Acute kidney injury (AKI) is common in hospitalized patients. Administration of iodinated contrast may impede kidney recovery but avoiding contrast may delay diagnosis and therapeutic interventions. There is limited data on the impact of contrast exposure in patients with established AKI receiving renal replacement therapy (RRT).

We conducted a retrospective cohort study which included all patients with AKI who received RRT at St Michael's Hospital in Toronto, Canada, from January 2007 to December 2022. The exposure was the receipt of iodinated contrast during the 14 days following RRT initiation and while the patient was still RRT-dependent. The primary outcome was RRT dependence at hospital discharge.

1597 patients with AKI received RRT and 754 patients were included in our analysis. Of these, 185 patients received iodinated contrast. After propensity score weighting, the exposure to contrast was associated with a higher likelihood of RRT dependence at hospital discharge (Odds Ratio 1.73, 95 % confidence interval 1.13-2.53).

The receipt of contrast in patients with AKI receiving RRT was associated with an increased risk of RRT dependence at hospital discharge. Contrast exposure in RRT-dependent patients may delay recovery from AKI. The benefits of contrast should be carefully weighed against this risk in patients with AKI receiving RRT.

Acute kidney injury (AKI) is a common clinical syndrome characterized by the rapid loss of renal filtration function. No standard therapeutic agent option is currently available. The development and progression of AKI is a continuous and dynamical pathological process. Oxidative stress and inflammatory responses are the primary influencing factors. Here, we developed a biomimetic nano-system (MM-PtNCs) with reactive oxygen species (ROS)-responsive platinum nanozyme clusters (PtNCs) wrapped in macrophage membrane (MM) to alleviate AKI by modulating oxidative stress and inflammation. The inflammatory cytokines receptors retained on MM surface allowed the biomimetic nano-system to target renal inflammation and neutralize these pro-inflammatory cytokines to ameliorate inflammation. PtNCs exhibit free radical scavenging-ability and catalase (CAT)-like activity to scavenge ROS and regulate the oxidative stress situations both in injured cells and tissues. Meanwhile, it could responsively dissociate into ultrasmall platinum nanoparticles under AKI-specific ROS conditions to eliminate ROS and eventually excreted through the renal filtration system. In a mouse model of ischemia/reperfusion-induced AKI, systemic injection of MM-PtNCs significantly reduced renal damage and restored kidney function. Additionally, MM-PtNCs effectively prevented the progression of AKI to chronic kidney disease. In conclusion, MM-PtNCs may propose a multi-faceted regulatory approach for clinical AKI treatment.

Recent studies have identified the neutrophil/lymphocyte ratio, platelet/lymphocyte ratio, and neutrophil/lymphocyte × platelet ratio as promising prognostic markers in patients with sepsis. This study aims to evaluate the discriminatory ability of these ratios to predict mortality and requirement for renal replacement therapy at discharge, in patients with septic acute kidney injury.

Diagnostic test study based on a multicenter retrospective cohort of adult patients with septic acute kidney injury requiring renal support. Hematologic ratios were calculated for three disease moments (admission, diagnosis of acute kidney injury, initiation of renal replacement therapy). Receiver operating characteristic curves were used to analyze the discriminative ability of the different hematological ratios at each disease moment.

A total of 152 patients were included. In-hospital mortality occurred in 61.8%, and 24.2% of survivors required renal replacement therapy at discharge. Measurements taken at the initiation of renal replacement therapy had the best discriminatory ability to predict adverse outcomes. For neutrophil/lymphocyte ratio the area under the curve to predict mortality was 0.596; (95% CI: 0.500-0.692), and to predict the requirement of renal replacement therapy 0.592 (95% CI: 0.286-0.898). In all proposed scenarios, the neutrophil/lymphocyte ratio and neutrophil/lymphocyte × platelet ratio demonstrated superior performance in comparison to the platelet/lymphocyte ratio. All three ratios exhibited comparable poor discriminatory ability.

Hematological ratios have poor discriminatory capacity for predicting adverse outcomes in cases of septic acute kidney injury. The neutrophil-to-lymphocyte ratio taken at the initiation of renal replacement therapy is a potentially useful, economical, and easily applicable tool to be included in predictive models of mortality and dialysis dependence.

Acute kidney injury (AKI) is a clinical syndrome characterized by the sudden loss of renal excretory function. Renal ischemia-reperfusion injury (IRI) is the most common clinical cause of AKI. This study investigated the therapeutic potential of vaccarin (VA), a flavonoid glycoside extracted from the seeds of the Chinese herb Vaccaria hispanica, in treating IRI in mice. We found that VA significantly reduced serum urea nitrogen and creatinine levels, ameliorated renal tubular histopathological injury, inhibited renal macrophage infiltration, and down-regulated the expression of kidney injury molecule-1 (KIM-1). In vitro, VA protected mouse tubular epithelial cells (mTECs) from hypoxia/reoxygenation (H/R) injury. VA decreased the expression of NOX4 in damaged mouse kidney and H/R treated mTECs. The anti-inflammatory effects of VA were evidenced by the decrease in phosphorylated p65, pro-inflammatory cytokines and macrophage infiltration. More importantly, VA decreases the levels of MDA and ROS, and increases the levels of GSH, suggesting an excellent anti-oxidative effect. Additionally, VA mitigated oxidative stress and ferroptosis, demonstrated by regulating the expression of glutathione peroxidase 4 (GPX4) and cystine/glutamate antiporter system (system Xc-), and by reducing malondialdehyde (MDA) and ROS levels. The study further demonstrated that VA interacts with NADPH oxidase 4 (NOX4) via cellular thermal shift assay and molecular docking, suggesting NOX4 is a potential therapeutic target of VA. Furthermore, the inhibition, knockdown, or overexpression of NOX4 did not significantly altered the protective effect of VA. Overall, these findings highlight the therapeutic potential of VA in treating IR-induced AKI.

Ischemia-reperfusion injury (IRI) is the primary cause of acute kidney injury (AKI), which can result in chronic kidney disease (CKD) with renal fibrosis. Magnesium lithospermate B (Mlb), a bioactive compound produced from Salvia miltiorrhiza Bunge, exerts nephroprotective effects against AKI. However, the significance of Mlb in the evolution of IRI-induced AKI in patients with CKD remains unclear. Notably, the specific mechanisms underlying the putative antifibrotic activities of Mlb during this progression remain to be fully elucidated.

This study sought to explore the therapeutic benefits of Mlb in AKI-to-CKD progression and uncover the potential mechanisms, with a special interest in its effects on renal fibrosis and cell cycle regulation.

Unilateral ischemia/reperfusion (UIR)-induced mouse AKI-to-CKD progression (in vivo) and HK-2 cells with TGF-β-induced fibrosis model (in vitro) were used in the study. The beneficial effects of Mlb on renal fibrosis and cell cycle-related signaling pathways were investigated using histological analysis, molecular assays, network pharmacology, and RNA sequencing.

Mlb treatment significantly reduced renal dysfunction, inflammation, apoptosis, and the G2/M phase cell cycle stalling in mice 14 days post-UIR-induced AKI, subsequently improving renal fibrosis. Mechanistically, Mlb promotes the activity of the CDK1/Cyclin B1 signaling pathway, thereby alleviating the G2/M phase cell cycle stalling. Network pharmacology and RNA sequencing analyses identified the KLF5/CDK1/Cyclin B1 signaling pathway as a potential target of the antifibrotic effects of Mlb, which was further verified in both in vivo and in vitro experiments. The KLF5 inhibitor ML264 attenuated the protective effects of Mlb by reducing CDK1/Cyclin B1 expression and reinstating the G2/M phase cell cycle stalling, highlighting the critical role of this pathway in Mlb-mediated renal protection.

Mlb decreases renal fibrosis by inhibiting the G2/M phase cell cycle stalling via the KLF5/CDK1/Cyclin B1 signaling pathway during AKI-to-CKD progression. Our findings offer new insight into the therapeutic potential of Mlb in preventing CKD progression following AKI and identify a previously unrecognized mechanism involving the KLF5/CDK1/Cyclin B1 pathway.

Acute kidney injury (AKI) remains a significant challenge in critical care medicine, affecting up to 50% of intensive care unit patients with substantial mortality rates. While traditional approaches to AKI assessment rely on static measurements like serum creatinine and urine output, the furosemide stress test (FST) has emerged as a dynamic functional tool for evaluating renal tubular function and predicting AKI progression. This comprehensive review examines the historical development, physiological basis, technical aspects, and clinical applications of FST in various patient populations. Originally developed and validated in 2013, FST has demonstrated superior predictive capabilities for AKI progression and the need for renal replacement therapy compared to conventional biomarkers. The test's mechanism relies on assessing the kidney's response to a standardized furosemide challenge, providing insights into both the structural integrity and functional reserve of the renal tubular system. Standardized protocols have been established for different clinical scenarios, though implementation challenges remain, including timing considerations, patient selection, and resource requirements. FST has shown utility in critical care, post-cardiac surgery, sepsis-associated AKI, and heart failure settings. Recent developments include integration with artificial intelligence, personalized medicine approaches, and combination with novel biomarkers. While limitations exist, including contraindications and technical challenges, ongoing research continues to refine protocols and expand applications. This review highlights FST's role as a valuable prognostic tool in modern AKI management and discusses future directions, including automated monitoring systems, protocol standardization efforts, and potential applications in different patient populations.

Kidney injury encompasses a broad spectrum of structural and functional abnormalities, directly associated with stem cell transplantation. Acute kidney injury and chronic kidney disease represent perilous complications of hematopoietic stem cell transplantation (HSCT), with an elevated risk of mortality and progression to end-stage renal disease. The early detection of these complications is, therefore, paramount, and research is increasingly focused on the identification of novel biomarkers of kidney damage. Recently, proenkephalin (PENK), a monomeric peptide that is freely filtered by the glomerulus and thus reflects glomerular filtration very well, has been shown to be an additional useful predictor of the occurrence of acute kidney injury and heart failure. Dickkopf-3 (DKK3) is a glycoprotein secreted by the renal tubular epithelium in response to stress and has been implicated in the development of interstitial fibrosis. It has therefore been evaluated primarily as a marker of fibrosis in chronic kidney disease (CKD), but may also help predict the development of acute kiney injury. Uromodulin is regarded as a renal marker. Previous studies have examined the potential of PENK, DKK-3 and uromodulin as a biomarker in individuals with preserved renal function. However, the urinary levels of PENK, DKK-3 and uromodulin in patients following HSCT have not yet been established. The objective of the present study was to assess urinary PENK, DKK-3, and uromodulin concentrations in patients who had been under ambulatory care of the Hematology, Transplantation and Internal Medicine Department for a minimum of three months following HSCT, and to investigate their correlations with kidney function, as reflected by serum creatinine and eGFR. The study population comprised 80 patients who had undergone allogeneic HSCT for various reasons, primarily hematological malignancies such as acute leukemias and lymphomas. In addition, 32 healthy volunteers were included in order to establish normal ranges for the biomarkers of interest. Urine concentrations of proenkephalin, DKK-3, and uromodulin were evaluated using a commercially available sandwich ELISA immunoassay. Demographic and clinical data were retrieved from the patients' records. Statistical analyses were conducted using XLSLAT 2022 (Lumivero, Denver, CO, USA) and STATISTICAv13.0 (StatSoft, Tulsa, OH, USA). The results showed that PENK and DKK-3 levels were significantly higher in patients after HSCT compared to healthy volunteers. Furthermore, when patients were divided according to kidney function (below and over 60 mL/min/1.72 m2), it was found that the concentration of PENK and DKK-3 were significantly higher in 23 patients with CKD stage 3 relative to patients with eGFR over 60 mL min 1.72 m2. In univariate correlations, PENK demonstrated an inverse relationship with eGFR (r: -0.21, p < 0.05), while DKK-3 exhibited no significant correlation with creatinine or eGFR.Patients following allogeneic HSCT, despite having normal or near-normal kidney function, exhibited evidence of kidney injury. However, further research is necessary to ascertain the clinical utility of the novel biomarker.

The occurrence of acute kidney injury (AKI) in critically ill patients is often associated with increased morbidity and mortality rates. Despite extensive research, a consensus is yet to be arrived, especially regarding the optimal timing and indications for initiation of kidney replacement therapy (KRT) for critically ill patients. There is no clear guidance available on the timing of weaning from KRT. More recently, various biomarkers have produced promising prognostic prediction in such patients, regarding the need for KRT and its termination. Most of these biomarkers are indicative of kidney damage and stress, rather than recovery. However, large-scale validation studies are required to guide the cutoff values of these biomarkers among different patient cohorts so as to identify the optimum timing for KRT. This article reviews the kidney biomarkers in detail and summarizes the individual roles of biomarkers in the decision-making process for initiation and termination of the KRT among critically ill AKI patients and the supportive literature.

Guidelines recommended volume expansion with albumin for 48 hours for patients with cirrhosis and acute kidney injury (AKI) to correct hypovolemia and rule out prerenal AKI. A recent update in the ADQI-ICA consensus guidelines suggested shortening this duration to 24 hours, primarily based on expert opinion. This study aimed to evaluate the response rates to albumin treatment after 24 and 48 hours and to compare and assess the prognostic significance of three different definitions of response to albumin therapy.

Data from 127 prospectively recruited patients with cirrhosis and AKI from two German centers were analyzed. We examined three response definitions after 24 and 48 hours: (1) serum creatinine (SCr) decrease >0.3 mg/dl, (2) SCr decrease >25%, and (3) SCr decrease in at least one AKI stage. Follow-up was prolonged until liver transplantation, death or hemodialysis.

Overall, 30-54% of the patients responded to albumin treatment depending on the definition, and response rates were balanced across AKI stages. Notably, a relevant number of patients who responded at 48 hours did not respond within the first 24 hours. Additional responses to albumin during the second 24 hours according to definitions 1, 2, and 3 were 28%, 22%, and 18%, respectively. Response according to definition 3 was associated with higher hemodialysis- and transplantation-free survival rates.

A substantial proportion of patients require 48 hours to respond to albumin treatment. Shortening the duration of albumin therapy may lead to overtreatment with terlipressin.

This study provides valuable insights into the optimal duration of albumin treatment for patients with cirrhosis and acute kidney injury, challenging the recent recommendation to shorten the duration of albumin treatment. Furthermore, the optimal definition for response to albumin (reduction of at least one acute kidney injury stage) has been assessed. The results of this study are highly clinically relevant since shortening albumin therapy may lead to overtreatment with terlipressin, and evidence to support a specific definition of response to albumin was lacking. Clinicians can use these findings to predict treatment outcomes better, avoid fluid overload, and improve patient prognosis, while also considering the potential risks of early intervention with terlipressin.

The management of hypertensive disease in pregnancy is currently guided by practice recommendations based largely on observational data from a half century ago and has changed only superficially since that time. These recommendations are both narrowly prescriptive (women without traditional features of severe disease should all be delivered at exactly 370/7 weeks) and at the same time frustratingly ambiguous (the presence of epigastric pain unresponsive to repeat analgesics precludes expectant management at any gestational age, regardless of laboratory studies). Guidelines that ignore recent data from the obstetric, pediatric, and internal medicine literature too often lead practitioners to be more aggressive than necessary in the delivery of very premature pregnancies, and, conversely, more complacent than patient safety would support in prolonging pregnancy with advanced fetal maturity. We present here an alternative, organ-specific-based approach to the management of gestational hypertension that allows and encourages practitioners to formulate a management plan based on a thoughtful and, when possible, evidence-based synthesis of the continuous variables of blood pressure, degree of organ dysfunction and response to treatment, gestational age, and patient balancing of maternal and fetal/neonatal risks. Such clinical care is more complex and nuanced than simply basing life-altering critical management decisions, including timing of delivery, on whether the patient does, or does not have any one of the conditions described by box 4 of the current American College of Obstetricians and Gynecologists practice guidelines. Nonetheless, we believe this approach will not only improve care but will also open the door to useful investigations into prevention and management of the various entities traditionally considered as the same disease process. KEY POINTS: · Traditional approaches to preeclampsia are not evidence based.. · The use of such approaches has resulted in stagnant maternal morbidity and mortality ratios.. · The consideration of disease severity as binary is particularly counterproductive.. · An organ-based approach will facilitate evidence-based individualization of care..

Acute kidney injury (AKI) is associated with a significant burden of mortality worldwide. Each episode of AKI increases the long-term risk of death, especially if there is no recovery or insufficient renal recovery (i.e. restoration of kidney function). This narrative review summarizes relevant studies on the definition and prediction of renal recovery. The following databases were searched for references: PubMed, Web of Science, Cochrane Library, Scopus. The period lasted from 1990 until 2024. The currently available criteria for renal recovery have been identified and discussed. Regarding restoration of kidney function prediction, seven studies on alternative or novel biomarkers have been reviewed. In the context of kidney replacement therapy and renal recovery, findings from four large, prospective randomized studies have been summarized. A standardized definition of renal recovery is presently not available. Specific biomarkers allow for an estimation of the likelihood of renal recovery under certain conditions. According to current knowledge, no dialysis method has been definitively shown to be advantageous for the recovery process.

While the relationship between glycemic variability (GV) and acute kidney injury (AKI) has been a subject of interest, the specific association of GV with persistent AKI beyond 48 hours postoperative after noncardiac surgery is not well-established.

This retrospective cohort study aimed to describe the patterns of different GV metrics in the immediate 48 hours after noncardiac surgery, evaluate the association between GV indices and persistent AKI within the 7-day postoperative window, and compare the risk identification capabilities of various GV for persistent AKI. A total of 10,937 patients who underwent major noncardiac surgery across 3 medical centers in eastern China between January 2015 and September 2023 were enrolled. GV was characterized using the coefficient of variations (CV), mean amplitude of glycemic excursions (MAGE), and the blood glucose risk index (BGRI). Multivariable logistic regression was used to examine the relationship between GV and AKI. Optimal cutoff values for GV metrics were calculated through the risk identification models, and an independent cohort from the INformative Surgical Patient dataset for Innovative Research Environment (INSPIRE) database with 7714 eligible cases served to externally validate the risk identification capability.

Overall, 274 (2.5%) of the 10,937 patients undergoing major noncardiac surgery met the criteria of persistent AKI. Higher GV was associated with an increased risk of persistent AKI (CV: odds ratio [OR] = 1.26, 95% confidence interval [CI], 1.08-1.46; MAGE: OR = 1.31, 95% CI, 1.15-1.49; BGRI: OR = 1.18, 95% CI, 1.08-1.29). Compared to models that did not consider glycemic factors, MAGE and BGRI independently contributed to predicting persistent AKI (MAGE: areas under the curve [AUC] = 0.768, P = .011; BGRI: AUC = 0.764, P = .014), with cutoff points of 3.78 for MAGE, and 3.02 for BGRI. The classification of both the internal and external validation cohorts using cutoffs demonstrated good performance, achieving the best AUC values of 0.768 for MAGE in the internal cohort and 0.777 for MAGE in the external cohort.

GV measured within 48 hours postoperative period is an independent risk factor for persistent AKI in patients undergoing noncardiac surgery. Specific cutoff points can be used to stratify at-risk patients. These findings indicate that stabilizing GV may potentially mitigate adverse kidney outcomes after noncardiac surgery, highlighting the importance of glycemic control in the perioperative period.

Acute kidney injury (AKI) is a frequent yet often overlooked complication. This study examines the incidence, unrecognized rate, and outcomes of AKI in adults at a large public Chinese hospital from 2010 to 2023. AKI rates were calculated, and outcomes were assessed using follow-up records. Multivariate logistic regression identified risk factors for unrecognized AKI. Among 2,790,540 patients, 5,080 met the AKI criteria, with an overall incidence of 0.18% (0.78% in hospitalizations, 0.05% in outpatients). The unrecognized AKI was 76.3%. In this group, 75% were stage 1, 16.7% stage 2, and 8.3% stage 3. Orthopedics had the highest unrecognized rate (94.5%) and ICUs the lowest (55.77%). Unrecognition of AKI improved from 90.3% in 2010-2011 to 70.2% in 2022-2023. AKI stage progression was linked to poorer survival. Patients with recognized AKI recovered faster than those with unrecognized AKI (8.0 vs. 9.0 days, p < 0.001). The mean follow-up time was 15.8 days, with similar rates at 28 and 90 days post-AKI for both groups. Risk factors for unrecognized AKI included lower AKI stage, baseline creatinine, absence of shock/heart disease/hypertension, and non-nephrology/surgery admissions. Non-nephrology physicians' unfamiliarity with AKI guidelines may contribute to low awareness. Improved early detection and monitoring in high-risk groups are needed.

Renal toxicity is a disorder that causes considerable issues in healthcare systems world, highlighting the critical importance of creating alternative treatments. Metallic nanoparticles have recently emerged as promising therapeutic agents for nephroprotection because of their remarkable properties. Numerous disciplines, including medicine, biotechnology, and the food industry, are currently investigating and exploring metallic nanoparticles, such as selenium, silver, and gold, with promising outcomes. In this overview, we provide the most current findings on cutting-edge nephroprotection through metallic nanoparticles, especially selenium, silver, and gold nanoparticles. While outlining the benefits, we outline possible methods for developing metallic nanoparticles, characterization techniques, and nephroprotection therapies. Selenium nanoparticles (SeNPs) minimize oxidative stress, a primary cause of nephrotoxicity through cell regeneration which protects kidneys. Silver nanoparticles (AgNPs) have anti-inflammatory capabilities that help alleviate kidney damage and nephrotoxicity. Gold nanoparticles (AuNPs), which are biocompatible and immune-modifying, reduce inflammation and promote renal cell regeneration, indicating nephroprotective advantages. Renal protection via the use of metallic nanoparticles represents a promising new frontier in the fight against kidney disease and other renal disorders. Metallic nanoparticles of selenium, silver, and gold can protect the kidneys by lowering oxidative stress, reducing inflammation, and improving cell repair. Through their mechanisms, these nanoparticles effectively safeguard and repair kidney function, making them suitable for treating renal diseases. The potential applications of selenium, silver, and gold nanoparticles, as well as their complex modes of action and renal penetration, provide fresh hope for improving renal health and quality of life in patients with kidney disease. The current study highlights therapeutic ability, stability, nephroprotection, and toxicity profiles, as well as the importance of continuous research in this dynamic and evolving field.

Acute kidney injury (AKI) is increasingly affecting hospitalized patients worldwide. Patients with inflammatory rheumatic diseases, although primarily impacted by functional impairment and sometimes structural damage to joints, bones, and muscle tissue, may also develop AKI during the course of their disease. This narrative review aimed to summarize potential causes of AKI and the associated disease patterns. The following databases were searched for references: PubMed, Web of Science, Cochrane Library, and Scopus. The search period covered from 1958 to 2024. Certain inflammatory rheumatic diseases increase the risk of AKI due to specific types of kidney disease. However, the most common conditions, such as rheumatoid arthritis and spondylarthritis, rarely cause AKI directly. Among the medications used for pain and sometimes disease activity control, nonsteroidal anti-inflammatory drugs (NSAIDs) can potentially induce AKI, even progressing to acute tubular necrosis. There is evidence that certain rheumatic diseases are associated with increased risk of AKI, independently of directly affecting kidney function or structure. However, the data on this topic are quite limited. AKI is a potentially significant issue for patients with inflammatory rheumatic diseases. Additional data on the increased risk of AKI, independent of direct kidney involvement, are needed.

Acute kidney injury (AKI) within the intensive care unit (ICU) is common but evidence is limited on longer-term renal outcomes. We aimed to model the trend of kidney function in ICU survivors using estimated glomerular filtration rate (eGFR), comparing those with and without AKI, and investigate potential risk factors associated with eGFR decline.

This observational cohort study included all patients aged 16 or older admitted to two general adult ICUs in Scotland between 1st July 2015 and 30th June 2018 who survived to 30 days following hospital discharge. Baseline serum creatinine and subsequent values were used to identify patients with AKI and calculate eGFR following hospital discharge. Mixed effects modelling was used to control for repeated measures and to allow inclusion of several exploratory variables.

3649 patients were included, with 1252 (34%) experiencing in-ICU AKI. Patients were followed up for up to 2000 days with a median 21 eGFR measurements. eGFR declined at a rate of -1.9 ml/min/1.73m2/year (p-value < 0.001) in the overall ICU survivor cohort. Patients with AKI experienced an accelerated rate of post-ICU eGFR decline of -2.0 ml/min/1.73m2/year compared to a rate of -1.83 ml/min/1.73m2/year in patients who did not experience AKI (p-value 0.007). Pre-existing diabetes or liver disease and in-ICU vasopressor support were associated with accelerated eGFR decline regardless of AKI experience.

ICU survivors experienced a decline in kidney function beyond that which would be expected regardless of in-ICU AKI. Long-term follow-up is warranted in ICU survivors to monitor kidney function and reduce morbidity and mortality.

Acute kidney injury (AKI) is a frequent clinical complication lacking early diagnostic tests and effective treatments. Novel biomarkers have shown promise for enabling earlier detection, risk stratification, and guiding management of AKI. We conducted a systematic review to synthesize evidence on the efficacy of novel biomarkers for AKI detection and management. Database searches yielded 17 relevant studies which were critically appraised. Key themes were biomarker efficacy in predicting AKI risk and severity before functional changes; potential to improve clinical management through earlier diagnosis, prognostic enrichment, and guiding interventions; emerging roles as therapeutic targets and prognostic tools; and ongoing challenges requiring further validation. Overall, novel biomarkers like neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), and cell cycle arrest markers ([TIMP-2] •[IGFBP7]) demonstrate capability for very early AKI prediction and accurate risk stratification. Their incorporation has potential to facilitate timely targeted interventions and personalized management. However, factors influencing biomarker performance, optimal cutoffs, cost-effectiveness, and impact on patient outcomes require robust validation across diverse settings before widespread implementation. Addressing these limitations through ongoing research can help translate novel biomarkers into improved detection, prognosis, and management of AKI in clinical practice.

Acute kidney injury (AKI) is a common, heterogeneous, multifactorial condition, which is part of the overarching syndrome of acute kidney diseases and disorders. This condition's incidence highest in low-income and middle-income countries. In the short term, AKI is associated with increased mortality, an increased risk of complications, extended stays in hospital, and high health-care costs. Long-term complications include chronic kidney disease, kidney failure, cardiovascular morbidity, and an increased risk of death. Several strategies are available to prevent and treat AKI in specific clinical contexts. Otherwise, AKI care is primarily supportive, focused on treatment of the underlying cause, prevention of further injury, management of complications, and short-term renal replacement therapy in case of refractory complications. Evidence confirming that AKI subphenotyping is necessary to identify precision-oriented interventions is growing. Long-term follow-up of individuals recovered from AKI is recommended but the most effective models of care remain unclear.

Growing evidence indicates that disruptions in mitochondrial quality management contribute to the development of acute kidney injury (AKI), incomplete or maladaptive kidney repair, and chronic kidney disease. However, the temporal dynamics of mitochondrial quality control alterations in relation to renal injury and its recovery remain poorly understood and are addressed in this manuscript.

ology: Male Wistar rats (n = 60) were subjected to varying durations of ischemia and reperfusion. Ischemia was instigated by clamping both renal arteries and for reperfusion, the clamps were removed to restore the blood flow. Renal injury, physiological function, mitochondrial assessment, and cellular mediators were analyzed.

Prolonging ischemia duration reduces bioenergetic function while disrupting the balance of mitochondrial fusion, fission, and mitophagy at the gene expression level while maintaining intact mitochondrial copy number. However, reperfusing a kidney after 45 min of ischemia with varying reperfusion times exacerbates mitochondrial dysfunction and significantly decreases mitochondrial copy number. These declines are particularly evident at 24 h of reperfusion, with some parameters improving by 7 days of reperfusion. Despite these improvements, 7 days of reperfusion did not correlate with renal injury indicators (CrCl- 0.46 ± 0.01, BUN-86.29 ± 4.9, Cr-1.75 ± 0.16) following 45 min of ischemia. Conversely, 15 min of ischemia followed by 7 days of reperfusion restored mitochondrial quality and renal function (CrCl- 7.33 ± 0.59, BUN-43.6 ± 3.16, Cr-0.93 ± 0.14).

The above findings emphasize that mitochondrial quality control alters with the extent of ischemia and subsequent reperfusion time, impacting not only mitochondrial copy number but also the resilience of mitochondria during tissue repair.

Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) mainly affects the respiratory tract, but different organs may be involved including the kidney. Data on acute kidney injury (AKI) in critical forms of coronavirus disease 2019 (COVID-19) are scarce. We aimed to assess the incidence, risk factors and prognostic impact of AKI complicating critical forms of COVID-19.

A retrospective descriptive case/control monocentric study conducted in a medical intensive care unit of a tertiary teaching hospital over a period of 18 months.

We enrolled 144 patients, with a mean age of 58±13 years old and a male predominance (sex-ratio: 1.25). Forty-one (28%) developed AKI within a median of 4 days (Q1: 3, Q3: 8.5) after hospitalization. It was staged KDIGO class 3, in about half of the cases. Thirteen patients underwent renal replacement therapy and renal function improved in seven cases. Diabetes (OR: 6.07; 95% CI: (1,30-28,4); p: 0.022), nephrotoxic antibiotics (OR: 21; 95% CI: (3,2-146); p: 0.002), and shock (OR: 12.21; 95% CI: (2.87-51.85); p: 0.031,) were the three independent risk factors of AKI onset. Mortality was significantly higher in AKI group (HR:12; 95% CI: (5.81-18.18); p:0.041) but AKI didn't appear to be an independent risk factor of poor outcome. In fact, age > 53 years (p: 0.018), septic shock complicating hospital acquired infection (p: 0.003) and mechanical ventilation (p<0.001) were the three prognostic factors in multivariate analysis.

The incidence of AKI was high in this study and associated to an increased mortality. Diabetes, use of nephrotoxic antibiotics and shock contributed significantly to its occurrence. This underlines the importance of rationalizing antibiotic prescription and providing adequate management of patients with hemodynamic instability in order to prevent consequent AKI.

The outcomes of patients with infective endocarditis (IE)-associated acute kidney injury (AKI) are poorly understood.

This retrospective cohort study was conducted in a tertiary hospital in China to analyze the short- and long-term outcomes among patients with IE-associated AKI. The risk factors for 90-day mortality, long-term outcomes and kidney non-recovery were analyzed via multivariable logistic regression, the Cox regression, and the Fine-Gray competing risk model, respectively.

Among 294 patients with IE-associated AKI, 14.3% died within 90 days, and the risk factors for 90-day mortality were similar to those identified in the general IE population. Among the 230 AKI survivors in whom 90-day kidney recovery could be assessed, 17.4% did not recover kidney function at 90 days. Kidney non-recovery at 90 days was associated with an increased risk of the long-term composite outcome of mortality, end-stage renal disease or sustained doubling of serum creatinine [hazard ratio (HR) 3.00, 95% confidence interval (CI) 1.19-7.59]. Five variables were related to kidney non-recovery: low baseline estimated glomerular filtration rate (eGFR) (HR 2.52, 95% CI 1.73-3.65), stage of AKI (HR 3.03, 95% CI 2.07-4.42 for stage 3), shock (HR 5.56, 95% CI 3.02-10.22), glomerulonephritis-related AKI (HR 3.04, 95% CI 1.93-4.77) and drug-related AKI (HR 2.77, 95% CI 1.86-4.13).

Patients with IE-associated AKI had a high 90-day mortality, and a substantial proportion of survivors did not recover kidney function at 90 days. Kidney non-recovery at 90 days was associated with adverse long-term outcomes. Low baseline eGFR, severe AKI, shock, drug-related AKI and glomerulonephritis-related AKI were risk factors for kidney non-recovery.

Accurate estimation of in-hospital outcomes for patients with acute kidney injury (AKI) is crucial for aiding physicians in making optimal clinical decisions. We aimed to review prediction models constructed by machine learning methods for predicting AKI prognosis using administrative databases.

A systematic review following PRISMA guidelines.

Adult patients diagnosed with AKI who are admitted to either hospitals or intensive care units.

We searched PubMed, Embase, Web of Science, Scopus, and Cumulative Index to Nursing and Allied Health for studies published between January 1, 2014 and February 29, 2024. Eligible studies employed machine learning models to predict in-hospital outcomes of AKI based on administrative databases.

Extracted data included prediction outcomes and population, prediction models with performance, feature selection methods, and predictive features.

The included studies were qualitatively synthesized with assessments of quality and bias. We calculated the pooled model discrimination of different AKI prognoses using random-effects models.

Of 3,029 studies, 27 studies were eligible for qualitative review. In-hospital outcomes for patients with AKI included acute kidney disease, chronic kidney disease, renal function recovery or kidney failure, and mortality. Compared with models predicting the mortality of patients with AKI during hospitalization, the prediction performance of models on kidney function recovery was less accurate. Meta-analysis showed that machine learning methods outperformed traditional approaches in mortality prediction (area under the receiver operating characteristic curve, 0.831; 95% CI, 0.799-0.859 vs 0.772; 95% CI, 0.744-0.797). The overlapping predictive features for in-hospital mortality identified from ≥6 studies were age, serum creatinine level, serum urea nitrogen level, anion gap, and white blood cell count. Similarly, age, serum creatinine level, AKI stage, estimated glomerular filtration rate, and comorbid conditions were the common predictive features for kidney function recovery.

Many studies developed prediction models within specific hospital settings without broad validation, restricting their generalizability and clinical application.

Machine learning models outperformed traditional approaches in predicting mortality for patients with AKI, although they are less accurate in predicting kidney function recovery. Overall, these models demonstrate significant potential to help physicians improve clinical decision making and patient outcomes.

CRD42024535965.

The lack of early renal function recovery among geriatric patients with acute kidney injury (AKI) in the intensive care unit (ICU) is a commonly observed and acknowledged poor prognostic factor, especially for older adults. However, no reliable prognostic biomarker is available for identifying individuals at risk of renal non-recovery or mortality in older adults. In this prospective observational cohort study, we enrolled critically ill older adults (aged ≥ 60 years) with AKI from the ICU and followed their disease progression. The primary endpoint was renal non-recovery within seven days of follow-up, while the secondary endpoint was the determinants of 30-day mortality after AKI. We assessed the predictive accuracy using receiver operating characteristic curves and performed between-group comparisons using the log-rank test. Among 209 older adults, 117 (56.0%) experienced renal recovery. Multiple regression analysis revealed that urine levels of tissue inhibitor of metalloproteinase-2 (TIMP-2) multiplied by insulin-like growth factor-binding protein 7 (IGFBP7) ([TIMP-2]*[IGFBP7]), AKI stages 2-3, and the Acute Physiology and Chronic Health Evaluation (APACHE II) score were independently associated with renal non-recovery. The regression model incorporating [TIMP-2]*[IGFBP7] demonstrated a fair predictive value (AUC 0.774, p < 0.001), with the optimal threshold set at 0.81 (ng/mL)2/1000. When [TIMP-2]*[IGFBP7] was combined with AKI severity and the APACHE score, the AUC increased to 0.851. In conclusion, urine [TIMP-2]*[IGFBP7] is a reliable biomarker associated with renal non-recovery in critically ill older adults, and its predictive efficacy can be further enhanced when combined with AKI severity and the APACHE score.

The purpose of this study was to evaluate the performance of urinary C-C motif chemokine ligand 14 (CCL14) and the renal resistive index (RI) in predicting persistent AKI in unselected critically ill patients.

This prospective observational study was conducted in a tertiary hospital's general intensive care unit (ICU). Consecutive adults who were admitted to the ICU were enrolled, with a primary endpoint of AKI lasting 48 h or longer. Urinary CCL14 was evaluated upon inclusion, and the renal RI was determined within 12 h of ICU admission. The individual discriminative ability of urinary CCL14 and the renal RI to predict persistent AKI was evaluated by the area under the receiver operating characteristic curve (AUC).

Overall, 166 patients were included, of whom 56 had persistent AKI. Urinary CCL14 showed good ability to predict persistent AKI, with an AUC of 0.817. However, the overall performance of the renal RI was fair, with an AUC of 0.739. Forty-nine patients presented with mild AKI at inclusion, and the values of CCL14 were significantly lower than those of patients with moderate or severe AKI (0.205 [0.125-0.300] vs. 0.302 [0.157-0.501]; p = 0.034). In the subgroup analysis, although the diagnostic performance of CCL14 was excellent in patients with moderate or severe AKI, it was fair in patients with mild AKI [AUC = 0. 738; 95% confidence interval (CI) 0.593-0.853].

Urinary CCL14 was an excellent predictor of persistent AKI in patients with moderate or severe AKI, but its performance was not good in patients with mild AKI. The renal RI cannot discriminate between transient and persistent AKI.

Carfilzomib, a new proteasome inhibitor indicated for patients with relapsed/refractory myeloma, has been associated with cases of thrombotic microangiopathy (CFZ-TMA). The role of variants in the complement alternative pathway and therapeutic potential of complement blockade with eculizumab remain to be determined.

We report 37 cases of CFZ-TMA recorded in the French reference center for TMA with their clinical characteristics, genetic analysis and outcome according to treatments.

A trigger was identified in more than half of cases, including eight influenza and five severe acute respiratory syndrome coronavirus-2 cases. All patients presented with acute kidney injury (AKI) [KDIGO stage 3 in 31 (84%) patients] while neurological (n = 13, 36%) and cardiac (n = 7, 19%) damage were less frequent. ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type I repeats-13) and complement activity were normal (n = 28 and 18 patients tested) and no pathogenic variant in the alternative complement pathway was found in 7 patients tested. TMA resolved in most (n = 34, 94%) patients but 12 (44%) still displayed stage 3 AKI at discharge. Nineteen (51%) patients were treated with therapeutic plasma exchange, 14 (38%) patients received corticosteroids and 18 (50%) were treated with eculizumab. However, none of these treatments demonstrated a significant impact on outcomes.

This study is the largest case series of CFZ-TMA since its approval in 2012. Patients present with severe AKI and experience frequent sequelae. Complement variants and blockade therapy do not seem to play a role in the pathophysiology and prognosis of the disease.

Haemodialysis is the primary kidney replacement therapy modality in Africa. In Ethiopia, the number of patients undergoing Haemodialysis is increasing, yet data on their outcomes is scarce. This study assesses the clinical characteristics and outcomes of Haemodialysis patients at Jimma Medical Center.

A retrospective cross-sectional study was conducted from April 08 to 12, 2024, involving patients who underwent Haemodialysis at Jimma Medical Center from June 2017 to March 2024. The data were coded and entered into EpiData version 3.1, then exported to the Statistical Package for Social Sciences version 26.0 for analysis. Descriptive statistics summarized the patients' clinical characteristics and outcomes, and Kaplan-Meier curves were used to assess survival status.

During the seven-year study period, 68 patients underwent Haemodialysis at Jimma Medical Center, with a predominance of males (69.1%). The average age of patients was 42.7 (± 12.8) years with 69.1% (95% CI: 57.5-79.1%) diagnosed with chronic kidney disease, while 30.9% (95% CI: 20.9-42.5%) had acute kidney injury. Among chronic kidney disease patients, common clinical features included nausea and vomiting (100%), proteinuria (95.7%), and body swelling (82.9%), while acute kidney injury patients frequently presented with oliguria (100%), nausea and vomiting (90.5%), and hematuria (52.4%). Hypertensive nephropathy was the leading cause of chronic kidney disease (40.4%), and acute glomerulonephritis (38.1%) and severe malaria (33.3%) were the predominant causes of acute kidney injury. Mortality was observed at 47.6% (95% CI: 27.7-68.6%) in acute kidney injury patients and 40.4% (95% CI: 27.3-54.7%) in chronic kidney disease patients. Emergency vascular access was required in 95.7% of chronic kidney disease and 100% of acute kidney injury patients.

This study highlights the substantial burden of chronic kidney disease and acute kidney injury among hemodialysis patients at Jimma Medical Center, revealing distinct clinical profiles and outcomes. Although acute kidney injury patients exhibited a longer median survival time, the significant mortality risk within the first year underscores the urgent need for improved treatment access and resource allocation. Enhancing early intervention and ensuring the availability of critical medications, such as erythropoietin, are essential for optimizing patient outcomes for both chronic kidney disease and acute kidney injury groups.

Not applicable.

This study aimed to assess the prognostic significance of serum ferritin levels in sepsis-associated acute kidney injury (SA-AKI) and their correlation with short-term mortality. Despite the established predictive value of serum ferritin in various serious diseases, its specific prognostic relevance in SA-AKI remains unexplored. Therefore, this study seeks to fill this research gap by investigating the association between serum ferritin levels and short-term mortality in patients with SA-AKI.

This retrospective cohort study utilized clinical data from the Medical Information Mart for Intensive Care-IV (MIMIC-IV) database, including all patients with SA-AKI admitted to the intensive care unit for the first time. The relationship between serum ferritin levels and 28-day mortality was explored using restricted cubic splines. Kaplan-Meier curves and Cox regression models were employed to evaluate the association between serum ferritin levels and mortality. Subgroup and sensitivity analyses were performed to verify the robustness of the results.

In this study, a total of 878 patients (486 males and 392 females) with a median age of 63.7 years were enrolled. The results indicated that increasing serum ferritin levels were linearly associated with a gradual increase in 28-day mortality rates. Specifically, patients in the highest quartile of serum ferritin had significantly higher 28-day mortality compared to those in the reference group (the first quartile of ferritin levels). After adjusting for various factors, the fully adjusted hazard ratio was 1.92 (95% CI: 1.24-2.96, p = 0.003).

In patients with SA-AKI, higher serum ferritin levels are associated with an increased 28-day mortality rate.

To determine the prevalence of functional, respiratory and renal impairments and of post-intensive-care-syndrome (PICS) among patients who had attended a post-ICU multidisciplinary consultation (post-ICU-MC) around 3 months after ICU discharge, we performed a retrospective, monocentric observational study, at Clermont Ferrand University hospital, France. We included patients who had attended a post-ICU-MC. Their characteristics during ICU stay and at the post-ICU-MC were collected. Functional status was assessed by the 6-min-walking test, handgrip test and peak inspiratory pressure, respiratory function by exploratory functional outcomes, mental status by SF-36 score, and quality of life by SF-36 score and European Quality of Life 5 Dimensions questionnaire. Overall, we enrolled 67 patients, of whom 70%, 74%, and 68% had functional, respiratory, and renal impairments, respectively, at the post-ICU-MC. Additionally, 40%, 28%, 19%, and 2.5% had three, two, one, and none of these impairments, respectively. All patients experienced mental disorders and a decline in quality of life. Functional impairment correlated with frailty score and sex, and respiratory function with age. To conclude, the prevalence of PICS in our cohort was high, as was that of functional, respiratory and renal failure.

Renal involvement in sarcoidosis is rare. We evaluated the pattern of renal involvement in sarcoidosis, its clinical course, renal histology, and response to treatment.

We retrospectively analyzed the data of all cases with sarcoidosis exhibiting renal involvement referred to our department between January 2010 and December 2021.

A total of 33 patients (age: 50.6 ± 12.6 years, males: 57.6%) were analyzed. Common presenting symptoms were weight loss (81.8%; n = 27), fever (75.8%; n = 25), and vomiting (63.6%; n = 21). A total of 14 (42.4%) patients had granulomatous interstitial nephritis (GIN), 13 (39.4%) had isolated hypercalcemia, and six (18.2%) had GIN along with hypercalcemia. Renal biopsy was performed in 20 (60.6%) patients, and all showed GIN, with concomitant glomerular disease in four (12.1%) patients. Mean serum creatinine and 24-h urine protein at presentation were 4.3 ± 2.1 mg/dL and 2.5 ± 0.9 g/day, respectively. All patients received oral prednisolone 1 mg/kg/day with subsequent tapering, concomitantly with azathioprine. Mycophenolate mofetil was used in three (9.1%) patients who developed azathioprine-induced hepatoxicity. After a median follow-up of 24 months (8-120 months), mean serum creatinine and 24-h urine protein improved to 1.9 ± 1.5 mg/dL and 1.1 ± 0.6 g/day, respectively, (P = 0.005). On follow-up, two patients (6.1%) became dialysis-dependent, and three (9.1%) succumbed: one due to a cardiovascular event and two to sepsis and septic shock.

Granulomatous interstitial nephritis was the most common diagnosis in sarcoidosis patients with kidney failure. Early steroid treatment improves kidney function.

Acute kidney injury (AKI) is common in cirrhotic patients, especially in the intensive care unit (ICU), and is often associated with poor prognosis. Albumin is often used for plasma volume expansion, but its efficacy in cirrhotic patients with AKI [excluding hepatorenal syndrome (HRS)] is debated. This study aimed to assess the impact of albumin therapy on prognosis in ICU patients with cirrhosis and non-HRS AKI.

A retrospective analysis was conducted using the MIMIC-IV 2.2 database. The primary endpoint was 28-day mortality. Inverse probability of treatment weighting (IPTW) was used to balance baseline characteristics between the albumin and non-albumin groups.

A total of 1,623 patients were included, with 586 receiving albumin. After IPTW, the sample sizes were 1,713 in the non-albumin group and 1,490 in the albumin group. Albumin administration was associated with higher rates of AKI recovery at 48 h but did not improve 28-day mortality in the overall cohort. Further analysis revealed that using 5% albumin concentration was associated with improved 28-day mortality (HR 0.68; 95% CI 0.49-0.95; p = 0.025), whereas 25% albumin did not show benefit. In patients with high bilirubin levels, albumin treatment significantly reduced 28-day mortality. However, albumin therapy may increase 28-day mortality in certain subgroups, including patients with chronic kidney disease and baseline albumin levels >3.3 g/dL.

Although albumin therapy improved 28-day mortality in some cases, it may also increase mortality in certain subgroups. The use of albumin in critically ill patients with cirrhosis and AKI should be approached with greater consideration of its risks and benefits.

Renal failure after cardiac surgery is associated with increased morbidity and mortality. There is a lack of data examining the rate of renal recovery after patients have started dialysis following cardiac surgery. We aimed to determine the frequency of and time to renal recovery of patients requiring dialysis after cardiac surgery.

All patients who developed new-onset renal failure requiring dialysis following cardiac surgery at our institution from 2011 to 2022 were included. Renal recovery, time to renal recovery, and mortality at 1 year were merged with patients' Society of Thoracic Surgeons Adult Cardiac Surgery Database files. Kaplan-Meier analysis was used to predict time to renal recovery; we censored patients who died or were lost to follow up. Cox regression was used for risk-adjustment.

A total of 312 patients were included in the final analysis. Mortality during index hospital admission was 33% (n = 105), and mortality at 1 year was 45% (n = 141). Of those surviving at 1 year, 69% (n = 118) remained renally recovered. Median renal recovery time was 56 (37-74) days. Accounting for mortality as a competing risk, 51% of patients were predicted to achieve renal recovery. Increasing age (hazard ratio, 0.98; 0.514-0.94, P < .026) and increasing total packed red blood cells (hazard ratio, 0.0958; 0.937-0.987, P < .001) received were found to be significant negative predictors of renal recovery in the Fine-Gray model for subhazard distribution.

More than two-thirds of patients with renal failure who survived the perioperative period had renal recovery within 1 year after surgery. Recovery was driven primarily by postoperative complications rather than comorbidities and intraoperative factors, suggesting renal failure in the postoperative cardiac surgery patient surviving to discharge is unlikely to be permanent.

In this study, we dynamically monitored the glomerular filtration rate and other assessment of renal function and markers of injury in various mice models of acute kidney injury. Male C57BL/6 mice were utilized to establish acute kidney injury models of sepsis, ischemia reperfusion, cisplatin, folic acid, aristolochic acid and antibiotic. In addition to the real time glomerular filtration rate, renal LCN-2 and HAVCR-1 mRNA expression levels, and serum creatinine, urea nitrogen and cystatin c levels were also used to evaluate renal function. In addition, the protein levels of LCN-2 and HAVCR-1 in renal, serum and urine were measured. Our results demonstrated that the changes in biomarkers always lagged the real time glomerular filtration rate during the progression and recovery of renal injury. Cystatin-c can reflect renal injury earlier than other markers, but it remains higher in the recovery stage. Perhaps the glomerular filtration rate does not reflect the greater injury caused by vancomycin plus piperacillin.

Acute kidney injury (AKI) is a multifactorial syndrome with a high risk of short- and long-term complications as well as increased health care costs. The traditional biomarkers of AKI, serum creatinine and urine output, have important limitations. The discovery of new functional and damage/stress biomarkers has enabled a more precise delineation of the aetiology, pathophysiology, site, mechanisms, and severity of injury. This has allowed earlier diagnosis, better prognostication, and the identification of AKI sub-phenotypes. In this review, we summarize the roles and challenges of these new biomarkers in clinical practice and research.

Introduction The severe consequences of acute kidney injury (AKI) have been well-documented in high-risk patient populations. However, the effects of milder forms in non-critically ill patients remain understudied, particularly in resource-limited settings. While the risk of mortality associated with these cases is considered low, it can still lead to various complications including prolonged hospitalization, which may influence long-term renal and patient survival. Hence, the objective of this study was to study the impact of non-dialysis-requiring AKI (NDR-AKI) on survival outcomes of non-critically ill medical patients admitted to St. Paul's Hospital Millennium Medical College in Ethiopia during the period from July 2019 to January 2022. Methods A retrospective cohort study was conducted among 300 non-critically ill medical patients, 93 with NDR-AKI and 207 without AKI. Descriptive statistics, including frequency distributions and median survival times, were employed to summarize the data. Kaplan-Meier curves and the log-rank test were utilized to compare survival experiences of groups. A Cox proportional hazards survival model was fitted to estimate the impact of NDR-AKI on time to recovery. Adjusted hazard ratio (AHR) with 95% confidence interval (CI) was used to report findings. Results Two hundred four (68.0%) were discharged after improvement and the median recovery time was 16 days (95%CI: 13.5-18.5 days). Having NDR-AKI was associated with a 43% lower rate of achieving recovery (AHR=0.57, 95%CI=0.38, 0.84, p-value=0.004). Females were found to have a 1.41 times higher rate of recovery (AHR=1.41, 95%CI=1.03,1.94, p-value=0.033). Additionally, having tuberculosis (AHR=0.41, 95%CI=0.23,0.72, p-value=0.002) and being on anticoagulant (AHR=0.67, 95%CI=0.47,0.95, p-value=0.027) were associated with a 59% and 33% lower rate of recovery, respectively. Conclusion NDR-AKI significantly delays recovery compared to patients without AKI suggesting that even milder forms of AKI in non-critically ill patients can negatively impact patient outcomes. Early identification, prompt management, and addressing underlying causes are key to improving recovery and reducing long-term morbidity and mortality. Strict screening and monitoring of high-risk groups such as men, patients with tuberculosis, and those on anticoagulants is also crucial.

The interplay between serum bicarbonate levels and kidney outcomes is not fully understood. We conducted a prospective cohort study in three intensive care units (ICUs) to evaluate the association of serum bicarbonate levels with acute kidney injury (AKI) and kidney function recovery in critically ill patients.

A prospective cohort study in three intensive care units (ICUs) was performed. The serum bicarbonate level in the first 24 h after ICU admission was categorized as low (< 22 mEq/L), normal (22-26 mEq/L), or high (> 26 mEq/L). Serum creatinine (SCr) levels according to the KDIGO AKI guideline were used for defining AKI within the first 7 days of ICU stay. At ICU admission, SCr ≥ 1.1 for women and ≥ 1.3 mg/dL for men were indicative of impaired kidney function. Mortality outcome was tracked up to 28 days, and kidney function recovery was assessed at hospital discharge.

A total of 2732 patients (66 ± 19 years and 55% men) were analyzed, with 32% having impaired kidney function at ICU admission. Overall, 26% of patients had low bicarbonate levels, while 32% had high bicarbonate levels. Notably, patients with preserved kidney function showed a lower prevalence of low bicarbonate levels compared to those with impaired kidney function (20% vs. 39%, p < 0.001), while higher rates were observed for high bicarbonate (35% vs. 24%, p < 0.001). Compared with patients with normal serum bicarbonate levels, those with low bicarbonate were 81% more likely to develop AKI (OR = 1.81; 95% CI 1.10-2.99), whereas those with high bicarbonate were 44% less likely (OR = 0.56; 95% CI 0.32-0.98) in the adjusted model for confounders. Neither those with high nor low serum bicarbonate levels were associated with an increased risk of mortality (HR = 1.03; 95% CI 0.68-1.56 and 0.99; 95% CI 0.68-1.42, respectively). In subgroup analysis, regardless of the kidney function at ICU admission, serum bicarbonate levels were not associated with the development of AKI and all-cause mortality. Regarding kidney function recovery, higher non-recovery rates were found for those with low bicarbonate.

In critically ill ICU patients, low bicarbonate levels were associated with the more likely development of AKI and subsequent non-recovery of kidney function, while high bicarbonate levels showed no such association. Therefore, low bicarbonate levels may be considered a risk factor for adverse kidney outcomes in critically ill patients.