Peritoneal dialysis (PD)-associated peritonitis is a leading cause of technique failure. We aimed to develop and internally validate a Cox regression‑based nomogram for predicting peritonitis‑free survival in incident PD patients. This single-center retrospective cohort study included 372 patients who underwent peritoneal dialysis between June 2018 and December 2024, with follow-up through December 2025. LASSO‑Cox regression was used to select predictors from 23 candidate variables. A nomogram was constructed to predict 6‑, 12‑, and 24‑month peritonitis‑free survival. Model performance was assessed by concordance index (C‑index), time‑dependent ROC, calibration curves, and decision curve analysis. Over a median follow‑up of 26.3 months, 92 (35.4%) and 34 (30.4%) peritonitis events occurred in the training and validation cohorts, respectively. Nine predictors (education, start age, BMI, hemoglobin, potassium, sodium, albumin, calcium, phosphorus) were retained. Independent predictors were lower education (≤9 vs >9 years: HR 1.93, 95% CI 1.03-3.64), lower hemoglobin (HR 0.99, 0.97-1.00), lower albumin (HR 0.92, 0.87-0.97), and lower phosphorus (HR 0.53, 0.29-0.99). The C‑index was 0.707 (95% CI 0.650-0.765). Time‑dependent ROCs in the training cohort were 75.8%, 77.5%, and 69.7% at 6, 12, and 24 months; in the validation cohort, they were 77.7%, 63.8%, and 58.4%, respectively. Calibration was satisfactory at 6 and 12 months (Brier scores 6.0%-11.1%), with wider clinical net benefit at 12-24 months. This nomogram using nine routinely available variables demonstrated moderate discrimination and satisfactory calibration for predicting peritonitis‑free survival in PD patients. While promising, the model requires external validation in larger, multicenter cohorts to confirm its generalizability before routine clinical use.

This study demonstrates that gamma-aminobutyric acid (GABA) ameliorates diabetic kidney disease (DKD) by modulating macrophage-driven inflammation and podocyte injury through the JAML/FPR2 signaling axis. In streptozotocin (STZ)-induced DKD mice, GABA administration significantly improved renal function by reducing serum creatinine, urea nitrogen, 24-hour urine protein, attenuated glomerular hypertrophy/mesangial expansion, and suppressed pro-inflammatory cytokine production (TNF-α, IL-1β, iNOS) in renal tissue and serum. GABA inhibited glomerular macrophage infiltration (CD68[+] cells) and M1 polarization while mitigating renal apoptosis and podocyte injury by restoring nephrin and podocin. In a high glucose (HG)-stimulated macrophage-podocyte co-culture model, GABA reduced HG-induced podocyte apoptosis in a macrophage ratio-dependent manner by reversing M1 polarization and inflammatory cytokine overproduction. Mechanistically, GABA normalized DKD-elevated JAML expression in renal tissues and podocytes, while JAML overexpression abolished GABA's renoprotective effects by reactivating inflammation, macrophage recruitment, and podocyte apoptosis. Co-IP confirmed JAML interacted with receptor formyl peptide receptor 2 (FPR2), which mediated DKD-driven macrophage infiltration, as FPR2 knockdown abrogated JAML-induced CD68[+] cell accumulation. Collectively, GABA alleviated DKD progression by disrupting the JAML/FPR2 axis to suppress macrophage-mediated inflammation and podocyte injury, highlighting its therapeutic potential for diabetic kidney disease.

Roxadustat, a hypoxia-inducible factor prolyl hydroxylase (HIF-PH) inhibitor, is effective for treating renal anemia, with efficacy noninferior to erythropoiesis-stimulating agents. However, data on its adverse effects remain scarce. In medical practice, roxadustat administration reportedly leads to central hypothyroidism; however, the frequency of its occurrence remains unclear. We investigated thyroid function in patients undergoing dialysis who received roxadustat at Saiseikai Yokohamashi Tobu Hospital, with particular focus on the timing of the decrease in serum thyroid-stimulating hormone (TSH) levels after roxadustat initiation and the subsequent course of thyroid function. HIF-PH inhibitors were administered to 43 chronic kidney disease patients including dialysis. After 2 weeks of roxadustat administration, we extracted the data of 16 hemodialysis patients who exhibited absence of residual urine and were able to undergo blood tests. All patients revealed decreased serum TSH levels. In contrast, changes in serum free triiodothyronine and free thyroxine levels were minor. None of the patients reported fatigue, bradycardia, or constipation, which are common symptoms of hypothyroidism. Our findings revealed that roxadustat may cause TSH reduction after 2 weeks of administration, though some patients showed subclinical hypothyroidism with high TSH levels. In a few cases, TSH levels decreased to one-tenth of the normal values. Despite these rapid changes, none of the patients exhibited clinical symptoms. Hence, regular thyroid hormone level monitoring is necessary with roxadustat administration, regardless of patients' history of thyroid function.

IgA nephropathy (IgAN) is the most common glomerulonephritis worldwide, characterized by a 4-hit pathogenesis primarily driven by mucosal immune dysregulation in the gut-associated lymphoid tissue (GALT). However, the specific environmental triggers initiating this cascade remain elusive. We propose a novel hypothesis that chronic exposure to ubiquitous micro- and nano-plastics (MNPs) serves as a primary environmental catalyst for IgAN. Through a proposed 5-step cascade, we outline how ingested MNPs directly degrade intestinal tight junctions, precipitating a 'leaky gut' that permits the synergistic influx of plastics and commensal bacterial antigens into the GALT. Acting as a 'Trojan horse,' MNP-corona complexes evade immune detection but trigger chronic inflammation and B-cell dysregulation upon internalization by phagocytes. This persistent immune stimulation drives the aberrant production of galactose-deficient IgA1. Furthermore, we hypothesize that circulating MNPs co-deposit in the renal mesangium alongside immune complexes, acting as a dual generator of both systemic immune complexes and direct structural kidney injury. This potential gene-environment interaction is supported by the intersecting high prevalence of environmental MNPs and IgAN in Asia. Finally, we delineate future in vivo, observational, and epidemiological investigations required to establish this pathophysiological link.

Automated peritoneal dialysis (APD) is a widely used dialysis modality for patients with end-stage kidney disease (ESKD). However, controversy remains regarding the rate of residual kidney function (RKF) decline between patients treated with APD and continuous ambulatory peritoneal dialysis (CAPD). This study aimed to investigate the effect of peritoneal dialysis modality on the rate of RKF decline in Chinese patients with new-onset ESKD. We conducted a single-center retrospective study to explore the association between PD modalities and RKF decline. A total of 53 patients with new-onset ESKD were enrolled. Of these, 19 patients started with APD and 34 with CAPD. The rates of RKF decline were compared between two groups. Multivariate linear regression was performed to identify risk factors for rapid decline of RKF. Baseline RKF and urine output were comparable between the APD and CAPD groups. At 6 months after PD initiation, RKF was 1.9 ± 1.6 mL/min/1.73 m[2] in the APD group, significantly lower than 3.0 ± 1.7 mL/min/1.73 m[2] in the CAPD group (p = 0.043). The APD group had a significantly faster mean rate of RKF decline (-6.6 ± 2.5 vs. -4.3 ± 2.3 mL/min/1.73 m[2]/year, p = 0.002). In multivariate linear regression adjusted for established risk factors, APD use (vs. CAPD) (β = 0.93; p = 0.004) and baseline RKF (β = 0.38; p < 0.001) were significantly associated with accelerated RKF decline. Our findings indicate that Chinese patients initiating dialysis with APD experience faster RKF decline within the first 6 months compared with those starting PD with CAPD. Furthermore, high baseline RKF is associated with rapid RKF decline.

Acute kidney injury (AKI) after liver transplantation (LT) is a frequent complication associated with adverse outcomes, yet practical early postoperative prediction tools remain limited. This retrospective study developed and internally validated an interpretable model for AKI after LT using perioperative variables available by the time of the first urgent postoperative blood test, generally obtained within 1 h after surgery. Adult LT recipients treated from June 2023 to January 2026 were screened. AKI was defined according to Kidney Disease: Improving Global Outcomes criteria. Among 146 screened recipients, 127 were included and randomly divided into training and validation cohorts at a 3:1 ratio. Least absolute shrinkage and selection operator regression selected estimated glomerular filtration rate calculated using the CKD-EPI equation, anhepatic phase time, postoperative natural logarithm-transformed D-dimer, and postoperative alanine aminotransferase. Multivariable logistic regression showed that lower estimated glomerular filtration rate and longer anhepatic phase time were independently associated with AKI. The nomogram achieved area under the receiver operating characteristic curve values of 0.861 in the training cohort and 0.761 in the validation cohort. Five-fold cross-validation and bootstrap internal validation were performed to assess model stability and optimism. Among five evaluated models, support vector machine showed the numerically highest validation AUC of 0.846. Shapley additive explanations identified estimated glomerular filtration rate as the dominant predictor. This early postoperative model may help identify high-risk recipients for intensified renal monitoring and individualized management. External multicenter validation is required before routine clinical implementation.

Lactate is frequently measured in patients with acute kidney injury (AKI), but its interpretation remains challenging because circulating lactate reflects systemic metabolic stress rather than kidney injury. Although elevated lactate levels are associated with adverse outcomes in critically ill patients with AKI, its biological and clinical significance varies according to disease context, timing, and the clinical question being addressed. This structured expert narrative review integrates mechanistic insights and clinical evidence to establish a context-dependent framework for interpreting lactate in AKI. We summarize the role of the kidney in lactate metabolism and discuss how impaired renal function, altered perfusion, mitochondrial dysfunction, and immune-metabolic remodeling contribute to lactate accumulation. We further evaluate clinical evidence regarding lactate in AKI risk assessment, severity evaluation, organ-support requirement, and mortality prediction, while emphasizing limitations related to confounding factors and clinical heterogeneity. Emerging clinical contexts, including extracorporeal membrane oxygenation-supported patients, are also considered. Overall, this framework supports a more precise interpretation of lactate as a context-dependent risk marker and metabolic signal rather than a kidney-specific biomarker.

Continuous renal replacement therapy (CRRT) is a vital organ support modality for critically ill patients. Adsorptive membranes, particularly AN69ST and oXiris, are increasingly used in clinical practice; however, their impact on the pharmacokinetics of antibiotics with a narrow target concentration range between efficacy and toxicity, such as vancomycin, remains incompletely defined. Considerable heterogeneity exists among available studies. Multiple in vitro dynamic circulation models reported adsorption of 12% to 19.5% of the initial vancomycin dose, whereas some static or open-model in vitro studies failed to detect significant adsorption. Retrospective studies have reported that adsorption accounted for approximately 15.9% with AN69ST membranes and 5.4% with oXiris membranes of total vancomycin elimination. However, the clinical significance of vancomycin removal by adsorptive membranes via adsorption remains unclear and warrants further investigation. Nevertheless, overlooking the additional clearance contributed by AN69ST or oXiris membranes during dose regimen design may lead to subtherapeutic vancomycin exposure, thereby increasing the risk of treatment failure and antimicrobial resistance. This article systematically reviews the current evidence on vancomycin elimination characteristics with adsorptive membranes, with an emphasis on adsorption mechanisms, influencing factors, and clinical dosing adjustment strategies. In current clinical practice, intensified therapeutic drug monitoring with dynamic dose adjustment based on measured concentrations remains an essential strategy to ensure the efficacy and safety of vancomycin therapy. A deeper understanding of membrane-specific adsorption kinetics is required to optimize antibiotic dosing in critically ill patients receiving CRRT with highly adsorptive membranes.

Renal ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury and is associated with mitochondrial dysfunction, excessive reactive oxygen species (ROS) production, and tubular cell apoptosis. Sigma-1 receptor (Sigma1R), an intracellular chaperone, helps maintain mitochondrial homeostasis and cell survival. Here, Sigma1R expression was significantly downregulated in renal IRI. Fluvoxamine treatment ameliorated renal dysfunction and reduced apoptosis in vivo, whereas Sigma1R overexpression preserved mitochondrial membrane potential and attenuated ROS accumulation in HK-2 cells subjected to hypoxia/reoxygenation. The findings support the functional involvement of Rac1 in Sigma1R-mediated enhancement of PINK1/Parkin-mediated mitophagy, which may facilitate the clearance of damaged mitochondria and restore mitochondrial quality control. Overall, Rac1 is involved in Sigma1R-mediated mitophagy and mitochondrial protection, highlighting Sigma1R as a potential therapeutic target for renal IRI.

Obesity is a major independent risk factor for chronic kidney disease (CKD). Population-level evidence linking immune dysregulation to CKD in obese individuals remains limited. In this cross-sectional study, we analyzed data from community-dwelling adults aged 65-85 years in Shanghai, China. The immune-inflammatory markers were compared between obese and non-obese groups. The associations between routinely measured immune-inflammatory markers (neutrophils, lymphocytes, platelet-to-lymphocyte ratio [PLR]) and CKD prevalence were evaluated using multivariable logistic regression, restricted cubic splines (RCSs). Obese individuals had higher neutrophil, monocyte, and lymphocyte counts and lower PLR than the non-obese group. Among participants with obese, elevated neutrophil and lymphocyte counts were independently associated with greater odds of CKD (adjusted odds ratio [aOR] for highest tertile: 1.42, 95% confidence interval [CI] 1.07-1.90; and 1.53, 95% CI 1.16-2.01, respectively), whereas higher PLR was associated with reduced odds (aOR 0.70, 95% CI 0.53-0.92). Adjusted RCS plots revealed nonlinear associations. Elevated neutrophils and monocytes together with lower PLR emerged as key immunoinflammatory markers that might be associated with obesity-associated CKD. These findings highlight the clinical potential of routine immune-inflammatory biomarkers for early and precise risk stratification of obesity-related CKD.

Hemorrhagic fever with renal syndrome (HFRS) is frequently complicated by acute kidney injury (AKI). Although most patients recover from AKI with supportive care, some progress to chronic kidney disease (CKD). The incidence and determinants of CKD progression in patients with HFRS-AKI remain uncertain. Here, 99 patients with HFRS-AKI treated at Jinling Hospital were analyzed retrospectively to determine the rate of CKD progression and identify associated risk factors. Patients were divided into complete recovery (CR) and incomplete recovery (ICR) groups according to CKD progression. Baseline clinical and laboratory data were collected and analyzed. Overall, 27.3% of patients with HFRS-AKI progressed to CKD despite receiving supportive care. Facial flushing was more frequent in the ICR group than in the CR group (40.7% vs. 18.1%, p = 0.033). Multivariate analysis revealed that treatment with Cordyceps sinensis preparations during the AKI phase was an independent protective factor against incomplete kidney recovery (OR: 0.323, 95% CI: 0.114-0.916, p = 0.034). Inverse probability weighting analysis further demonstrated that the use of Cordyceps sinensis preparations was inversely associated with incomplete kidney recovery (β: -1.184, 95% CI: -2.224 - -0.144, p = 0.026). Survival analysis confirmed that Cordyceps sinensis preparation therapy was associated with improved kidney outcomes (log-rank test, p = 0.004). This study provides the first clinical evidence that adjunctive therapy with Cordyceps sinensis preparations during HFRS-AKI is associated with improved kidney outcomes, suggesting that Cordyceps sinensis preparations represents a promising therapeutic approach for viral-induced AKI.