Objective To investigate the association between serum klotho level and risk of all-cause mortality in the population with diabetic kidney disease (DKD). Methods It was a retrospective cohort study. DKD patients from the National Health and Nutrition Examination Survey (NHANES) database in the United States, which covered five survey cycles from 2007 to 2016 were selected. Relevant demographic and laboratory examination data were collected, and all-cause mortality was regarded as the endpoint event. Patients were divided into high serum klotho group and low serum klotho group according to the optimal klotho threshold of predicting survival outcomes, and the differences of baseline characteristics between the two groups were compared. The weighted Kaplan-Meier method was used to draw the survival curves of the high and low serum klotho groups during the follow-up period. Log-rank test was used to compare the survival rates between the two groups. Weighted Cox proportional hazards regression analysis and further stratified analysis were used to estimate the correlation between serum klotho level and the risk of all-cause mortality. Results A total of 633 DKD patients were included in this study, with age of 65 (56, 72) years, and 323 (51.03%) males. Among them, there were 510 patients in the high klotho level (>556.6 ng/L) group, and 123 patients in the low klotho level (≤556.6 ng/L) group. The serum creatinine level in the high klotho level group was significantly lower than that in the low klotho level group (Z=-2.650, P=0.010), while the estimated glomerular filtration rate (eGFR, Z=2.489, P=0.015) and fasting blood glucose (Z=2.275, P=0.026) were significantly higher than those in the low klotho level group. There was no statistically significant difference between the two groups in terms of age, gender distribution, racial distribution, proportion of smoking, body mass index, proportion of hypertension, total cholesterol, triglyceride, and urine albumin/creatinine ratio (all P>0.05). The follow-up time was 81 (49, 116) months, and a total of 204 (32.23%) all-cause death events occurred. Kaplan-Meier survival analysis showed that the survival rate of the high klotho level group was significantly higher than that of the low klotho level group (Log-rank test, χ²=4.21, P=0.040). Cox proportional hazards regression analysis showed that, after adjusting for gender, age, race, smoking, body mass index, hypertension, blood glucose, triglyceride, total cholesterol and eGFR, the risk of all-cause death in the low klotho level group was 1.63 times than that in the high klotho level group (HR=1.63, 95% CI 1.03-2.63). Further stratified analysis showed that there was no interaction effect of age, gender, race and eGFR on the impact between low serum klotho level and the risk of all-cause death (all P>0.05), indicating that the correlation between low serum klotho level and the risk of all-cause death was consistent when DKD individuals were divided into different subgroups. Conclusions Low serum klotho level are significantly associated with increased risk of all-cause mortality in the DKD population. Maintaining an adequate serum klotho level may reduce the risk of death in DKD patients.

Objective To evaluate effectiveness of finerenone in patients with type 2 diabetes mellitus (T2DM) and chronic kidney disease (CKD) in the real world, and to analyze the associated factors of renal function progression during treatment. Methods It was a single-center retrospective study. The patients diagnosed with T2DM and CKD who received finerenone treatment for 3 months in Beijing Anzhen Hospital, Capital Medical University between April 1 and October 1, 2023 were included. The clinical data before and after finerenone treatment were collected. Based on urinary albumin-to-creatinine ratio (UACR) and estimated glomerular filtration rate (eGFR), the patients were divided into different groups, and the differences of clinical data before and after treatment were compared respectively. Logistic regression models was used to analyze the correlated factors of renal function changes during the treatment. Results A total of 151 patients were included with age of 63 (54, 70) years, and 103 males accounted for 68.2%. UACR level after 3 months of finerenone treatment was significantly lower than those before treatment (Z=-5.051, P<0.001), whereas there was no statistically significant change in eGFR (P>0.05). Both patients with baseline eGFR ≥60 ml·min^-1·(1.73 m²)^-1 (Z=-4.543, P<0.001) and those with baseline eGFR <60 ml·min^-1·(1.73 m²)^-1 (Z=-2.610, P=0.009) showed significant reductions in UACR after treatment. Both patients with baseline UACR ≥300 mg/g (Z=-4.681, P<0.001) and those with baseline UACR <300 mg/g (Z=-1.979, P=0.048) exhibited significantly lower UACR levels after treatment. The percentage reduction in UACR was greater in patients with baseline UACR ≥300 mg/g than in those with baseline UACR <300 mg/g (Z=-2.102, P=0.036).After 3 months of finerenone therapy, serum potassium level was slightly higher than baseline, but the difference was not statistically significant (P>0.05).The incidence of hyperkalemia after treatment was higher than baseline in patients with baseline eGFR <60 ml·min^-1·(1.73 m²)^-1 (χ² =2.558, P=0.039). During the treatment, 74 patients (49.0%) experienced renal function progression. Multivariate logistic regression analysis identified increased baseline serum albumin <45 g/L was an independent correlated factor of renal function progression during finerenone therapy (OR=1.934, 95% CI 1.157-3.231, P=0.012). Conclusions UACR in patients with T2DM and CKD can be reduced significantly after short-term treatment of finerenone. Increased baseline serum albumin level <45 g/L is independently associated with renal function progression during finerenone therapy.

Objective To conduct a comprehensive analysis of the clinical, pathological characteristics and prognosis of patients with secondary oxalate nephropathy manifested by acute kidney injury. Methods A retrospective analysis study was conducted on secondary oxalate nephropathy presenting with acute kidney injury and diagnosed by renal biopsy in the Department of Nephrology of the Second Affiliated Hospital of Anhui Medical University from August 2020 to July 2023. The general demographic characteristics, complications and laboratory tests were collected. All patients were followed from the time of diagnosis of oxalate nephropathy until death, loss to follow-up or the end of the study (October 2024). The primary endpoint event was the recovery of renal function. Results During the study period, a total of 329 patients underwent renal biopsies. Among them, 12 patients (3.65%) with secondary oxalate nephropathy were included in this study, including 7 males (7/12) and 5 females (5/12), with age of 56.5 (50.0, 69.0) years. In terms of comorbidities, 5 patients (5/12) had diabetes mellitus, 8 patients (8/12) had hypertension, and 3 patients (3/12) had gastrointestinal diseases. Among the causes, 3 patients (3/12) were identified as having a high-oxalate diet, 1 patient (1/12) underwent gastric cancer surgery, and 3 patients (3/12) took medications that could induce hyperoxalemia. Additionally, no definitive cause was identified in 5 patients (5/12). All 12 patients exhibited acute tubulointerstitial injury on renal pathology, with 8 patients also demonstrating chronic tubulointerstitial lesions. Management strategies included the removal of causative factors, adequate hydration to promote oxalate excretion, and sodium bicarbonate to alkalize urine and vitamin B6 to reduce oxalate production, along with renal replacement therapy if necessary. During the follow-up of 28 (16, 39) months, 6 patients (6/10) achieved complete recovery of renal function, 4 patients (4/10) showed partial recovery, and 2 patients were lost to follow-up. Conclusions The prevalence of secondary oxalate nephropathy at our center is 3.65%. Renal pathology in all patients demonstrates acute tubulointerstitial injury, with most patients exhibiting chronic tubulointerstitial lesions. Overall, the clinical prognosis remains favorable.

Objective To investigate the mechanism by which microRNA-183 (miR-183) regulates the progression of diabetic nephropathy (DN) through targeting phosphatase and tensin homolog deleted on chromosome 10 (PTEN) and modulating the AKT signaling pathway, and to identify potential therapeutic targets for DN. Methods (1) Bioinformatic analysis of miRNA expression: MiRNA expression datasets from diabetic nephropathy (DN) and control samples were obtained from the Gene Expression Omnibus database. Differential expression analysis was performed, and differentially expressed miRNAs (DEmiRNAs) were identified using thresholds of an absolute log₂ (fold changes) >1 and an adjusted P-value<0.05. The results were visualized in a volcano plot and a heatmap. (2) Animal model establishment and in vivo interventional studies: A DN rat model was induced by administration of a high-fat/high-sucrose diet combined with an intraperitoneal injection of streptozotocin. Rats were randomly assigned into four groups (n=10 per group) using a random number table: control group, DN model group, miR-183 inhibitor negative control (NC) group, and miR-183 inhibitor group. The latter two groups received tail vein injections of the miR-183 inhibitor NC or the miR-183 inhibitor, respectively, for eight consecutive weeks. Parameters including fasting blood glucose, 24-hour urinary protein excretion, urinary albumin excretion rate (UAER), serum creatinine, and blood urea nitrogen (BUN) were measured. Renal histopathological changes were assessed by HE and PAS staining. Furthermore, the expression of candidate miRNAs from patient data was validated, and the mechanism of action of miR-183 was investigated using quantitative real-time PCR and Western blotting. (3) In vitro mechanistic investigations in cultured podocytes: Mouse podocyte clone-5 (MPC5) cells were cultured in vitro and subjected to the following conditions: normal glucose (5.3 mmol/L glucose), high glucose (30 mmol/L glucose), and osmotic control (5.3 mmol/L glucose+19.5 mmol/L mannitol). Cells in the logarithmic growth phase were transfected with the miR-183 inhibitor (100 nmol/L), miR-183 mimic (50 nmol/L), or their corresponding negative controls. A dual-luciferase reporter assay was conducted to validate the binding interaction between miR-183 and the 3'-untranslated region (3'UTR) of PTEN. The effects of miR-183 on the AKT signaling pathway, apoptosis-related proteins, and cell viability were evaluated by quantitative real-time PCR, Western blotting, and the cell counting kit-8 assay, respectively. Results MiR-183 expression was markedly upregulated in renal tissues from DN patients and DN model rats (both P<0.05). Inhibition of miR-183 significantly reduced renal miR-183 levels by 90.2% (P<0.01), decreased fasting blood glucose by 65.3% (P<0.01), and improved renal function parameters, including reductions in urinary protein (40.3%), blood urea nitrogen (32.1%), urinary albumin excretion rate (22.5%), and serum creatinine (40.2%) (all P<0.01). Histological analyses showed attenuation of glomerular lesions and glycogen accumulation. Bioinformatic prediction and experimental validation identified PTEN as a direct target of miR-183, confirmed by dual-luciferase assays. In vitro, miR-183 inhibition increased PTEN expression, reduced AKT phosphorylation, promoted podocyte proliferation, and suppressed apoptosis (upregulation of Bcl-2 and downregulation of cleaved-caspase-3). These effects were abolished upon PTEN knockdown. Conclusions miR-183 aggravates DN by targeting PTEN and activating the AKT signaling pathway. Inhibition of miR-183 improves renal function and reduces podocyte apoptosis, suggesting miR-183 as a potential therapeutic target for DN.

This was a single-center retrospective case series study. This study evaluated the efficacy and safety of percutaneous covered stent endovascular exclusion under digital subtraction angiography (DSA) for removing dialysis catheters misplaced in arteries. The clinical data from 7 patients treated in the First Affiliated Hospital of Zhejiang University School of Medicine from January 2012 to October 2023 were analyzed. All patients had dialysis catheters confirmed to be misplaced in arteries via chest CT, X-ray radiography or computed tomography angiography. Percutaneous covered stent endovascular exclusion under DSA was used to remove the catheters. The results showed that except for one elderly patient died during waiting for surgery, the remaining 6 patients achieved satisfactory outcomes with no postoperative bleeding. There was no related complication observed during a 6-month follow-up. Arterial misplacement of dialysis catheters is a serious complication requiring prompt removal. Percutaneous covered stent endovascular exclusion under DSA offers a minimally invasive, effective, and safe approach with a high technical success rate and a low complication rate, making it a viable surgical option for similar clinical cases.

T-cell large granular lymphocyte leukemia (T-LGLL) is a rare chronic lymphoproliferative disorder. This paper presents a T-LGLL patient who had been on maintenance hemodialysis for over 20 years. Three years prior, the patient developed erythropoietin hyporesponsiveness, with hemoglobin levels declining from 100 g/L to 49 g/L over eight months, accompanied by mild leukopenia and thrombocytopenia. Initial bone marrow biopsy and peripheral blood tests yielded inconclusive results. A ^99mTc-labeled red blood cell spleen scintigraphy revealed evidence of hypersplenism, which prompted a splenectomy. Following surgery, leukopenia and thrombocytopenia resolved, but anemia persisted. Subsequently, lymphocyte counts increased, and reticulocyte progressively declined. Further investigations, including bone marrow biopsy, blood smear analysis, immunophenotyping, and T-cell receptor gene analysis, ultimately confirmed the diagnosis of T-LGLL with pure red cell aplasia. Treatment with cyclosporine resulted in a significant improvement in hemoglobin, reaching 117 g/L in 6 months. This case contributes to enhancing clinicians' awareness and understanding of this disease.

Joubert syndrome is a rare primary ciliopathy characterized by hypoplasia of the midbrain and vermis cerebellum, with or without extracerebral organs involvement. This article reports a case of Joubert syndrome with RPGRIP1L mutation, presented with anemia, renal dysfunction, growth retardation, and mental retardation. The patient reached end-stage renal disease at the age of 13 years old. Magnetic resonance imaging of the brain revealed slight elongation of the superior cerebellar peduncles, mild hypoplasia of the cerebellar vermis, and the characteristic "molar tooth sign". Elevated transaminase and γ-glutamyl transpeptidase levels were detected at the age of 14 years old. Genetic analysis showed a compound heterozygous mutation in the RPGRIP1L gene (c.1290_1291delGT, c.3764T>C). Joubert syndrome is a clinically heterogeneous disorder and easy to be missed. Early diagnosis and standard treatment contribute to a better prognosis.

This article reports a case of membranous nephropathy in an adolescent accompanied by monoclonal IgG1-κ deposition. The 16-year-old female patient was hospitalized for experiencing proteinuria and hematuria for more than 20 days. The patient had a history of mycoplasma infection and acute kidney injury, and renal pathology revealed glomerular membrane lesions accompanied by crescent formation. Electron microscopy showed electron dense deposits in the subepithelial and mesangial regions, and immunofluorescence demonstrated monotypic IgG1?κ deposits in the glomerulus. Bone marrow examination did not find any abnormal plasma cells, nor were there significant abnormalities in serum or urine free light chain κ/λ ratio. The diagnosis was proliferative glomerulonephritis characterized by membranous lesions with monoclonal IgG1?κ deposits. This disease is rare in children and adolescents, and currently there is limited understanding of its mechanism, with limited clinical treatment experience. This article aims to provide clinical insights through case analysis and literature review.

Patients with chronic kidney disease (CKD) are at increased risk of fractures, and accurate assessment of this risk remains a major clinical challenge. Traditional tools such as bone mineral density and fracture risk assessment tool show limited predictive performance in CKD population. In recent years, novel approaches including trabecular bone score, vertebral fracture assessment, hip structural analysis, quantitative computed tomography, high-resolution peripheral quantitative computed tomography, artificial intelligence, and bone turnover markers have been introduced for fracture risk assessment. These emerging techniques provide more comprehensive evaluation strategies, yet their clinical utility remains to be fully validated. This review summarizes current research progress on fracture risk assessment methods in CKD patients and highlights potential directions for improving risk prediction in CKD population.

Immune-related kidney disease is one of the causes of end-stage renal disease and an important disease type that threatens public health. Farnesoid X receptor (FXR) is a nuclear receptor activated by bile acids, involved in regulating gene expression related to bile acid, lipid, and glucose metabolism. In recent years, the role of FXR in renal immune regulation has received attention. FXR participates in the occurrence and development of immune-related kidney diseases by regulating the differentiation, polarization, activation, recruitment, adhesion, infiltration, and cytokine release of immune cells such as macrophages, dendritic cells, natural killer cells, T lymphocytes, and B lymphocytes. This article reviews renal immune-regulatory mechanisms of FXR in recent years and its potential role in immune-related kidney diseases, to provide a theoretical basis for the prevention and treatment of immune-related kidney diseases targeting FXR.

Chronic kidney disease (CKD) during the peridialysis period (CKD-PeriDialysis) includes two stages: predialysis and initial dialysis. During this period, patients have a high incidence of complications and comorbidities, a high mortality rate, high treatment costs, and a rapid decrease in glomerular filtration rate. In the early stage of dialysis, due to the particularity, variability, and limitations of dialysis technology, the patients' internal environment undergoes drastic changes, and the mortality rate increases instead of decreasing. Therefore, there is an urgent need for guiding documents for the management of CKD patients during the peridialysis period in clinical practice. In view of this, the Clinical Practice Guidelines for the Management of CKD during Peridialysis in China (2025) Working Group of the Kidney Disease Dialysis Special Committee of the China Association of Non-Public Medical Institutions has developed this clinical practice guidelines for management of CKD during peridialysis in China (2025). This guideline is based on evidence-based medicine and clinical experience, comprehensively elaborating on the disease evaluation indicators and frequency, the timing and mode selection of renal replacement therapy, the assessment of dialysis adequacy, and the diagnosis and management of common complications during the peridialysis in CKD patients during the peridialysis. This guideline reflects new perspectives and future development trends in the diagnosis and treatment of CKD patients during the peridialysis, which is conducive to further strengthening the understanding of nephrologists on CKD during the peridialysis, standardizing clinical management processes, thereby improving survival rates and quality of life of the patients, and reducing medical burden.