Acute kidney injury (AKI) frequently complicates acute heart failure (AHF), predicting worse outcomes. Early risk identification is crucial. The stress hyperglycemia ratio (SHR), reflecting acute dysglycemia, may predict AKI, but its utility in AHF remains unestablished. We analyzed 1,241 AHF patients stratified by SHR. Associations with outcomes were assessed using logistic and Cox regression. The relationship between continuous SHR and AKI development was evaluated with restricted cubic splines (RCS). The primary endpoint was incident AKI during hospitalization. AKI occurred in 79.7% of patients. After multivariable adjustment, SHR demonstrated a linear association with AKI risk. For 28-day mortality, the relationship with SHR was U-shaped, with an inflection point at 0.841. An SHR >0.841 was associated with significantly increased mortality (OR=2.086; 95% CI: 1.368-3.182). An elevated SHR was consistently associated with higher AKI risk across all patient subgroups, with an overall adjusted OR of 1.60 (95% CI: 1.15-2.22). The study demonstrates a linear association between the SHR and AKI, in contrast to a U-shaped relationship with 28-day in-hospital mortality among AHF patients. An SHR of 0.841 represents a critical threshold for evaluating in-hospital mortality risk.

Acute respiratory distress syndrome and acute kidney injury in critically ill patients: A scoping review on this lung-kidney crosstalk.

BackgroundThe goal of this study was to evaluate the impact of contrast administration on the subsequent development of acute kidney injury (AKI) in trauma patients.MethodsTrauma patients at a level one trauma center were identified and stratified by administration of contrast during their initial diagnostic evaluation. Outcomes including mortality, AKI, and need for renal replacement therapy were collected and compared. Multivariable logistic regression analysis was performed to determine the impact of contrast administration on the development of AKI in trauma patients.Results839 patients were identified: 551 who received contrast and 288 who did not. Only 58 (6.9%) developed AKI and 3 (0.3%) required new renal replacement therapy (RRT). Those exposed to contrast had a higher injury severity score (10 vs 9, P < .001), admission serum creatinine (1.02 vs 0.91, P < .001), initial vasopressor requirements (3.8% vs 0.3%, P = .003), and 24-hour packed red blood cell transfusions (PRBC) (4 vs 2 units, P < .001). Despite this, those exposed to intravenous contrast had lower rates of acute kidney injury (9.4% vs 5.6%, P = .042) and no difference in the need for new RRT (0.5% vs 0%, P = .2). Multivariable logistic regression identified age, 24-hour PRBC transfusions, admission SBP, and admission serum creatinine as the only independent predictors of acute kidney injury.DiscussionIn the diagnostic evaluation of trauma patients, the administration of intravenous contrast was not associated with the subsequent development of acute kidney injury.

Introduction Daboia siamensis envenoming is a major cause of hematotoxicity and acute kidney injury in Southeast Asia. In Thailand, D. siamensis is a clinically important snake, yet detailed national data on its bites are limited. Hence, we aimed to determine the clinical characteristics, management, and outcomes of D. siamensis bites in Thailand, identify factors associated with acute kidney injury and hemodialysis, and analyze antivenom administration with reference to acute kidney injury and hemodialysis. Methods We conducted a 10-year retrospective cross-sectional study using data from the Ramathibodi Poison Center Toxic Exposure Surveillance System (2014–2023). All diagnosed D. siamensis bites were reviewed. Definite cases were defined when the snake species was identified via a live specimen, carcass, or photograph. Results A total of 185 patients were included, with 101 definite cases. Most (82.7%) were male, and the mean (±SD) age was 43.0 ± 16.6 years. Overall clinical manifestations included local effects (20.5%), coagulopathy (89.2%), acute kidney injury (50.3%), thrombocytopenia (31.4%), and rhabdomyolysis (28.1%). Antivenom was administered in 89.2% of cases. The median (IQR) length of hospital stay was 5 (3–7) days. The mortality rate was 3.8%. Tachycardia at presentation, initial proteinuria, and rhabdomyolysis were found to prognosticate the development of acute kidney injury. Metabolic acidosis at presentation and rhabdomyolysis were predictors of the requirement for hemodialysis. In addition, receiving antivenom within two hours may reduce the need for hemodialysis (odds ratio 0.153, 95% CI 0.035–0.674). Discussion Discrepancies between our findings and those of others on D. siamensis bites may have resulted from geographic variation in the venom composition and/or differences in the study period and population. Although antivenom treatment did not reverse renal injury, it may have prevented progression. Conclusions Systemic hematotoxicity and nephrotoxicity generally developed after a D. siamensis bite. Several clinical characteristics are potential markers of acute kidney injury and hemodialysis requirement after a D. siamensis bite, and early administration of antivenom may reduce the need for hemodialysis.

We aimed to identify risk factors for the development of acute kidney injury (AKI) during treatment of Staphylococcus aureus bacteremia (SAB), with particular emphasis on the roles of cloxacillin and cefazolin, and the contribution of other antibiotics. We performed a retrospective, observational, single-center study of a prospective cohort of patients with SAB receiving cloxacillin or cefazolin as definitive therapy and with serum creatinine available at baseline and days 5, 10, and 15. The primary outcome was the highest AKI stage between days 5 and 15; the secondary outcome was 30 day mortality. Univariate and multivariate analyses were performed to identify independent predictors of outcomes. A total of 470 patients were included in the study, and 103 (21.9%) developed AKI during hospitalization. Independent predictors of AKI were age >64 years (adjusted odds ratio [aOR] 1.76; 95% CI 1.08-2.87), peripheral arterial disease (aOR 2.23; 95% CI 1.02-4.88), chronic kidney disease (aOR 3.77; 95% CI 2.07-6.89), need of mechanical ventilation (aOR 3.33; 95% CI 1.62-6.86), and cloxacillin as definitive treatment with prior glycopeptide exposure (aOR 3.45; 95% CI 1.74-6.84). AKI occurred in 42.6% (23/52) of patients receiving empirical glycopeptide followed by cloxacillin, compared with 21.0% (61/290) in those treated with cloxacillin without prior glycopeptide exposure. The development of AKI during admission was an independent predictor of 30 day mortality (aOR 3.50; 95% CI 1.88-6.52). The only modifiable factor associated with AKI was the use of cloxacillin as definitive therapy after prior exposure to glycopeptides. These data reinforce the need to consider non-nephrotoxic alternatives.

ASSOCIATION OF SITE OF RIGHT CORONARY ARTERY OCCLUSION AND RECOVERY OF COMPLETE HEART BLOCK IN ACUTE INFERIOR WALL MYOCARDIAL INFARCTION UNDERGOING PRIMARY ANGIOPLASTY: THE RECOVER-CHB STUDY.

The safety of a low-osmolar contrast agent, iopromide (Ultravist, Bayer, Leverkusen, Germany), currently being used is unknown. This study aimed to evaluate whether iopromide use was associated with acute kidney injury (AKI) in patients undergoing contrast-enhanced computed tomography (CT) imaging. This retrospective cohort study included 1915 participants who had CT scans during 2023. AKI was defined as an absolute rise in serum creatinine (sCr) ≥26.5 µmol/L within 48hours or≥1.5 times increase from baseline within seven days. The differences in the means of pre-CT and post-CT sCr with and without contrast exposure were determined using the independent samples t-test and variance ratio (F-test). Paired t-test was used to find the mean difference between pre- and post-CT creatinine levels. Pearson's chi-squared (X2) test, along with pairwise correlation analysis, was applied to find the relationship between contrast exposure and AKI as well as AKI and renal outcomes. To find out the independent predictors of contrast-associated acute kidney injury (CA-AKI), a multivariable binary logistic regression model was conducted. Of 1915 participants who underwent CT imaging, 869 (45.4%) were exposed to contrast, while 1046 (54.6%) were not exposed to contrast. No statistically significant difference was found between exposed and non-exposed groups for the development of AKI (10.6% vs. 8.8%; p=0.188). Both groups were found to have lower mean post-procedure sCr compared to pre-procedure sCr (-2.2 and -12.7 µmol/L, respectively). The AKI occurrence was not directly associated with whether patients were exposed to iopromide or not (r=0.03; p=0.178). Noteworthy risk factors identified were active malignancy (aOR: 2.43; 95% CI: 1.54-3.84; p<0.001), pre-existing renal dysfunction (aOR: 2.31; 95% CI: 1.27-4.18; p=0.006), and cardiac disease (aOR: 2.09; 95% CI: 1.22-3.58; p=0.007). Use of low-osmolar contrast agents for CT imaging was not independently associated with AKI. Our results suggest that contrast-enhanced CT may be considered when clinically indicated without unnecessary delay while acknowledging that individual patient risk assessment remains essential. Greater emphasis should instead be placed on identifying and optimizing certain factors, like active malignancy, pre-existing renal dysfunction, and cardiac diseases, to prevent CA-AKI.

Periprosthetic joint infection (PJI) is a devastating complication of joint arthroplasty and is commonly treated with two-stage revision. During two-stage revision, the insertion of a temporary antibiotic-loaded bone cement spacer (ALCS) in infected joints exerts a direct and effective anti-infection effect but may increase the risk of developing acute kidney injury (AKI). This article reviews the latest research progress on AKI after ALCS insertion for PJI treatment and discusses the definition, incidence and outcome of AKI. We focused on analyzing the risk factors for AKI in terms of demographic characteristics, comorbidities, medication history, perioperative management, and types and doses of antibiotics in ALCS patients. The results revealed that advanced age, excessive obesity, a history of diabetes mellitus, a history of hypertension, the use of angiotensin-converting enzyme inhibitor (ACEI) or angiotensin-II receptor blocker (ARB) medications, a history of chronic kidney disease (CKD), preoperative anemia or hypoalbuminemia, the use of nonsteroidal anti-inflammatory drugs (NSAIDs), high intraoperative blood loss, insufficient perioperative rehydration, and transfusions significantly increased the incidence of AKI. The associations between the development of AKI and antibiotic type and dosage in ALCS are still unclear. Further exploration is still necessary to help clinicians identify PJI patients with a high risk of AKI early and improve their prognosis.

Renal pulsatility index assessment by intraoperative doppler ultrasound is associated with acute kidney injury after cardiac surgery: a prospective observational study.

Acute kidney injury (AKI) is characterized by high incidence and mortality rates, and a lack of specific targeted therapies. Inflammatory responses mediated by immune cells and direct damage to renal tubular epithelial cells underlie AKI development. Melanocortin exerts renoprotective effects through systemic immune regulation; however, the renoprotective role of melanocortin 1 receptor (MC1R) remains unclear. MC1R-deficient (e/e) mice developed higher serum creatinine levels, more severe renal dysfunction, and greater histological damage than wild-type (WT) mice following folic acid-induced AKI. Treatment with MC1R agonist MS05 improved experimental nephritis in WT mice; however, this effect was less pronounced in e/e mice. The exacerbation of AKI in e/e mice was associated with damage to renal tubular epithelial cells and macrophage infiltration, where MC1R is highly expressed. MC1R alleviates tubular cell inflammation by inhibiting the nuclear factor-κB pathway and suppresses the polarization of M1 macrophages. Chimeric mice were generated through transplantation of bone marrow-derived macrophages after irradiation. Macrophages from e/e mice with MC1R dysfunction exacerbated kidney injury in WT mice, whereas those from WT mice mitigated kidney injury in e/e mice. Targeting MC1R in renal tubular epithelial cells and macrophages provides a novel treatment concept for AKI.

Acute kidney injury (AKI), a life-threatening disorder marked by abrupt renal dysfunction, is increasingly recognized as a global healthcare challenge. It not only triggers immediate organ dysfunction but also heightens long-term risks of chronic kidney disease (CKD). The senescence of proximal tubular epithelial cells (PTECs) has a major impact on the occurrence and development of AKI. This review systematically analyzes existing evidence, which suggests that the senescence of PTECs may have a dual effect. Acute cellular senescence typically mitigates uncontrolled replication of damaged cells by inducing cell cycle arrest, thereby limiting the further expansion of tissue damage. In contrast, the pathological retention of chronic senescent cells and the excessive production of the senescence-associated secretory phenotype (SASP) exacerbate the local inflammatory response and the process of fibrosis, accelerating the transformation of AKI into CKD. Despite incomplete elucidation of the spatiotemporal mechanisms governing the transition from acute to chronic cellular senescence, therapeutic interventions can be precisely targeted to specific disease stages based on their characteristic progression dynamics. This review summarizes the intervention strategies applicable at different stages of AKI, including prevention, early induction of senescence, senoreverse, senolysis, and senomorphics. Additionally, we highlight potential therapeutic targets to provide a theoretical basis for optimizing clinical management.

Patient vulnerability associated with acute kidney injury after pulsed field ablation: A role for baseline biomarkers and haptoglobin phenotype.

Serum creatinine frequently increases during hospitalizations for acute heart failure (AHF) meeting criteria for acute kidney injury (AKI), but the significance of this increase is variable. We evaluated whether admission levels of kidney tubule and cardiac biomarkers are associated with increases in serum creatinine and adverse in-hospital events. In a nested case-control, we identified 214 cases with at least stage 1 AKI defined by the 2012 Kidney Disease Improving Global Outcomes criteria within seven days of admission in the Acute Kidney Injury Neutrophil Gelatinase-Associated Lipocalin Evaluation of Symptomatic Heart Failure Study and matched with 214 controls who did not experience AKI. The primary outcome was the development of AKI within the first seven days; secondary outcomes were the development of severe AKI (stages 2 or 3) and a composite of adverse in-hospital events. Associations of 6 blood and 14 urine biomarkers were assessed with logistic regression and Receiver Operating Characteristic Area Under the Curve (ROC-AUC) curve analysis. Individuals were 71±13 years; 64% were men; with median admission creatinine 1.3 [IQR 1.0-1.8] mg/dL. Among AKI cases, 181 (85%), 16 (8%), and 17 (8%) were stages 1, 2, and 3, respectively. Compared to the lowest tertile, only the highest tertiles of fractional excretion of sodium (FeNa≥3.65; OR 1.7, 95% CI 1.0-2.9) and urinary MCP-1 (≥ 433ng/g; OR 1.7, 95% CI 1.0-2.8) were associated with AKI risk, though discrimination was poor (ROC-AUC<0.60). Neither was associated with severe AKI. Only elevated B-type natriuretic peptide (≥ 932 pg/mL) predicted the composite adverse in-hospital event (OR 2.3, 95% CI 1.2-4.2). Kidney tubule and cardiac biomarkers at admission for AHF are not associated with risk for increases in creatinine or adverse in-hospital events reaffirming that creatinine changes in AHF are largely functional in nature.

This study investigated the incidence, risk factors, and prognostic implications of acute kidney injury (AKI) after transjugular intrahepatic portosystemic shunt (TIPS). This multicenter retrospective study included patients who underwent TIPS at three hospitals in China. AKI risk factors were identified using multivariate logistic regression in the overall cohort. Propensity score matching was performed to balance baseline covariates. Survival differences were assessed using the Kaplan-Meier method, and the association between AKI and mortality was evaluated using stratified Cox regression models. A total of 995 patients were included, of whom 4.92% developed postoperative AKI. Multivariable analysis identified older age (OR: 1.07, 95% CI: 1.04–1.10), higher preoperative neutrophil percentage (OR: 1.05, 95% CI: 1.02–1.08), elevated preoperative creatinine (OR: 1.01 [per μmol/L], 95% CI: 1.00–1.01), and an increased Child-Pugh score (OR: 1.27, 95% CI: 1.01–1.59) as independent risk factors for AKI. AKI was strongly associated with increased overall mortality (p < 0.001). In the propensity score-matched cohort, postoperative AKI remained an independent predictor of worse long-term survival (HR: 4.09, 95% CI: 1.97–8.50). In conclusion, age, preoperative neutrophil percentage, creatinine level, and Child-Pugh score were independent risk factors for AKI following TIPS, and the development of AKI is strongly associated with a poor prognosis in these patients.

Aim : To identify predictors of acute kidney injury (AKI) after coronary artery bypass grafting (CABG) in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). Material and methods. The study included patients with NSTE-ACS and multivessel coronary artery disease, for whom the cardiac team determined indications for CABG. Initially, during the first 7 days after CABG and prior to discharge from the hospital, creatinine levels in the blood were measured using the Jaffe method (Synchron CX Systems, USA), and the initial levels of N-terminal pro-brain natriuretic peptide (Nt-proBNP) were examined using an immunochemical method (Elecsys, Roche). Chronic kidney disease (CKD) was diagnosed if the glomerular filtration rate (GFR) was less than 60 ml/min/1,73 m 2 . GFR was calculated using the CKD-EPI formula. CABG was performed either on a "beating heart" or under conditions of artificial circulation. AKI was diagnosed according to KDIGO criteria (2012). In-hospital complications of CABG including AKI, intraoperative myocardial infarction (MI), bleeding, multiple organ failure and cardiac deathwere recorded. The cumulative incidence rate of in-hospital complications, including thoselisted, was calculated, taking into account the first occurrence of the event. Results . We examined 70 patients with NSTE-ACS, 32,9% of whom had MI. The mean age was 65 years, and 77,1% of the patients were men. They had multivessel coronary artery disease. All patients had arterial hypertension, 31,4% had type 2 diabetes mellitus, and 17,1% had CKD. The initial Nt-proBNP level was 168 (54-902) pg/ml. After CABG, AKI developed in 15 (21,4%) patients, with stage 1 AKI occurring in 17,1%, and stage 2 and 3 in 4,1%. Parameters associated with the development of postoperative AKI included a higher incidence of stages 3 and 4 CKD (p=0,05), an initial left ventricular ejection fraction &lt; 50% (p=0,031), intraoperative MI (p=0,036), the use of adrenaline to stabilize hemodynamics (p=0,001), and a higher initial Nt-proBNP level (909, 278-1394 pg/ml, p=0,011). Nt-proBNP was found to be a predictor of AKI after CABG. A level above the median value of 900 (278-1394) pg/ml increased the likelihood of AKI development by an average factor of 9,0 times. Patients with AKI after CABG showed a tendency toward a higher cumulative incidence of in-hospital complications compared to those without AKI (40% and 16,4%, respectively, p=0,05). Conclusion . The incidence of AKI after CABG in patients with NSTE-ACS was 24,1%. On average, the likelihood of developing AKI after CABG was 9,0 times higher for patients with an initial Nt-proBNP level above the median value (900, 278-1394 pg/ml). Patients who developed AKI after CABG were more likely to experience adverse in-hospital complications than those without postoperative AKI.

Acute kidney injury (AKI) impairs renal function in the short term and may eventually progress to chronic kidney disease (CKD) in the long term. The activation of Smad3 and an imbalance in hypoxia-inducible factors-α (HIF-α) expression constitute vital mechanisms leading to the AKI-CKD transition. We have designed a Smad3-targeted Proteolysis-Targeting Chimera (PROTAC) named P1705434, which recruited VHL to degrade Smad3 and meanwhile stable HIF-2α levels. We established a cisplatin nephrotoxicity model and folic acid nephropathy (FAN) model to explore its role and possible mechanisms in the early stage and development of AKI. The results demonstrated that P1705434 alleviated inflammation and fibrosis in progressing AKI by degrading Smad3 and increasing HIF-2α. This was confirmed in both the cisplatin nephrotoxicity and FAN mice models, as evidenced by the reduction percentage of maladaptive proximal tubular cells (PT) and down-regulation of the TNF pathway, which ameliorated injury in S3-PT. Furthermore, we identified a transitional collecting duct (tCD) cell type that had a trend to differentiate into fibroblast but P1705434 treatment reduces the propensity of tCD cells and mitochondrial injury in CD cells by up-regulating the oxidative phosphorylation (OXPHOS) pathway.

Soluble Cluster of Differentiation 14 as a Prognostic Marker in Decompensated Cirrhosis With Water Retention.

IntroductionManaging fluid balance in COVID-19 patients can be challenging, particularly if acute kidney injury (AKI) develops.Aim of the studyWe study the relationship between fluid net input and output (FNIO) in COVID-19 patients with development of AKI, time to development of AKI, in-hospital length of stay (LOS), and in-hospital mortality.Material and MethodsRetrospective study of 403 patients with COVID-19. Data for FNIO were from day 1 through day 10 or earlier if AKI occurred.ResultsAKI occurred in 22.8%, in-hospital mortality occurred in 26.3%, mean days to AKI were 7.7 (SD=6.3), and mean LOS was 11.5 (SD=13.2) days. In the multivariate logistic regression analyses, increased FNIO mean was significantly associated with slightly increased odds for mortality (OR=1.001, 95% CI:1.0001, 1.0011, p=0.02) but was not significantly associated with AKI. In the multivariate linear regression analyses, increased FNIO mean was significantly associated with lesser days to AKI (B=−6.63*10−5, SE=<0.001, p=0.003) in the whole sample, greater days to AKI in the subset of those with ICU treatment (B=<0.001, SE=<0.001, p<0.001), while FNIO mean was not significantly associated with LOS.ConclusionsPositive fluid balance was associated with faster onset of AKI and increased mortality. Fluid administration in patients with COVID-19 should be guided by routinely measuring FNIO. A restrictive fluid management regimen rather than usual care should be practiced.

Association between β-lactam exposure and clearance of bacteraemia and acute kidney injury in patients with methicillin-resistant Staphylococcus aureus bloodstream infections-a post hoc analysis of the CAMERA2 trial.

Contrast-induced nephropathy or contrast-induced acute kidney injury (CI-AKI) has been regarded for decades as arelevant complication of iodinated contrast medium administration, particularly in perioperative and intensive care settings. However, recent epidemiological and clinical data increasingly challenge this presumed causal relationship and suggest that the associated risk is substantially overestimated. The aim of this article is to critically appraise the current evidence and to reassess the clinical relevance of contrast medium administration within the context of multifactorial acute kidney injury development. This editorial is based on anarrative and commentary-driven analysis of selected clinical studies, meta-analyses, and current recommendations regarding the use of iodinated contrast media in perioperative and intensive care settings. The published data were evaluated with aparticular emphasis on patient-related risk factors and clinically relevant practical aspects. The majority of contemporary studies demonstrate no or only amarginal causal association between the administration of iodinated contrast media and the development of AKI. Instead, the occurrence of AKI closely correlates with patient-related factors such as pre-existing chronic kidney disease, hemodynamic instability, sepsis, and systemic inflammation. Preventive measures beyond individualized volume therapy and hemodynamic optimization have not shown consistent effectiveness. Contrast medium administration frequently appears to be amarker of severe disease rather than aprimary trigger for AKI. The long-assumed nephrotoxicity of iodinated contrast media requires reevaluation. From an anesthesiological perspective, the focus should shift away from contrast avoidance towards ensuring adequate organ perfusion and hemodynamic stability. Unwarranted reluctance to perform urgently indicated imaging may lead to diagnostic delays and potentially compromises patient safety. Arational evidence-based approach to contrast medium administration within an interdisciplinary risk-benefit assessment is essential.