidemiology, use of novel biomarkers in risk stratification, and therapeutic modalities for AKI in burn, pediatrics, sepsis, trauma, cardiac, and liver disease, contrast-induced AKI, as well as the evidence assessing goal-directed fluid therapy.

Recent studies address the use of risk stratification models and biomarkers, more sensitive than creatinine, in the preoperative identification of patients at risk for AKI. Although exciting, these scores and models need validation. There is a need for research assessing whether early AKI detection improves outcomes. Enhanced recovery after surgery utilizing goal-directed fluid therapy has not been shown to make an appreciable difference in the incidence of AKI. Reducing perioperative AKI requires a multi-pronged and possibly disease-specific approach.

Contrast-induced nephropathy (CIN) is an impairment of renal function that occurs after the administration of an iodinated contrast medium (CM). Kidney dysfunction in CIN is considered transient and reversible in most cases. However, it is the third most common cause of hospital-acquired acute kidney injury and is associated with increased morbidity and mortality, especially in high-risk patients. Diagnostic and interventional procedures that require intravascular CM are being used with increasing frequency, especially among the elderly, who can be particularly susceptible to CIN due to multiple comorbidities. Therefore, identifying the exact mechanisms of CIN and its associated risk factors is crucial not only to provide optimal preventive management for at-risk patients, but also to increase the feasibility of diagnostic and interventional procedure that use CM. CM induces kidney injury by impairing renal hemodynamics and increasing the generation of reactive oxygen species, in addition to direct cytotoxicity. Periprocedural hydration is the most widely accepted preventive strategy to date. Here, we review the latest research results on the pathophysiology and management of CIN.