Recurrent Abdominal Pain Due to Acute Renal Failure With Loin Pain and Patchy Renal Ischemia After Anaerobic Exercise.

Acute renal failure with severe loin pain and patchy renal ischemia after anaerobic exercise (ALPE) is a rare condition characterized by severe loin pain and patchy renal ischemia following vigorous exercise. Moreover, its diagnosis relies on clinical manifestations. Here, we present the case of a 16-year-old male with recurrent abdominal pain attributed to ALPE. He developed recurrent abdominal pain after he started playing handball, and no definite cause could be identified despite a thorough examination. His symptoms worsened when he resumed handball practice after a one-month interruption. This case underscores the varied presentations of ALPE and the importance of considering it in the differential diagnosis of recurrent abdominal pain, particularly following strenuous exercise. Moreover, caution should be exercised when resuming exercise after periods of detraining, as this may predispose individuals to ALPE. Healthcare providers should be vigilant in recognizing and managing this condition, especially in individuals with recent exercise initiation following detraining.

Bidirectional pressure: a mini review of ventilator-lung-kidney interactions.

Acute kidney injury and respiratory failure that requires mechanical ventilation are both common complications of critical illnesses. Failure of either of these organ systems also increases the risk of failure to the other. As a result, there is a high incidence of patients with concomitant acute kidney injury and the need for mechanical ventilation, which has a devasting impact on intensive care unit outcomes, including mortality. Despite decades of research into the mechanisms of ventilator-lung-kidney interactions, several gaps in knowledge remain and current treatment strategies are primarily supportive. In this review, we outline our current understanding of the mechanisms of acute kidney injury due to mechanical ventilation including a discussion of; 1) The impact of mechanical ventilation on renal perfusion, 2) activation of neurohormonal pathways by positive pressure ventilation, and 3) the role of inflammatory mediators released during ventilator induced lung injury. We also provide a review of the mechanisms by which acute kidney injury increases the risk of respiratory failure. Next, we outline a summary of the current therapeutic approach to preventing lung and kidney injury in the critically ill, including fluid and vasopressor management, ventilator strategies, and treatment of acute kidney injury. Finally, we conclude with a discussion outlining opportunities for novel investigations that may provide a rationale for new treatment approaches.

Perioperative Marinobufagenin (MBG) Measurement May Improve Acute Kidney Injury Risk Assessment in Patients Undergoing Major Cardiac Surgery: A Proof-of-Concept Study.

Background and Objectives: Acute kidney injury (AKI) remains a significant complication following major cardiac surgery. Marinobufagenin (MBG), a cardiotonic steroid involved in sodium balance and blood pressure regulation, has been linked to organ damage after ischemia-reperfusion events. This pilot, prospective study investigates the utility of circulating MBG to improve AKI risk assessment in cardiac surgery patients as a stand-alone biomarker and after inclusion in a validated risk model (STS-AKI score). Materials and Methods: We included 45 patients undergoing elective cardiac surgery. The MBG levels were measured preoperatively and at 4, 8, and 12 h post-surgery. The AKI was defined according to the KDIGO guidelines. Statistical analyses assessed the diagnostic and prognostic utility of MBG and its integration with the STS-AKI score. Results: An AKI occurred in 26.7% of the patients. The STS-AKI score performed well in this cohort (AUC: 0.736). The MBG levels displayed a decreasing trend in the whole population after surgery (p = 0.02). However, in the AKI patients, MBG increased at 4 and 8 h before decreasing at 12 h post-surgery. The MBG changes from the baseline to 8 h and from 8 to 12 h post-surgery showed a remarkable diagnostic accuracy for an AKI (AUCs: 0.917 and 0.843, respectively). Integrating these MBG changes with the STS-AKI score significantly improved the model performance, including discrimination, calibration, and risk reclassification. Conclusions: The MBG measurement, particularly any dynamic changes post-surgery, enhances AKI risk stratification in cardiac surgery patients. Integrating MBG with the STS-AKI score offers more accurate risk predictions, potentially leading to better patient management and outcomes.

Acute Kidney Injury in Inflammatory Bowel Disease Patients: A Nationwide Comparative Analysis.

Rationale & Objective: About 25%-40% of patients with inflammatory bowel disease (IBD) may have extraintestinal manifestations, mainly involving the liver, skin, and joints. Kidney involvement in patients with IBD has been reported, but there are no estimates of its prevalence in population-based studies in the United States. We compared the frequency of acute kidney injury (AKI) among hospitalizations with IBD with that among hospitalizations with collagen vascular diseases and hospitalizations with neither condition. Study Design: Retrospective, population-based cohort study. Setting & Participants: Healthcare Cost and Utilization Project-Nationwide Inpatient Sample database. Outcomes: AKI and AKI requiring dialysis. Analytical Approach: Regression models were used to compare the occurrence of AKI among groups. Inverse probability of treatment weighting was applied to balance groups on covariates. Results: The final sample comprised 5,735,804 hospitalizations, including 57,121 with IBD, 159,930 with collagen vascular diseases, and 5,518,753 with neither IBD nor collagen vascular diseases. AKI was observed in 13%, 15%, and 12.2% of hospitalizations with IBD, collagen vascular diseases, and the general population, respectively. When adjusting for demographic, hospital, and clinical characteristics using inverse probability of treatment weighting, hospitalizations with IBD had higher odds of being diagnosed with AKI than both those with collagen vascular diseases (odds ratio [OR], 1.32; 95% confidence interval [CI], 1.27-1.38) and the general population (OR, 1.27; 95% CI, 1.23-1.31) and also had higher odds of being diagnosed with AKI requiring dialysis than those with collagen vascular diseases (OR, 1.59; 95% CI, 1.31-1.94) or than the general population (OR, 1.45; 95% CI, 1.25-1.68). Limitations: Cross-sectional analysis, underreporting of International Classification of Diseases codes, and analyses relevant to in-hospital stays only. Conclusions: The prevalence and risk of AKI among hospitalizations with IBD is greater than that of hospitalizations with collagen vascular diseases and the general population. Coexisting kidney disease should be considered among patients with a known diagnosis of IBD.

As a nephrologist, we have evaluated many patients with inflammatory bowel disease with various forms of kidney disease, both inflammatory and noninflammatory. Based on a multitude of factors, we have always wondered if there are shared immune mechanisms between the gut and kidney that could explain the underlying inflammation in both organs. In addition, based on recent studies of other autoimmune/inflammatory diseases, there is growing interest in the role of the gut microbiome (microorganisms that reside in our gut) and its influence on the immune system as well as how both the altered microbiome and immune system affect the kidneys. As a first step, we wanted to understand if some forms of kidney disease are more prevalent in patients with inflammatory bowel disease than in the general population, which possibly suggests a shared pathogenesis.

An unusual presentation of fungal brain abscess in immunocompetent host.

Focal area of necrosis, with a surrounding membrane within the brain parenchyma, usually resulting from an infectious process or rarely from a traumatic process known as brain abscess. We report a case of young female, who presented with multiple abscess in left frontal and right occipital region of brain, she was otherwise immunocompetent, lacking any known risk factor for opportunistic infection. And this fungal abscess manifest with unusual presentation of bilateral lower limb weakness along with seizures and fever. This infection leads to acute kidney injury (AKI), necessitating kidney replacement therapy (RRT) in term of intermittent hemodialysis (IHD). After drainage of abscess and antifungal therapy, she responded well, her acute kidney injury resolved and she showed clinical and radiological improvement.

Assessing the prevalence and severity of cisplatin-induced nephrotoxicity in a minority- low socioeconomic population in the Bronx, New York.

Studies evaluating Cisplatin-induced nephrotoxicity in minorities are limited. We conducted a retrospective review of adult patients receiving cisplatin from 2019 to 2023 at an inner-city hospital. Renal indices were obtained at baseline and after cycles 1, 2, and 3 of Cisplatin. A total of 93 patients were included, 46% were male. Median age was 57 years. About 40% were Black, 13% White, and 42% Hispanic. About 54% were uninsured. About 16% of the patients developed AKI after cycle 1 of cisplatin, 5% after cycle 2%, and 17% after cycle 3. There was no statistically significant correlation between race, sex, BMI and development of cisplatin-induced AKI. Repeated measures ANOVA test indicated a statistically significant and cumulative rise in creatinine level following cisplatin therapy [Wilks' Lambda = 0.003, F(1,26)=13.7, η2 = 0.44]. Our study in a minority, low socioeconomic population highlights the progressive kidney injury following each cycle of cisplatin therapy. Further studies targeting this specific population are warranted to develop tailored interventions.

Role of CDKL1-SOX11 signaling axis in Acute Kidney Injury.

The biology of CDKL (Cyclin-Dependent Kinase-Like) kinase family remains enigmatic. Contrary to their nomenclature, CDKLs do not rely on cyclins for activation and are not involved in cell cycle regulation. Instead, they share structural similarities with MAPKs (Mitogen-Activated Protein Kinases) and GSK3 (glycogen synthase kinase 3), though their specific functions and associated signaling pathways are still unknown. Previous studies have shown that the activation of CDKL5 kinase contributes to the development of acute kidney injury (AKI) by suppressing the protective SOX9-dependent transcriptional program in tubular epithelial cells. In the current study, we measured the functional activity of all the five CDKL kinases and discovered that, in addition to CDKL5, CDKL1 is also activated in tubular epithelial cells during AKI. To explore the role of CDKL1, we generated a germline knockout mouse which exhibited no abnormalities under normal conditions. Notably, when these mice were challenged with bilateral ischemia reperfusion and rhabdomyolysis, they were found to be protected from AKI. Further mechanistic investigations revealed that CDKL1 phosphorylates and destabilizes SOX11, contributing to tubular dysfunction. In summary, these studies have unveiled a previously unknown CDKL1-SOX11 axis that drives tubular dysfunction during AKI.

BK polyomavirus infection: more than 50 years and still a threat to kidney transplant recipients.

BK polyomavirus (BKPyV) is a ubiquitous human polyomavirus and a major infection after kidney transplantation, primarily due to immunosuppression. BKPyV reactivation can manifest as viruria in 30%-40%, viremia in 10%-20%, and BK polyomavirus-associated nephropathy (BKPyVAN) in 1%-10% of recipients. BKPyVAN is an important cause of kidney graft failure. Although the first case of BKPyV was identified in 1971, progress in its management has been limited. Specifically, there is no safe and effective antiviral agent or vaccine to treat or prevent the infection. Even in the current era, the mainstay approach to BKPyV is a reduction in immunosuppression, which is also limited by safety (risk of de novo donor specific antibody and rejection) and efficacy (graft failure). However, recently BKPyV has been getting more attention in the field, and some new treatment strategies including the utilization of viral-specific T-cell therapy are emerging. Given all these challenges, the primary focus of this article is complications associated with BKPyV, as well as strategies to mitigate negative outcomes.

Visualization of intracellular ATP dynamics in different nephron segments under pathophysiological conditions using the kidney slice culture system.

ATP depletion plays a central role in the pathogenesis of kidney diseases. Recently, we reported spatiotemporal intracellular ATP dynamics during ischemia reperfusion (IR) using GO-ATeam2 mice systemically expressing an ATP biosensor. However, observation from the kidney surface did not allow visualization of deeper nephrons or accurate evaluation of ATP synthesis pathways. Here, we established a novel ATP imaging system using slice culture of GO-ATeam2 mouse kidneys, evaluated the ATP synthesis pathway, and analyzed intracellular ATP dynamics using an ex vivo IR-mimicking model and a cisplatin nephropathy model. Proximal tubules (PTs) were found to be strongly dependent on oxidative phosphorylation (OXPHOS) using the inhibitor oligomycin A, whereas podocytes relied on both OXPHOS and glycolysis using phloretin an active transport inhibitor of glucose. We also confirmed that an ex vivo IR-mimicking model could recapitulate ATP dynamics in vivo; ATP recovery in PTs after reoxygenation varied depending on anoxic time length, whereas ATP in distal tubules (DTs) recovered well even after long-term anoxia. After cisplatin administration, ATP levels in PTs decreased first, followed by a decrease in DTs. An organic cation transporter 2 inhibitor, cimetidine, suppressed cisplatin uptake in kidney slices, leading to better ATP recovery in PTs, but not in DTs. Finally, we confirmed that a mitochondria protection reagent (Mitochonic Acid 5) delayed the cisplatin-induced ATP decrease in PTs. Thus, our novel system may provide new insights into the energy dynamics and pathogenesis of kidney disease.

Discovery of mmu-lncRNA129814/hsa-lncRNA582795 as a Potential Biomarker and Intervention Target for Ischemia Reperfusion Injury-Induced AKI.

Background: Acute kidney injury (AKI) is associated with higher perioperative mortality and morbidity, as well as increased medical expenses. The molecular mechanisms underlying ischemia-reperfusion (I/R)-induced AKI remain unclear. Methods and Results: We applied an RT-qPCR assay to measure the expression of mmu-lncRNA129814, hsa-lncRNA582795, and miRNA-494-5p, immunoblotting to detect IL-1α and cleaved caspase-3 expression, and TUNEL staining and flow cytometry (FCM) to evaluate apoptosis. The experiments were conducted using BUMPT and HK-2 cells, as well as C57BL/6J mice. Mechanistically, mmu-lncRNA129814 could sponge miRNA-494-5p and upregulate IL-1α expression to promote cell apoptosis. Furthermore, knockdown of mmu-lncRNA129814 ameliorated I/R-induced progression of AKI by targeting the miRNA-494-5p/IL-1α pathways. Interestingly, hsa-lncRNA582795, a homolog of mmu-lncRNA129814, also promoted I/R-stimulated HK-2 cell apoptosis and AKI progression by regulating the miRNA-494-5p/IL-1α axis. Finally, we found that patients with I/R-induced AKI exhibited significantly elevated plasma and urinary levels of hsa-lncRNA582795 compared to those who underwent ischemia-reperfusion without developing AKI. Spearman's test demonstrated a significant correlation between serum creatinine and plasma hsa-lncRNA582795 in I/R patients. Plasma hsa-lncRNA582795 showed high sensitivity but low specificity (86.7%) compared to urinary hsa-lncRNA582795. Conclusion: The mmu-lncRNA129814/hsa-lncRNA582795/miRNA-494-5p/IL-1α axis was found to modulate the progression of ischemic AKI, and hsa-lncRNA582795 could act as a diagnosis biomarker and potential therapy target of I/R-induced AKI.

Galectin-3 protects distal convoluted tubules in rhabdomyolysis-induced kidney injury.

Advanced glycation endproducts (AGEs) contribute to cellular damage of various pathologies, including kidney diseases. Acute kidney injury (AKI) represents a syndrome seldom characterized by a single, distinct pathophysiological cause. Rhabdomyolysis-induced acute kidney injury (RIAKI) constitutes roughly 15% of AKI cases, yet its underlying pathophysiology remains poorly understood. Using a murine model of RIAKI induced by muscular glycerol injection, we observed elevated levels of AGEs and the AGE receptor galectin-3 (LGALS3) in the kidney. Immunofluorescence localized LGALS3 to distal nephron segments. According to transcriptomic profiling via next-generation sequencing, RIAKI led to profound changes in kidney metabolism, oxidative stress, and inflammation. Cellular stress was evident in both proximal and distal tubules, as shown by kidney injury markers KIM-1 and NGAL. However, only proximal tubules exhibited overt damage and apoptosis, as detected by routine morphology, active Caspase-3, and TUNEL assay, respectively. In vitro, distal convoluted tubule (DCT) cells challenged with AGEs underwent apoptosis, which was markedly enhanced by Lgals3 siRNA treatment. Thus, in RIAKI, the upregulation of LGALS3 may protect the distal nephron from AGE-mediated damage, while proximal tubules lacking LGALS3 stay at risk. Thus, stimulating LGALS3 in the proximal nephron, if achievable, may attenuate RIAKI.

Early neutrophil gelatinase-associated lipocalin (NGAL) measurement could rule out future acute kidney injury in patients with acute coronary syndrome-Prospective observational study.

Background and Aims: The diagnosis of acute kidney injury (AKI) is of importance among patients with ST segment elevation (STEMI) undergoing primary coronary intervention (PCI). It is often delayed given the need in serial measurements of creatinine or other serum markers. Neutrophil gelatinase-associated lipocalin (NGAL) is a proven marker for AKI, although its role as an early predictor in this setting was scarcely addressed before and was the aim of our study. Methods: Prospective observational study including 133 patients with STEMI treated with PCI. Plasma NGAL was drawn immediately before PCI (NGAL-0) and 24 h after (NGAL-24). Similar analysis of C-reactive protein (CRP) was performed for additional comparison. Results: Mean age was 62 ± 13 years, 78% were men, and 20 (15%) developed AKI after admission. Patients with AKI after admission demonstrated higher levels of NGAL-0 (164 vs. 95 ng/mL; p < 0.001) and NGAL-24 (142 vs. 93 ng/mL; p < 0.001). Levels of NGAL-0 and NGAL-24 were similar within the AKI and non-AKI groups. Using ROC curve analysis, NGAL-0 had best predictive ability for AKI development (AUC 0.841, 95% CI 0.80-0.96), compared with NGAL-24 (0.783, 95% CI 0.74-0.85), CRP-0 (0.701, 95% CI 0.58-0.83), and CRP-24 (0.781, 95% CI 0.66-0.90). The optimal NGAL-0 cutoff for AKI prediction was 125 ng/mL, with 70% sensitivity, 84% specificity, and 94% negative predictive value. Conclusions: Among STEMI patients, NGAL measurement upon admission are associated with AKI and may serve as a reliable marker for early AKI detection. Future studies may direct risk stratification using this single test can direct personalized evaluations during the admission, and focused interventions to prevent AKI.

Predictive enrichment for the need of renal replacement in sepsis-associated acute kidney injury: combination of furosemide stress test and urinary biomarkers TIMP-2 and IGFBP-7.

BACKGROUND: In sepsis, initial resuscitation with fluids is followed by efforts to achieve a negative fluid balance. However, patients with sepsis-associated acute kidney injury (SA-AKI) often need diuretic or renal replacement therapy (RRT). The dilemma is to predict whether early RRT might be advantageous or diuretics will suffice. Both the Furosemide Stress Test (FST) and measurements of the urinary biomarkers TIMP-2*IGFBP-7, if applied solely, do not provide sufficient guidance. We tested the hypothesis that a combination of two tests, i.e., an upstream FST combined with downstream measurements of urinary TIMP-2*IGFBP-7 concentrations improves the accuracy in predicting RRT necessity. METHODS: In this prospective, multicenter study 100 patients with sepsis (diagnosed < 48h), AKI stage ≥ 2, and an indication for negative fluid balance were included between 02/2020 and 12/2022. All patients received a standardized FST and urinary biomarkers TIMP-2*IGFBP-7 were serially measured immediately before and up to 12 h after the FST. The primary outcome was the RRT requirement within 7 days after inclusion. RESULTS: 32% (n = 32/99) of SA-AKI patients eventually required RRT within 7 days. With the FST, urine TIMP-2*IGFBP-7 decreased within 2 h from 3.26 ng2/mL2/1000 (IQR: 1.38-5.53) to 2.36 ng2/mL2/1000 (IQR: 1.61-4.87) in RRT and 1.68 ng2/mL2/1000 (IQR: 0.56-2.94) to 0.27 ng2/mL2/1000 (IQR: 0.12-0.89) and non-RRT patients, respectively. While TIMP-2*IGFBP-7 concentrations remained low for up to 12 h in non-RRT patients, we noted a rebound in RRT patients after 6 h. TIMP-2*IGFBP-7 before FST (accuracy 0.66; 95%-CI 0.55-0.78) and the FST itself (accuracy 0.74; 95%-CI: 0.64-0.82) yielded moderate test accuracies in predicting RRT requirement. In contrast, a two-step approach, utilizing FST as an upstream screening tool followed by TIMP-2*IGFBP-7 quantification after 2 h improved predictive accuracy (0.83; 95%-CI 0.74-0.90, p = 0.03) compared to the FST alone, resulting in a positive predictive value of 0.86 (95%-CI 0.64-0.97), and a specificity of 0.96 (95%-CI 0.88-0.99). CONCLUSIONS: The combined application of an upstream FST followed by urinary TIMP-2*IGFBP-7 measurements supports highly specific identification of SA-AKI patients requiring RRT. Upcoming interventional trials should elucidate if this high-risk SA-AKI subgroup, identified by our predictive enrichment approach, benefits from an early RRT initiation.

Renal Infarction in SARS-CoV-2 Infection: A Case Report.

The novel coronavirus disease 2019 (COVID-19) is an infectious disease caused by SARS-CoV-2 and associated with a wide spectrum of clinical manifestations ranging from asymptomatic carrier states to fulminant respiratory distress and multiple organ dysfunction. The intravascular arterial and venous thrombotic phenomena are one of the most prevalent and devastating consequences and tend to occur in patients with a severe disease state. Here we present a 45-year-old male with a medical history of essential hypertension (HTN) who presented with severe left flank pain accompanied by dry cough and fever for five days. He was found to have acute kidney injury (AKI) with concomitant renal infarction in computed tomography angiography (CTA) in the setting of a COVID-19 infection. He was eventually managed with novel oral anticoagulation (NOAC) and was discharged after a short hospital stay. Follow-up thereafter showed stable baseline renal function with no relevant symptoms.

A two-tier feature selection method for predicting mortality risk in ICU patients with acute kidney injury.

Acute kidney injury (AKI) is one of the most important lethal factors for patients admitted to intensive care units (ICUs), and timely high-risk prognostic assessment and intervention are essential to improving patient prognosis. In this study, a stacking model using the MIMIC-III dataset with a two-tier feature selection approach was developed to predict the risk of in-hospital mortality in ICU patients admitted for AKI. External validation was performed using separate MIMIC-IV and eICU-CRD. The area under the curve (AUC) was calculated using the stacking model, and features were selected using the Boruta and XGBoost feature selection methods. This study compares the performance of a stacking model using two-tier feature selection with a model using single-tier feature selection (XGBoost: 85; Boruta: 83; two-tier: 0.91). The predictive effectiveness of the stacking model was further validated by using different datasets (Validation 1: 0.83; Validation 2: 0.85) and comparing it with a simpler model and traditional clinical scores (SOFA: 0.65; APACH IV: 0.61). In addition, this study combined interpretable techniques and causal inference to analyze the causal relationship between features and predicted outcomes.

Efficacy and Safety Factors Related to Plasma Concentration-Optimized Polymyxin B Therapy in Treating Carbapenem-Resistant Gram-Negative Bacterial Infections in China.

Background: Polymyxin B (PMB)-based combination therapies are used to treat severe carbapenem-resistant gram-negative bacterial (CR-GNB) infections. This observational study investigated the relationship between clinical factors, including PMB concentration, and clinical efficacy and safety. Patients and Methods: Polymyxin B regimens were optimized through therapeutic drug monitoring (TDM) and area under the concentration-time curve (AUC). In all, 382 samples were tested from 130 patients. Logistic regression was used to analyze the relationships between variables with clinical efficacy and 30-day mortality factors were analyzed by Cox regression. The sensitivity and specificity of Cmin and AUC for the occurrence of acute kidney injury (AKI) were determined by ROC curve analysis. Results: The clinical effectiveness of PMB was 65.4%. Multivariate logistic regression analysis revealed that lung infection, continuous renal replacement therapy, and C-reactive protein were independent factors significantly associated with efficacy. AKI occurred in 14.6% of the patients during treatment; age > 73 years (OR: 3.63; 95% CI: 1.035-12.727; P = 0.044), Cmin greater than 2.3 µg/mL (OR: 7.37; 95% CI: 1.571-34.580; P = 0.011), combined vancomycin (OR: 9.47; 95% CI: 1.732-51.731; P = 0.009), and combined piperacillin-tazobactam (OR: 21.87; 95% CI: 3.139-152.324; P = 0.002) were independent risk factors. The identified PMB cut-offs for predicting AKI were Cmin = 2.3 µg/mL and AUC = 82.0 mg h/L. Conclusion: Polymyxin B-based combination regimens are effective in treating CR-GNB infections, particularly bloodstream infections, but have shown unsatisfactory for lung infections. Cmin ≥ 2.3 µg /mL and AUC ≥ 82.0 mg h/L may increase PMB-associated AKI incidence. PMB dose should be adjusted based on TDM to ensure efficacy.

Acknowledging acute kidney disease following ureteroscopy and laser lithotripsy: results from a tertiary care referral center.

BACKGROUND: Acute kidney disease (AKD) is a recently described syndrome consisting of kidney function abnormalities lasting less than 3 months. Little is known regarding AKD following ureteroscopy (URS) and laser lithotripsy. OBJECTIVE: To evaluate the occurrence and evolution of AKD in stone patients treated with URS. MATERIALS AND METHODS: Data from 284 patients treated with URS for urinary stones were retrospectively analyzed. According to the KDIGO 2020 criteria, AKD was defined as postoperative acute kidney injury (AKI) occurrence, estimated glomerular filtration rate (eGFR) decrease ≥ 35%, or serum creatinine (SCr) increase ≥ 50%. AKI was defined as SCr increase ≥ 0.3 mg/dL or ≥ 50%. AKD evolution was evaluated 60 days post-URS. Data were analyzed using descriptive statistics. Univariable (UVA) and multivariable (MVA) logistic regression analyses tested the association of patients' characteristics and perioperative data with the occurrence of AKD. RESULTS: Overall, postoperative AKD occurred in 32 (11.3%) patients. Recovery from AKD was found in 26 (82%) patients and persistent AKD occurred in 6 (18%) patients. At UVA, age at surgery (p = 0.05), baseline SCr (p = 0.02), baseline CKD category (p = 0.006), Charlson comorbidity index (p = 0.01), operative time (p = 0.04) and postoperative complications (< 0.001) were associated with AKD. At MVA, CKD category (OR 2.99, 95% CI = 1.4-6.3; p = 0.004), operative time (OR 1.01, 95% CI = 1.001-1.018; p = 0.023) and postoperative complications (OR 3.5, 95% CI = 1.46-8.49; p = 0.005) were independent predictors of AKD. CONCLUSIONS: AKD is a frequent complication in patients treated with URS. Moreover, AKD persists in a non-neglectable percentage of patients at medium-term follow-up. Therefore, nephrological assessment should be considered, especially in high-risk patients. Current findings should be considered for the peri-operative management of stone patients.

Quercetin Attenuates Acute Kidney Injury Caused by Cisplatin by Inhibiting Ferroptosis and Cuproptosis.

Ferroptosis, an iron- and ROS-dependent form of regulated cell death. Cuproptosis is a novel form of cellular demise mode. Quercetin, a natural flavonoid, has demonstrated a range of pharmacological activities, including anti-cancer, anti-inflammatory, and antioxidant properties. In this research, we investigated the quercetin effect on cisplatin-induced acute kidney and its mechanism associated ferroptosis and cuproptosis. The HK-2 cells were used in this research. Cell viability was evaluated using the CCK-8 assay. Acute kidney injury (AKI) models were established to perform in vivo experiments. Renal tissue homogenate was used to determine ROS, LPO, MDA, PA, etc., to assess ferroptosis and cuproptosis. To perform bioinformatic analysis, microarray data from the GEO database was utilized. Real-time PCR analysis and ELISA was explored the mechanism of ferroptosis and cuproptosis. We found that ferroptosis and cuproptosis in AKI were abnormally activated caused by cisplatin, and that quercetin attenuated AKI by inhibiting ferroptosis and cuproptosis. QCT suppressed ferroptosis by reducing malondialdehyde (MDA) and ROS levels and increasing glutathione (GSH) levels and alleviated cuproptosis by reducing copper ion, pyruvate (PA) and HSP70 levels. Moreover, bioinformatic analysis revealed that the ferroptosis-related gene SLC7A11 and the cuproptosis-related genes ATP7B and GLS were the differential expression genes. And QCT significantly increased the expression or activity of SLC7A11, GPX4, ATP7B, and GLS in Cis-AKI mice. Our findings highlight the clinical importance of quercetin, which guards against cisplatin-induced acute kidney injury by suppressing ferroptosis and cuproptosis.

Clinically Evident Cardiopulmonary Congestion Does Not Significantly Impact the Prognosis of Patients With Septic Acute Kidney Injury.

Background: Acute kidney injury (AKI) is a common issue among in-hospital patients, with high mortality rates. Sepsis is a primary cause of AKI, particularly in the intensive care unit. Patients with septic AKI often experience cardiovascular congestion, leading to the formal classification of cardiorenal syndrome type 5. The study aimed to evaluate the prognosis of septic AKI patients with and without clinical evidence of cardiovascular congestion. Methods: This was a retrospective observational study. AKI patients were identified using the in-hospital AKI alert system. Sepsis was diagnosed based on laboratory, clinical, and hemodynamic characteristics, with additional consideration of the quickSOFA score. Cardiovascular congestion was diagnosed by assessing clinical (edema), radiographic (pulmonary congestion), echocardiographic (e.g., wall motion abnormalities), and laboratory variables (e.g., N-terminal pro-B-type natriuretic peptide). Endpoints included in-hospital survival, the need for kidney replacement therapy (KRT), and recovery of kidney function (ROKF). Results: In total, 102 patients were included, and cardiopulmonary congestion was diagnosed in 78.4%. Individuals with congestion did not differ from patients without congestion in any of the pre-defined endpoints. Conclusions: It is justified not to consider clinically apparent cardiovascular congestion in septic AKI patients as a risk factor for death per se. Rather, especially in the case of sepsis, clinically apparent positive fluid balance does not seem to be a disadvantage in terms of survival, KRT, and ROKF.