Objective To investigate the association between homocysteine (Hcy) and left ventricular remodeling (LVR) in patients with IgA nephropathy (IgAN). Methods In this single-center retrospective study, IgAN patients admitted to Sun Yat-sen Memorial Hospital, Sun Yat-sen University between April 2014 and July 2023 were enrolled. LVR was defined as elevated left ventricular mass index (LVMI) or relative wall thickness (RWT) (LVMI >115 g/m2 for males and LVMI >95 g/m2 for females, or RWT>0.42). Logistic regression analysis was used to analyze the correlation between Hcy and LVR, and LVR subclasses. Results There were 257 IgAN patients included in this study, with 126 males (49.03%) and age of 34.00 (28.00, 46.00) years old. There were 74 patients (28.79%) with LVR. Compared with the non-LVR group, LVR group had higher proportion of males (χ²=10.431, P=0.002), age (Z=4.110, P<0.001), proportion of hypertension (χ²=37.782, P<0.001), body mass index (Z=4.798, P<0.001), mean arterial pressure (Z=5.179, P<0.001), Hcy (Z=5.130, P<0.001), serum creatinine (Z=6.103, P<0.001), cystatin C (Z=6.536, P<0.001), blood urea nitrogen (Z=5.626, P<0.001), serum uric acid (t=3.568, P<0.001), 24 h-urine protein excretion (Z=5.088, P<0.001), triglyceride (Z=4.292, P<0.001) and high-sensitivity C-reactive protein (Z=4.501, P<0.001), and lower high-density lipoprotein (Z=-3.104, P=0.003), hemoglobin (Z=-2.370, P=0.018) and serum bicarbonate (Z=-3.007, P=0.003). Univariate logistic regression analysis identified that sex, age, body mass index, mean arterial pressure, hypertension, serum creatinine, blood urea nitrogen, cystatin C, serum uric acid, Hcy, high-sensitivity C-reactive protein, serum phosphorus, triglyceride, hemoglobin, serum bicarbonate, tubular atrophy or interstitial fibrosis, thickening arterial wall and hyaline degeneration were significantly correlated with LVR in IgAN patients (all P<0.05). Multivariate logistic regression analysis indicated that serum Hcy was not independently correlated with LVR in IgAN patients with (P>0.05). LVR subtypes revealed that serum Hcy was independently correlated with left ventricular eccentric hypertrophy (OR=1.109, 95% CI 1.018- 1.208, P=0.018). Serum Hcy was not correlated with centripetal remodeling or centripetal hypertrophy (both P>0.05). Conclusions Serum Hcy is not significantly associated with LVR in IgAN patients, but an independent correlation exists between Hcy and the eccentric hypertrophy subtype of LVR.

Objective To investigate the impact of the degree of proteinuria remission on the prognosis of patients with IgA nephropathy (IgAN). Methods This study was a single-center retrospective cohort study. The data from patients diagnosed with IgAN via renal biopsy in the Department of Nephrology, the First Affiliated Hospital of the University of Science and Technology of China from December 2019 to March 2023 was retrospectively analyzed. Based on proteinuria levels 6 months after initial treatment, patients were divided into complete remission (CR), partial remission (PR), and no remission (NR) groups. Differences in baseline clinical and pathological characteristics among the three groups were compared. The follow-up period began on the day of the patient's renal biopsy and ended on June 1, 2024. The endpoint event was defined as a ≥30% decline in estimated glomerular filtration rate (eGFR) from baseline, or the onset of end-stage renal disease [eGFR<15 ml·min^-1·(1.73 m²)^-1], initiation of dialysis, or all-cause mortality. Logistic regression was used to analyze the factors related to the remission of proteinuria. The Kaplan-Meier method was used to calculate the cumulative renal survival rates for the three groups, and Cox regression analysis was applied to evaluate factors influencing endpoint events. Results Of 342 patients diagnosed with IgAN, 226 patients with primary IgAN were ultimately included. After 6 months of initial treatment, proteinuria status was CR in 110 patients (48.7%), PR in 43 patients(19.0%), and NR in 73 patients (32.3%). Multivariate logistic regression analysis was conducted with the relief of proteinuria (CR and PR) as the dependent variable. The results showed that baseline 24-hour urine protein quantity ≤ 1 g (OR=3.954, 95% CI 1.803-8.670, P=0.001), history of hypertension (OR=0.348, 95% CI 0.183-0.660, P=0.001), and tubular atrophy or interstitial fibrosis (T1+T2/T0, OR=0.405, 95% CI 0.187-0.875, P=0.021) were independent correlated factors for the relief of proteinuria within 6 months of treatment in patients. The follow-up period was 22.5 (12.0, 34.0) months. Among the 50 patients (22.1%), 50 events occurred as the endpoint. Specifically, 1 patient (0.9%) in the CR group, 10 patients (23.3%) in the PR group, and 39 patients (53.4%) in the NR group experienced the event. Kaplan-Meier survival analysis showed that there was a statistically significant difference in renal survival rates among the three groups (Log-rank test, χ²=70.289, P<0.001). Among them, the renal survival rates of patients in the CR group and the PR group were significantly higher than that of the NR group, respectively (Log-rank test, χ²=70.699, P<0.001; χ²=7.930, P=0.048, respectively). Further grouping based on the subgroup analysis of baseline proteinuria revealed that, among patients with a baseline urinary protein quantification of <1 g/d, the CR group showed a significantly higher renal cumulative survival rate compared to both the PR and NR groups respectively (Log-rank test, χ²=14.206, P<0.001; χ²=25.823, P<0.001, respectively). However, the difference in renal survival rate between the PR and NR groups was not statistically significant (Log-rank test, χ²=0.659, P=0.417). Among patients with a baseline urinary protein quantification of 1 to 2 g/d, the CR group also demonstrated a significantly higher renal cumulative survival rate than the PR and NR groups respectively (Log-rank test, χ²=7.583, P=0.006; χ²=20.706, P<0.001, respectively). Similarly, no statistically significant difference in renal survival rate was observed between the PR and NR groups (Log-rank test, χ²=2.494, P=0.114). In patients with baseline urinary protein quantification >2 g/d, the CR group's cumulative renal survival rate was superior to the PR and NR groups respectively (Log?rank test, χ²=6.495, P=0.011; χ²=18.461, P<0.001, respectively), and importantly, the PR group's survival rate was significantly better than the NR group (Log?rank test, χ²=6.233, P=0.013). Multivariate Cox regression analysis showed that achieving proteinuria CR at 6 months of treatment was correlated with a 98.6% reduction in the risk of reaching the endpoint event (HR=0.014, 95% CI 0.002-0.103, P<0.001) and the risk of renal composite endpoint events in the proteinuria PR group was reduced by 55.2% (HR=0.448, 95% CI 0.213-0.941,P=0.034) compared with the NR group. Furthermore, Hypertension (HR=2.145, 95% CI 1.081-4.260, P=0.029), serum albumin <35 g/L (HR=3.400, 95% CI 1.747-6.619, P<0.001), and uric acid (HR=1.005, 95% CI 1.002-1.007, P=0.001) were also significant factors correlated with the occurrence of renal composite endpoint events in patients with IgAN. Conclusions Achieving CR of proteinuria 6 months after treatment improves renal prognosis in IgAN patients, and achieving PR also provides some benefit. Therefore, proteinuria in IgAN patients should be actively managed, with efforts made to achieve CR whenever possible, regardless of baseline urinary protein levels.

Objective To analyze the incidence and the risk factors of bleeding complications after percutaneous renal biopsy and provide a theoretical basis for identifying renal biopsy patients with high risk factors. Methods It was a retrospective study. The clinical data of patients who underwent ultrasound-guided percutaneous renal biopsy in the Department of Nephrology, Jinling Hospital, Affiliated Hospital of Nanjing University Medical School between January 1, 2015 and September 30, 2020 were collected. Patients were classified into hemorrhage and non-hemorrhage groups based on the presence of hemorrhagic complications within 30 days following renal biopsy, and the clinical data between the two groups were compared. Logistic regression model was used to analyze the risk factors of post-renal biopsy hemorrhage. Results There were 16 013 renal biopsy patients enrolled in the study, with age of 40 (29, 65) years old and 8 577 males (53.6%). There were 519 patients (3.2%) experiencing bleeding within 30 days post renal biopsy, and 229 patients (1.4%) required intervention, including endovascular treatment, blood transfusion, and administration of hemostatic agents such as pituitrin, thrombin, or others. There were statistically significant differences in the proportion of females (χ2=39.219, P<0.001), age (Z=2.146, P=0.032), body mass index (BMI) (Z=-5.616, P<0.001), BMI classification (χ2=34.753, P<0.001), proportion of diabetes mellitus (χ2=8.547, P=0.003), platelet (Z=-5.511, P<0.001), preoperative hemoglobin (Z=-10.337, P<0.001), postoperative hemoglobin (Z=-12.856, P<0.001), the difference of hemoglobin before and after the operation (Z=-3.683, P<0.001), decreased hemoglobin >15 g/L (P<0.001), D-dimer (Z=-3.623， P<0.001), 24-hour urinary protein (Z=-2.040, P=0.041), estimated glomerular filtration rate classification (χ2=10.739, P=0.030), proportion of nephrotic syndrome (χ2=49.772, P<0.001), type of renal diseases (χ2=89.219, P<0.001) between the two groups. Multivariate regression analysis identified that females (OR=1.284, 95% CI 1.040-1.587), diabetes mellitus (OR=1.546, 95% CI 1.100-2.174), hypertensive kidney damage (OR=3.170, 95% CI 2.008-5.004), plasma cell dyscrasia-related kidney injury (OR=3.151, 95% CI 1.592-6.236), nephrotic syndrome (OR=0.446, 95% CI 0.354-0.562), BMI≥25 kg/m² (OR=0.794, 95% CI 0.635-0.993), hemoglobin (OR=0.984, 95% CI 0.980-0.989) and platelet (OR=0.998, 95% CI 0.997-0.999) were independent correlated factors of post-renal biopsy bleeding. Of the 34 severe bleeding patients requiring blood transfusions or interventional therapy, all patients recovered to preoperative hemoglobin levels after 1 month of active treatment. Conclusions The incidence of bleeding complications after renal biopsy is 3.2%, and 1.4% patients requires intervention treatment. Female, diabetes mellitus, hypertensive renal damage, plasma cell disease-related renal injury, nephrotic syndrome, BMI≥25 kg/m2, hemoglobin and platelet are independent related factors of bleeding complications after renal biopsy. Comprehensive risk assessment before renal biopsy is of great importance.

Objective To evaluate the relationship between estimated pulse wave velocity (ePWV) and functional dependence in maintenance hemodialysis (MHD) patients. Methods A cross-sectional study was conducted. The clinical data of MHD patients in the Second Affiliated Hospital of Soochow University from June to December 2023 were retrospectively collected. The Katz and Lawton-Brody questionnaires scales were used to assess the patients' functional status. Patients were classified into normal functional group (total scores ≥36) and functional dependence group (total scores <36) based on these scores. ePWV was calculated based on age and blood pressure and categorized into elevated and normal groups using a threshold of 9.945, and the differences of the functional dependence status between the two groups were compared. Spearman's correlation analysis method was used to analyze the correlation between ePWV and functional dependence scores in MHD patients. Logistic regression analysis method was used to identify risk factors of functional dependence. Receiver-operating characteristic curve was used to evaluate ePWV's predictive value for functional dependence. Results A total of 161 MHD patients were included, with age of (58.45±14.42) years and 95 males (59.01%). Among them, 39 patients (24.22%) were combined with diabetes, 145 patients (90.06%) were combined with hypertension, and 80 patients (49.69%) had functional dependence. The functional dependence group had significantly higher age (Z=5.669, P<0.001), proportion of diabetes (χ²=4.277, P=0.039), pulse pressure difference (Z=3.571, P<0.001) and ePWV (Z=5.296, P<0.001), and lower diastolic blood pressure (t=-2.841, P=0.005), serum creatinine (t=-3.327, P=0.001), serum albumin (Z=-4.797, P<0.001), triglyceride (Z=-2.142, P=0.032) and total cholesterol (Z=-2.491, P=0.013). The normal ePWV group had significantly higher activity of daily living scores, instrumental activity of daily living scores, and physical function dependence scores (all P<0.05). Spearman correlation analysis showed negative correlation between ePWV and activity of daily living scores (r=-0.254, P=0.001), instrumental activity of daily living scores (r=-0.440, P<0.001), and functional dependence scores (r=-0.436, P<0.001). Multivariate logistic regression analysis showed that ePWV (OR=4.043, 95% CI 1.247-13.107, P=0.020), combined diabetes (OR=3.013, 95% CI 1.079-8.419, P=0.035) and serum albumin (OR=0.792, 95% CI 0.689-0.910, P=0.001) were independent correlated factors of functional dependence. The receiver-operating characteristic curve showed that the area under the curve (AUC) for ePWV in predicting functional dependence was 0.742 (95% CI 0.664-0.819, P<0.001), marginally higher than that for serum albumin (AUC=0.720, 95% CI 0.641-0.799, P<0.001). The optimal cut-off value for ePWV was 10.664 m/s, with sensitivity of 85% and specificity of 60%. Conclusion ePWV≥10.664 m/s has the value of predicting functional dependence in MHD patients.

Objective To analyze the structural data related to hospital infection quality control in the Beijing Blood Purification Quality Control Center and provide a reference for further enhancing the level of overall hospital infection quality control system. Methods It was a cross-sectional study. Under the guidance of an expert committee, in accordance with the hospital infection management guidelines and standard operating procedures for hemodialysis stipulated by national health management authorities, the research team defined the investigation scope and procedures, thus establishing an on-site hospital infection quality control framework, encompassing 13 dimensions. A total of 183 survey data items were meticulously examined through various means, including on-site operations, random inspections, on-site audits, and interviews. From January to March 2024, a sampling survey was conducted on blood purification centers across Beijing. The collected data were then collated and analyzed. Results A total of 41 hemodialysis centers and 26 peritoneal dialysis centers within the jurisdiction of Beijing were investigated. The on-site assessment results of nosocomial infection quality control showed that the items with the highest detection rates of risky behaviors were qualifications and allocation of blood purification personnel (56.72%, 38/67), zoning and layout of blood purification centers (47.76%, 32/67), and implementation of rules and regulations (43.28%, 29/67). There were statistically significant differences among different-level medical institutions in terms of the qualifications and allocation of personnel in blood purification centers (χ²=7.236, P=0.027), the implementation of regulations and rules (χ²=10.973, P=0.004), and the prevention and control of nosocomial infections (Fisher value=7.474, P=0.018). Conclusions The main weak links in the quality control and management of nosocomial infections at the Beijing Blood Purification Center are the qualifications and allocation of personnel in the blood purification center, the zoning and layout of the blood purification center, and the implementation of rules and regulations. In future quality control initiatives and the daily management of blood purification centers, it is advisable to prioritize the rectification of core vulnerable areas. Moreover, establishing a differentiated supervision and dynamic monitoring mechanism can contribute to optimizing hospital infection quality control.

Objective To assess the growth and development status of children with idiopathic nephrotic syndrome (INS) and to explore associated factors of stunting. Methods It was a single-center, cross-sectional study. The general information, clinical data, and laboratory test data from INS children under 18 years old initially diagnosed at the Children's Hospital of Zhejiang University School of Medicine between January 1, 2020 and April 30, 2024 were retrospectively collected. Among children receiving medium-to long-term glucocorticoid (GC) therapy (≥3 months), the relationship between the duration of GC treatment and height development was analyzed from two perspectives: differences of GC treatment duration among different height development grade groups, and differences of the distribution of height development grades among different GC treatment durations groups. In children with complete clinical data, patients were divided into growth retardation (GR) group (short stature or below-average height) and growth normal (GN) group (normal criteria) based on the evaluation standard for children and adolescents. Differences of related data between the two groups were compared. Multivariate logistic regression analysis was used to identify factors associated with GR in INS children Results A total of 720 children with INS were included, of whom 499 children (69.9%) were males. The baseline age was (7.10±4.19) years, and the height was (119.81±32.75) cm. 31.81% (229/720) of the children had a height development grade classified as below-average height or short stature. Among children receiving medium- to long-term GC therapy, the incidence of below-average height and short stature showed an increase with longer treatment duration, but the differences of these proportions among the various treatment duration groups were not statistically significant (all P>0.05). Among the 152 children with complete clinical data, 53 patients were in the GR group and 99 patients in the GN group. Intergroup comparisons showed that alkaline phosphatase (Z=-2.395, P=0.017) and serum creatinine (Z=-2.267, P=0.023) in the GR group were lower than those in the GN group, while triglyceride (Z=2.018, P=0.044) and serum pH value (t=2.530, P=0.012) were higher than those in the GN group. Multivariate logistic regression analysis revealed that increasing serum pH value was an independent correlated factor of GR in children with INS (OR=2.353, 95% CI 1.051-5.265, P=0.037). Subgroup analysis showed that among male children, the GR group had lower alkaline phosphatase (Z=-2.606, P=0.009), serum creatinine (Z=-2.607, P=0.009) and serum magnesium (Z=-1.996, P=0.046) than the GN group, while triglyceride (Z=2.222, P=0.026) and serum pH value (t=2.987, P=0.003) in the GR group were higher than those in the GN group. Age group analysis indicated that among male children with INS aged 0 to <9 years, the GR group had lower serum magnesium (Z=-2.248, P=0.025) and higher serum pH value (t=2.049, P=0.044) than the GN group. Among male children with INS aged 9 to <18 years, the GR group had higher serum albumin (t=2.193, P=0.035), prealbumin (t=3.155, P=0.003), triglyceride (Z=1.985, P=0.048) were higher than the GN group, while serum creatinine (t=-2.966, P=0.005) in the GR group were lower than those in the GN group. Furthermore, bone metabolism analysis showed that the GR group had significantly lower serum phosphorus (t=-2.151, P=0.040), β-crosslaps (Z=-2.095, P=0.037), osteocalcin (Z=-2.570, P=0.009), and parathyroid hormone (Z=-2.846, P=0.004) than the GN group. Conclusions 31.81% of children with INS had GR. Among children receiving medium- to long-term GC therapy, the incidence of both below-average height and short stature increases with the duration of treatment, suggesting that the duration of GC therapy may be a relevant factor contributing to GR in children with INS.

Objective To summarize the clinical characteristics and genetic variants of children with Dent disease, thereby improving clinicians' understanding of this disorder. Methods It was a retrospective case series study. A retrospective analysis was conducted of the clinical characteristics and genetic testing results of children with Dent disease admitted to the Nephrology Department of Wuhan Children's Hospital, Tongji Medical College, Huazhong University of Science＆Technology. between June 2016 and June 2023, with evaluation of the clinical progression. The effects of different mutation sites on the protein structure of the pathogenic genes chloride voltage-gated channel 5 (CLCN5) and oculocerebrorenal syndrome of Lowe (OCRL) were further analyzed. Results All enrolled 12 patients with Dent disease were males, with diagnosed age ranging from 9 months to 14 years and 5 months. All patients presented with low-molecular- weight proteinuria and hypercalciuria. Ten children had nephrocalcinosis or nephrolithiasis, and none showed evidence of rickets. Renal biopsy was performed in one patient and revealed minimal glomerular lesions with focal thinning of the basement membrane on electron microscopy. Gene testing revealed 12 mutations, including 2 unreported nonsense mutations in the OCRL gene, c.556A>T (p.K186X) and c.218T>A (p.L73X); The 10 mutations of CLCN5 gene, including missense mutations c.478T>C (p.C160R) and c.1790A>G (p.E597G), nonsense mutation c.1429C>T (p.R417X), splice site mutation c.316-2 (IVS5) A>C, and deletion mutation loss (exon: 4-15), had been reported for the first time in the literature. Three- dimensional protein structure simulations suggested that the p.C160R and p.E597G missense mutations altered internal chemical bonds within the protein, thereby disrupting its structural stability. All newly identified nonsense or deletion mutations resulted in truncated proteins. Notably, deletion of exons 4-15 led to complete loss of the CLCN5 protein. The remaining five types of mutations had been previously reported in the domestic and international literature. After diagnosis, nine children were treated with potassium citrate, hydrochlorothiazide and fosinopril, and the urinary calcium-to-creatinine ratio was maintained within the normal range. The remaining three children did not receive oral pharmacological treatment and were not followed up regularly. Conclusions low-molecular- weight proteinuria and hypercalciuria are important indicators for the diagnosis of Dent disease. Genetic testing should be actively considered in children presenting with low-molecular-weight proteinuria and hypercalciuria to establish a definitive diagnosis of Dent disease and to avoid misdiagnosis or missed diagnosis. By correlating clinical phenotypes with genotypes, this study expands the mutation spectrum of Dent disease and provides a theoretical basis for future investigations into its molecular mechanisms.

Objective To investigate the expression changes of glutaminase 2 (GLS2) in peritoneal mesothelial cells during peritoneal dialysis (PD) and its role in the epithelial- mesenchymal transition (EMT) of peritoneal mesothelial cells. Methods This study was divided into two parts: clinical samples analysis and in vitro experimental verification. (1) Peritoneal tissues were collected from healthy controls, uremic patients, and patients with ultrafiltration failure during PD. HE and Masson staining were used to observe the morphological changes of peritoneal tissues. (2) The PD effluent was collected from nocturnal abdominal retention in uremic patients with initial PD, PD short dialysis duration and PD long dialysis duration. Primary human peritoneal mesothelial cells were isolated and cultured. Proteins and RNA were extracted for Western blotting and real-time fluorescent quantitative PCR to detect the protein and mRNA expression levels of GLS2, E?cadherin, and α?smooth muscle actin (α?SMA). (3) The human peritoneal mesothelial cell line HMrSV5 was cultured in vitro and stimulated with different concentrations of glucose to construct the EMT models. The cells were divided into a low-glucose control group (5.6 mmol/L D-glucose), a hypertonic control group (5.6 mmol/L D-glucose+133.4 mmol/L D-mannitol), a 1.5% high-glucose group (83 mmol/L D-glucose), and a 2.5% high-glucose group (139 mmol/L D-glucose). GLS2 was specifically knocked down by small interfering RNA (siRNA), and the cells were divided into a GLS2 knockdown negative control group (139 mmol/L D-glucose+siNC) and a GLS2 knockdown group (139 mmol/L D-glucose+siGLS2). The expression of EMT markers (E?cadherin and α?SMA) was observed. Results (1) Compared with the healthy control and uremic groups, the peritoneal tissues of PD ultrafiltration failure patients were thickened and had increased collagen deposition(both P<0.01). (2) Compared with the PD initial dialysis group, the expression of E?cadherin in the peritoneal dialysis effluent of the PD short dialysis duration and long dialysis duration groups was down-regulated (both P<0.01), with a progressive decline correlating with longer dialysis duration; while the expressions of α?SMA and GLS2 were up-regulated (both P<0.05), and the expression of both significantly up-regulated with increasing dialysis duration. (3) In vitro cell experiments showed that compared with the low- glucose group, the expression of E?cadherin in the HMrSV5 cell line was significantly down-regulated in the high-glucose group (P<0.05); while the expression of α?SMA and GLS2 were significantly up- regulated (both P<0.05). (4) Compared with the negative control group, the expression of E?cadherin in the GLS2 knockdown group was significantly up-regulated (P<0.05), and the expression of α?SMA was significantly down-regulated (P<0.05). Conclusion GLS2 is significantly over-expressed in high glucose-induced EMT of peritoneal mesothelial cells, and specific knockdown of GLS2 can effectively alleviate high glucose-induced EMT. It is suggested that GLS2-mediated glutaminolysis may be a key regulatory pathway of high glucose-induced peritoneal fibrosis.

It was a single-center cross-sectional study. The maintenance hemodialysis (MHD) patients from the Suzhou Ninth People's Hospital Affiliated to Soochow University from June to August 2024 were selected as the research subjects to investigate the prevalence and influencing factors of functional constipation (FC) in patients undergoing MHD. The general data, clinical data, laboratory examination results, and oral medication history data were collected. The questionnaires surveys were conducted among the patients. The questionnaires included the Diagnostic Questionnaire for Functional Constipation in Adults (RomeⅣ), the International Physical Activity Questionnaire (IPAQ), and the 24 h Dietary Recall Questionnaire. Based on the results of FC diagnosis, the patients were divided into FC and non-FC groups. The differences of related data between the two groups were compared. Multivariate logistic regression analysis was performed to identify influencing factors of FC in the MHD patients. A total of 206 MHD patients were included, with 132 males (64.08%) and age of (61.36±13.44) years. The prevalence of FC was 44.17% (95% CI 37.32%-51.24%). There were statistically significant differences between FC and non-FC groups in terms of age (t=2.772, P=0.006), proportion of diabetes (χ ²=13.733, P<0.001), serum ferritin (Z=2.670, P=0.008), IPAQ scores (Z=-2.344, P=0.019), triglyceride (Z=-2.903,P=0.004), proportion of lanthanum carbonate (χ² =5.040, P=0.025) and proportion of calcium channel blockers (χ ²=5.572, P=0.018). Multivariable logistic regression analysis revealed that age ≥60 years (OR=3.004, 95% CI 1.554-5.807, P=0.001), comorbid diabetes (OR=3.824, 95% CI 1.852-7.897, P<0.001), serum ferritin ≥100 μg/L (OR=2.279, 95% CI 1.162-4.471, P=0.017), IPAQ scores ≥1 500 (OR=0.485, 95% CI 0.246-0.958, P=0.037), consumption of aquatic products (OR=0.373, 95% CI 0.183-0.759, P=0.007), carbohydrate intake ≥150 g (OR=0.420, 95% CI 0.206-0.854, P=0.017), use of lanthanum carbonate (OR=2.835, 95% CI 1.239-6.485, P=0.014), and use of calcium channel blockers (OR=1.958, 95% CI 1.004-3.819, P=0.049) were independently correlated with FC in MHD patients. The study shows that, the prevalence of FC is relatively high in MHD patients. Age ≥60 years, comorbid diabetes, serum ferritin ≥100 μg/L, IPAQ scores ≥1 500, carbohydrate intake ≥150 g, consumption of aquatic products, use of lanthanum carbonate, and use of calcium channel blockers are related factors of FC in MHD population.

Pure red cell aplasia caused by anti-erythropoietin (EPO) antibody is a rare but serious disease. This report describes a 41-year-old male peritoneal dialysis patient who developed anti-EPO antibody mediated-pure red cell aplasia following treatment with recombinant human EPO. Initially, the patient showed poor response to oral corticosteroids and cyclophosphamide, with persistently low EPO level and markedly elevated transferrin saturation. After switching to cyclosporine, the anemia was promptly corrected, accompanied by a significant rebound in EPO level. This case suggests that EPO level and transferrin saturation may not only aid in diagnosis but also serve as potential indicators for assessing the efficacy of immunosuppressive therapy.

Autosomal dominant tubulointerstitial kidney disease (ADTKD) is a group of single-gene inherited kidney diseases characterized by autosomal dominant inheritance and progressive tubulointerstitial damage. The paper reports a case of ADTKD caused by a new mutation in the uromodulin (UMOD) gene (ADTKD-UMOD). The patient presented with hyperuricemia, gout, mildly elevated serum creatinine, and a family history of elevated serum creatinine. Genetic testing revealed a heterozygous variant in the UMOD gene (c.856T>C, p.Tyr286His). Through strict management of serum uric acid level and regular monitoring of renal function, the patient maintained stable renal function throughout the follow-up one-year. By reporting this case and reviewing recent advances in ADTKD-UMOD, this article highlights the diagnostic role of genetic testing in unexplained tubulointerstitial injury.

Paroxysmal nocturnal hemoglobinuria (PNH) is a rare acquired clonal disease caused by genetic mutations in hematopoietic stem cells. Kidney injury is a common and easily ignored complication. Eculizumab significantly improves the therapeutic efficacy of PNH by inhibiting terminal complement activation. The paper reports a PNH patient with episodic gross hematuria after repeated upper respiratory tract infections, diagnosed with hemosiderin-containing renal tubular disease through renal biopsy. After treatment with standard dose of eculizumab, intravascular hemolysis and kidney damage were significantly improved. There were no infection events during treatment and follow-up, and the clinical condition remained stable. This case emphasizes the importance of improved recognition of PNH-associated kidney damage. Furthermore, it indicates that eculizumab therapy is both effective and safe for treating this complication.

Acute kidney injury (AKI) is a common clinical syndrome characterized by a rapid decline in renal function. Previous studies have proposed multiple predictive biomarkers for the occurrence of AKI. However, the development of AKI is heterogeneous. Recent studies have demonstrated that distant organs can influence the kidney through various pathways, and the corresponding early predictive indicators differ accordingly. This review summarizes the specific roles of different distant organs including the heart, lung, brain, gastrointestinal tract, and liver in the development and progression of AKI, and highlights early predictive markers associated with each organ system, aiming to provide a basis for early identification and mechanism-based interventions of AKI across diverse clinical settings.

Renal anemia is one of the most common complications of chronic kidney disease. Recently, the development of hypoxia-inducible factor-prolyl hydroxylase inhibitors (HIF?PHI) has provided new therapeutic options for patients with renal anemia. This article systematically reviews the mechanisms of action of HIF?PHIs, comprehensively elaborates on the pharmacological characteristics of different drugs, and summarizes the overall efficacy and safety data from clinical studies. In addition, based on clinical practice in nephrology, it addresses key issues and considerations in the application of HIF?PHIs, aiming to support rational clinical use.

Chronic kidney disease (CKD) affects a large number of people. Vascular calcification in CKD patients can increase the incidence of cardiovascular events, posing a serious threat to the life safety of CKD patients. At present, many studies are actively exploring the pathogenesis of CKD-related vascular calcification, among which the discovery of vascular calcification biomarkers holds significant clinical and scientific research value. The paper reviews the research progress on calcification markers of coronary artery, thoracic aorta, abdominal aorta, and intracranial artery related to CKD, and its possible mechanism in the pathogenesis of vascular calcification, aiming to provide new ideas for further in-depth researches and future clinical applications.

Calciphylaxis is a rare and progressive vascular calcification disease characterized by microvascular calcification in subcutaneous fat and dermis, microthrombus formation, and endothelial damage. It commonly occurs in patients with end-stage kidney disease, and progresses rapidly, with a 1-year mortality rate of up to 80% when accompanied by ulceration and infection. Despite its severity, the underlying mechanism of calciphylaxis remains unclear, and the existing therapies are limited to multidisciplinary approaches without established effective methods. In recent years, mesenchymal stem cells (MSCs) have emerged as a potential therapeutic approach for complex and challenging diseases due to their promoting regeneration, inhibiting vascular calcification, anti-infection, regulating immunity, and anti-coagulant properties. This review summarizes the epidemiological characteristics and clinical manifestations, pathogenesis, and current therapeutic status of MSCs for calciphylaxis in recent years, along with the potential therapeutic applications of MSC.

The 2025 Kidney Disease: Improving Global Outcomes (KDIGO) clinical practice guideline for IgA nephropathy represented a comprehensive update to the 2021 edition, emphasizing early diagnosis, risk stratification, and precision therapy. The guideline recommended that patients with proteinuria ≥0.5 g/d and no contraindications should undergo timely renal biopsy to confirm pathological type and assess risk. Proteinuria ≥0.5 g/d was defined as the threshold for progressive renal risk, warranting treatment initiation. For the first time, the new guideline advocated for simultaneous initiation of interventions targeting the two key pathological processes of IgA nephropathy: (1) etiological intervention to suppress the formation of galactose-deficient IgA1 (Gd-IgA1) and its immune complexes, and (2) management of the secondary responses following nephron loss. Budesonide enteric capsules are currently the only agent proven to significantly reduce Gd-IgA1 and related immune complexes by targeting gut mucosal immunity and decreasing pathogenic IgA production, thereby interrupting the "four-hit" pathogenesis at its source. Clinical studies have demonstrated that budesonide markedly reduces proteinuria, slows estimated glomerular filtration rate decline, and can be safely re-administered, providing evidence for its role in long-term maintenance therapy. Sodium-glucose cotransporter-2 inhibitors and sparsentan are recommended to mitigate compensatory injury following nephron loss. A comprehensive management approach combining etiological and symptomatic therapies, along with lifestyle modification and blood pressure control, is essential to improve the long-term prognosis of patients with IgA nephropathy.