Objective To develop and validate a predictive model for the transition to hemodialysis (HD) or death within 30 days in peritoneal dialysis (PD) patients with peritoneal dialysis-associated peritonitis (PDAP). Methods This study was a retrospective analysis of a single-center prospective cohort. Clinical data from patients who experienced their first episode of PDAP during follow-up at the peritoneal dialysis center of Peking University First Hospital between January 1, 2008, and December 31, 2021 were collected and analyzed. The study population was randomly divided into a training set and a validation set at a ratio of 7:3. Univariate and multivariate logistic regression analysis were performed in the training set to identify potential predictors, and a predictive model was constructed using logistic regression, followed by the development of a nomogram. The area under the receiver operating characteristic curve (AUC) was calculated, and the calibration curves were generated. The Hosmer-Lemeshow test was conducted to assess model performance. Results A total of 528 patients were enrolled in the study and randomly divided into a training set (n=369) and a validation set (n=159). In the training set, 78 patients (21.1%) experienced transition to hemodialysis or death within one month after peritonitis, versus 26 patients (16.4%) in the validation set. A basic model was constructed based on the available general clinical characteristics before the occurrence of PDAP, and an extended model was further developed by incorporating peritonitis-related information into the basic model. After variable selection, the variables of basic model included serum albumin and dialysis vintage; the variables of extended model included serum albumin, dialysis vintage, and pathogenic microorganisms. In the training set, AUCs for the basic and extended models were 0.657 [95% confidence interval (CI)0.583-0.731] and 0.735 (95% CI 0.670-0.800), respectively; in the validation set, the corresponding AUCs were 0.638 (95% CI 0.518-0.758) and 0.766 (95% CI 0.659-0.874), respectively. Based on data from both the training and validation sets, calibration curves for the two models demonstrated good agreement between predicted and observed outcomes. The Hosmer-Lemeshow test indicated good model fit for both models [in training set: basic model, χ2=9.563, degree of freedom (df)=8, P=0.297; extended model, χ2=2.701, df=8, P=0.952; in validation set: basic model, χ2=7.884, df=8, P=0.445; extended model, χ2=1.538, df=8, P=0.992]. Conclusions The basic and the extended prediction models can be applied to identify high-risk individuals at different stages: the basic model upon peritonitis diagnosis, and the extended model after the causative microorganism is identified. The nomograms derived from these two models may aid clinicians in tailoring treatment strategies and evaluating prognosis.

Objective To investigate the association between iron metabolism disorders and development of osteoporosis in maintenance hemodialysis (MHD) patients. Methods It was a cross-sectional study. The MHD patients treated at the blood purification center of Hainan Provincial People's Hospital in September 2024 were collected. Patients were divided into osteoporosis and non-osteoporosis groups based on osteoporosis status. Demographic information and laboratory examination data were collected. Dual-energy X-ray absorptiometry was used to measure the bone mineral density. Multivariate logistic regression analysis was performed to identify risk factors for osteoporosis in MHD patients. Results A total of 222 MHD patients were enrolled. The age was (54.17±13.22) years old. Among them, 124 (55.9%) patients were males, and 84 (37.8%) patients had osteoporosis. The age (t=-2.543, P=0.012), female (χ²=24.939, P<0.001), proportion of fragility fracture (χ²=5.099, P=0.024), and proportion of iron overload (χ²=4.102, P=0.043) of the osteoporosis group were all higher than those of the non-osteoporosis group, and the body mass index (Z=2.932, P=0.003), blood phosphorus (t=2.715, P=0.007) and serum albumin (t=2.402, P=0.017) were lower than those of the non-osteoporosis group. Multivariate logistic regression analysis identified that female (OR=5.856, 95% CI 2.911-11.781, P<0.001), age (OR=1.037,95% CI 1.009-1.066, P=0.010), body mass index < 18.5 kg/m²(≥24.0 kg/m² as a reference, OR=5.849, 95% CI 1.586-21.564, P=0.008), serum phosphorus (OR=0.494, 95% CI 0.264-0.925, P=0.028), serum iron (OR=1.250, 95% CI 1.028-1.518, P=0.025), and transferrin saturation (OR=1.105, 95% CI 1.019- 1.198, P=0.015) were the independent correlated factors of osteoporosis in MHD patients. There was no association between systemic inflammatory markers and osteoporosis (all P>0.05). Conclusions Female, increased age, low body mass index, low blood phosphorus, and iron metabolism disorders are the independent associated factors for osteoporosis in MHD patients. Clinical interventions targeting iron metabolism may reduce the risk of osteoporosis in MHD patients.

Objective To compare the safety and efficacy of calcium-containing replacement fluid and calcium-free replacement fluid in an citrate anticoagulation system for continuous renal replacement therapy (CRRT) patients. Methods This was a single-center, randomized controlled trial that included patients who received CRRT at West China Hospital, Sichuan University, from June 2021 to June 2023. All patients underwent CRRT using an integrated citrate anticoagulation system and were randomized via a computer-generated sequence to be assigned to either a calcium-containing or a calcium-free replacement fluid group. General patient data and CRRT-related parameters were collected. The primary endpoint was the lifespan of the extracorporeal circuit, which was evaluated using Kaplan-Meier survival analysis. Secondary endpoints included CRRT-related parameters, hospital mortality rate, kidney function recovery rate, and complications. Results A total of 60 patients were randomly assigned, and 57 patients were finally included, with 29 (50.9%) in the calcium-containing replacement fluid group and 28 (49.1%) in the calcium-free replacement fluid group, comprising 109 sets of extracorporeal circuits (58 sets in the calcium-containing replacement fluid group and 51 sets in the calcium-free replacement fluid group). The median circuit lifespans were 52.25 (23.75, 72.00) hours in the calcium-containing replacement fluid group and 45.00 (24.00, 72.00) hours in the calcium-free replacement fluid group, with no statistically significant difference (Z=0.107, P=0.744). Kaplan-Meier survival analysis results indicated that there was no statistically significant difference in the survival rate of the extracorporeal circulation circuits between the two groups (Log-rank test, χ²=0.093, P=0.760). There were no significant differences between the calcium-containing replacement fluid group and the calcium-free replacement fluid group in sodium citrate infusion rate [179.00(171.66, 191.25) ml/h vs. 182.00(178.25, 192.00) ml/h, Z=0.685, P=0.737], pre-filter ionized calcium level [(1.02±0.11) mmol/L vs. (1.02±0.13) mmol/L, t=0.029, P=0.977], or post-filter ionized calcium level [(0.29±0.05) mmol/L vs. (0.26±0.07) mmol/L, t=1.945, P=0.055]. However, the calcium supplementation rate in the calcium-containing replacement fluid group was significantly lower than that in the calcium-free replacement fluid group, and the difference was statistically significant [4.00 (0, 9.19) ml/h vs. 30.50 (6.82, 41.00) ml/h, Z=2.830, P<0.001]. No statistically significant differences were found between the two groups in in-hospital mortality or renal function recovery rate (P>0.05). There was no statistically significant difference in the occurrence of hyponatremia and citrate accumulation between the calcium-containing replacement fluid group and the calcium-free replacement fluid group [1 episode (1.72%) vs. 2 episodes (3.92%), P=0.249; 2 episodes (3.45%) vs. 5 episodes (9.80%), P=0.598]. No other serious complications occurred in either group. Conclusions In the integrated citrate anticoagulation system for CRRT, the use of calcium- containing replacement fluid may be a safe and feasible alternative. Compared to calcium-free replacement fluid, calcium-containing replacement fluid can reduce the need for calcium supplementation and simplify clinical operations. However, due to the limitations of the single- center design and sample size, further large-scale, multicenter studies are required to verify the long-term safety and clinical application value.

Objective To evaluate the clinical efficacy of intraoperative transluminal angioplasty (ITA) performed simultaneously with autogenous arteriovenous fistula (AVF) creation in patients with small-diameter radial arteries. Methods This prospective interventional study enrolled stage 5 chronic kidney disease patients who were scheduled for forearm AVF creation at Haidian Hospital of Peking University Third Hospital between March 1, 2022, and February 28, 2023, and the inner diameter of the radial artery was less than 1.5 mm. All patients underwent radial artery ITA during AVF creation. Regular follow-up was conducted to assess AVF maturation at 4, 8, and 12 weeks, and AVF patency at 6 and 12 months. Results A total of 26 patients were included, all of whom successfully underwent AVF creation combined with radial artery ITA. Postoperative radial artery spasm occurred in 8 patients. One patient experienced loss of AVF bruit within 0.5 hours after surgery, which resolved after local manual massage. The overall technical success rate was 96.2% [25/26, 95% (confidence interval,CI) 80.4%-99.9%]. No patients experienced complications such as radial artery rupture or dissection. The proportion of patients achieving AVF maturation at 4, 8, and 12 weeks were 30.8% (8/26, 95% CI 14.3%-51.8%), 50.0% (13/26, 95% CI 29.9%-70.1%), and 92.3% (24/26, 95% CI 74.9%-99.1%), respectively. The median time to AVF maturation was 8.00 (4.00, 12.00) weeks. The primary patency rate at 6 months was 69.2% (18/26, 95% CI 48.2%-85.7%), and the secondary patency rate at 12 months was 92.3% (24/26, 95% CI 74.9%-99.1%). Conclusions Performing radial artery ITA simultaneously with AVF creation in patients with small-diameter radial arteries is feasible and safe, with favorable AVF maturation and long-term patency outcomes. This combined approach offers a viable option for establishing AVF in end-stage renal disease patients whose arterial diameter would otherwise be considered insufficient.

Objective To analyze the clinical characteristics and prognosis of IgA vasculitis-associated nephritis (IgAVN) patients presenting as nephrotic syndrome (NS) and compare it with IgA nephropathy (IgAN) to enhance the understanding of IgAVN. Methods It was a single-center retrospective study. The patients aged ≥14 years old diagnosed with IgAVN or IgAN and met the clinical criteria of NS at nephrology department of Peking Union Medical College Hospital between January 2001 and March 2022 were collected. The follow-up period was more than 6 months. The clinical and pathological data of the patients were collected. For patients who underwent renal biopsy after 2010, the proportion of sclerotic glomeruli and interstitial fibrosis in renal pathology were measured. The extrarenal characteristics and prognosis in IgAVN patients with NS were analyzed, and the short-term prognosis and potential risk factors between IgAN and IgAVN groups were compared. Results A total of 36 patients with IgAVN and 76 patients with IgAN were included in this study. The patients in the IgAVN group were younger than that in the IgAN group when renal biopsy was performed [23.00 (16.00, 43.00) years vs. 33.50 (27.75, 42.25) years, Z=-2.425, P=0.015]. Baseline serum creatinine [80.00 (60.94, 108.00) μmol/L vs. 113.50 (85.75, 159.25) μmol/L, Z=-3.564, P<0.001] and proportion of renin-angiotensin system inhibitors use (47.22% vs. 67.11%, χ2=4.049, P=0.044) were lower, and estimated glomerular filtration rate was higher [(110.08±93.42) ml·min^-1·(1.73 m²)^-1vs. (65.20±29.44) ml·min^-1·(1.73 m²)^-1, t=2.779, P=0.009] in the IgAVN group than those in the IgAN group. There were no statistical differences between the two groups in terms of gender distribution, disease duration, baseline blood pressure, urinary sediment red blood cell count, 24-hour urinary protein excretion, serum albumin, IgA and IgG levels (all P>0.05). Two patients did not receive immunosuppressive therapy, 4 patients received glucocorticoids only, and 30 patients received glucocorticoids combined with immunosuppressive agents (cyclophosphamide, mycophenolate mofetil, or cyclosporine) in the IgAVN group. Seven patients received monotherapy glucocorticoids and 69 patients received combination therapy in the IgAVN group. There was no statistical difference in the proportion of patients receiving glucocorticoids combined with immunosuppressive agents between the two groups (83.33% vs. 90.79%, χ2=0.697, P=0.404). Six months after discharge, the estimated glomerular filtration rate decline was more significant in the IgAVN group than that in the IgAN group [-8.76%(-25.45% ,1.74%) vs. 3.29%(-10.95%, 19.42%), Z=-2.982, P=0.003]. The multivariate linear regression analysis showed that the improvement rate of eGFR=-0.091+0.005×age (years)-0.196×disease classification (where disease classification was a binary variable, including IgAVN and IgAN, with IgAN as the reference), and the results indicated that IgAVN was correlated with the improvement rate of eGFR (t=-2.499, P=0.014). Further analysis of renal pathology in some patients revealed that IgAN group had higher level of baseline interstitial fibrosis than that in the IgAVN group [8.42%(4.68%, 18.70%) vs. 19.64% (7.47%, 37.23%), Z=-2.295, P=0.022]. Conclusions IgAVN patients presenting as NS achieve a comparable level of urinary protein to those with IgAN. However, the short-term decline of estimated glomerular filtration rate in the IgAVN group is significantly more pronounced than that in the IgAN group.

Objective To explore the protective effect of time-restricted fasting (TRF) on the kidneys of diabetic kidney disease (DKD). Methods Twelve 8-week-old male C57BL/6J mice were adaptively fed for 1 week, and then fed with the high-fat diet for 8 weeks. The mice were intraperitoneally injected with streptozotocin (50 mg/kg) for 5 days. After 2 weeks, if random blood glucose level was more than 16.7 mmol/L, it was considered that type 2 diabetes mellitus models had been successfully established. After an additional 8 weeks of feeding, urinary protein was presented, confirming the successful establishment of the DKD model. DKD mice were randomly divided into non-fasting group (DKD group) and fasting group (DKD TRF group), with 4 h feeding, 20 h fasting per day. Six mice were in each group, and continuously treated for 4 weeks. Body weight and blood glucose were monitored weekly, and blood and urine samples were collected to assess kidney function and blood lipid levels. Visceral fat and kidney tissues were collected and weighed after the mice were sacrificed. PAS staining, sirius red staining, and oil red O staining were used to observe the pathological changes in kidney tissues. Immunofluorescence was performed to analyze the expression levels of podocyte markers, kidney tubular injury markers, adipose differentiation-related protein, inflammatory cytokines, apoptosis-related molecules, and fibrosis markers. Results Compared with the DKD group, the DKD TRF group showed significant reductions in kidney weight, visceral fat mass, serum creatinine, blood urea nitrogen, urine protein quantity, triglyceride, total cholesterol, and low-density lipoprotein levels (all P<0.05). Oil red O staining and immunofluorescence revealed significantly reduced ectopic fat deposition of renal tissues in the DKD TRF group than that in the DKD group (both P<0.05). PAS staining showed reduced glomerular area and mesangial expansion in the DKD TRF group than those in the DKD group (both P<0.05). Immunofluorescence analysis showed higher positive area percentages of Wilms' tumor 1 and higher fluorescence intensity of podocin, while kidney injury molecule-1, neutrophil gelatinase-associated lipocalin, interleukin-6, tumor necrosis factor-α, caspase-3, α- smooth muscle actin, and collagen type I α1 had significantly reduced fluorescent areas in the DKD TRF group than those in the DKD group (all P<0.05). Sirius Red staining showed a decrease in the kidney fibrosis-positive area in the DKD TRF group than that in the DKD group (P<0.05). Conclusions TRF can reduce the kidney weight, visceral fat mass and blood lipid levels in DKD mice, and improve renal pathological damage and renal function, providing experimental evidence for the treatment of DKD.

Trimethyltin chloride (TMT), an organotin compound used as a heat stabilizer in plastics, can cause life-threatening poisoning if ingested excessively. This case report describes a 58-year-old woman who presented with fatigue, headache, convulsion, impaired consciousness, memory deficits, metabolic acidosis, severe hypokalemia, paradoxical alkaline urine, and a normal anion gap. Urinary TMT testing was positive, confirming a diagnosis of severe renal tubular acidosis due to acute TMT poisoning. Following treatment with potassium supplementation, acidosis correction, and supportive care, her symptoms improved. At a two-month follow-up, her serum potassium had normalized. Given that TMT poisoning typically presents with predominant neurological symptoms, often leading to initial neurological consultation, and rarely manifests primarily as renal tubular acidosis, this case aids in enhancing clinicians' awareness of TMT poisoning.

The patient was an elderly female who presented with proteinuria, with history of hypertension and diabetes mellitus. On admission, urine protein quantification was 0.96 g/24 h, serum albumin 36.9 g/L, serum creatinine 73.1 μmol/L, estimated glomerular filtration rate (eGFR) 77.8 ml·min^-1·(1.73 m²)^-1. Under light microscopy, there was deposition of pink, homogeneous, structureless material within the glomerular mesangium and renal interstitium. Immunofluorescence examination revealed deposition of IgG, kappa, and lambda along the capillary loops, and IgA deposition in the mesangial area.Anti-M-type phospholipase A2 receptor (PLA2R) antibody was positive. Congo red staining was positive, with characteristic apple- green birefringence observed under polarized light. Immunohistochemistry demonstrated positive staining for leukocyte chemotactic factor 2 (LECT2) protein in segmental glomeruli and renal interstitium. Mass spectrometry analysis identified LECT2 protein in the renal interstitium and PLA2R protein in the glomerular region. Final clinical diagnosis was LECT2-associated renal amyloidosis with stage Ⅱ membranous nephropathy (PLA2R-mediated) and IgA nephropathy. Literature review indicates this is the first reported case of LECT2-associated renal amyloidosis with PLA2R-mediated membranous nephropathy and IgA nephropathy. By reporting this case and reviewing the pathogenesis, clinical-pathological manifestations, and prognosis of such cases, clinicians' awareness of the disease may be raised.

Polyamines represent a class of cationic compounds that are widely distributed among organisms and participate in a diverse array of life activities. In recent years, there has been a growing number of studies that have focused on the significant role of maintaining polyamine homeostasis in the pathogenesis and intervention of autoimmune-related diseases. Systemic lupus erythematosus (SLE) is a common group of autoimmune diseases, with lupus nephritis (LN) representing the most common and severe form of target organ damage observed in SLE. This review summarizes the emerging role of polyamine metabolism in SLE or LN. Highlighting the biphasic regulatory effects of polyamine concentration changes, it explores the association of polyamine dysregulation with aberrant T and B cell activation, excessive interferon signaling, and autophagy dysfunction, with a view to informing novel preventative and therapeutic strategies for this challenging disease.

IgA nephropathy (IgAN) is the most common primary glomerular disease worldwide, with high heterogeneity and the risk of progression to end-stage kidney disease. To improve clinicians' diagnosis and treatment of IgAN, Clinical practice guidelines working group organized national nephrologists to revise and compile this article through several rounds of discussion on 60 common questions in clinical practice of IgAN. The content covered epidemiological features, pathogenesis, clinical manifestations, diagnostic approaches, therapeutic strategies, and prognostic evaluation of IgAN, with particular emphasis on the clinical application of targeted-release formulation of budesonide—the first targeted etiological treatment, marking a new era in IgAN management. Additionally, comprehensive discussions were provided on management strategies for IgAN patients in various clinical scenarios, such as blood pressure management, treatment of special populations, and post-transplant recurrence. This article aims to offer practical and standardized clinical guidance to optimize the precise treatment of IgAN and improve patients' prognosis.

Objective To compare the safety and efficacy of erythropoietin (EPO) and roxadustat in the treatment of anemia in patients with chronic kidney disease (CKD) during the peri-dialysis period, providing a reference for clinical practice. Methods This was a multicenter retrospective cohort study. Clinical data of peri-dialysis patients with CKD stage 5 and anemia treated with EPO or roxadustat between January 1, 2015, and December 31, 2021, were collected from 82 hospitals (42 tertiary and 40 secondary hospitals) on the health medical big data platform of Tianjin. Patients were divided into EPO group and roxadustat group based on their treatment regimens. After propensity score matching was performed at a 1:4 ratio between the two groups and baseline characteristics were compared. The incidence rates of cardio-cerebrovascular events, thrombotic events, major adverse cardiovascular events (MACE), and hospitalization rate due to complications, as well as the length of hospital stay, were compared between the two groups during different time periods (within 6 and 12 months of initial treatment, within 3 months after the initiation of dialysis, and within 12 months after the peri-dialysis period). Kaplan-Meier method was used to analyze the cumulative event-free rates of cardiovascular and cerebrovascular events as well as thrombotic events between the two groups. Changes of hemoglobin (Hb) levels from baseline during the 3-month treatment period were recorded. Results A total of 35 324 peri-dialysis patients with CKD stage 5 and anemia were included, comprising 6 017 patients in the EPO group and 548 patients in the roxadustat group. After propensity score matching, 545 patients were included in the roxadustat group and 1 804 in the EPO group. There were no statistically significant differences in baseline characteristics between the two groups (all P>0.05). The incidence of cardio-cerebrovascular events [83.7% (456/545) vs. 66.9% (1 206/1 804), χ2=57.213, P<0.001; 87.9% (479/545) vs. 76.9% (1 388/1 804), χ2=30.771, P<0.001; 71.7% (391/545) vs. 54.4% (982/1 804), χ2=51.632, P<0.001], MACE [52.7% (287/545) vs. 29.8% (538/1 804), χ2=95.806, P<0.001; 62.8% (342/545) vs. 40.7% (735/1 804), χ2=81.665, P<0.001; 42.4% (231/545) vs. 20.5% (370/1 804), χ2=105.200, P<0.001], and the rate of hospitalizations due to complications [70.6% (385/545) vs. 53.9% (972/1 804), χ2=48.203, P<0.001; 75.8% (413/545) vs. 63.0% (1 137/1 804), χ2=30.330, P<0.001; 60.2% (328/545) vs. 44.8% (808/1 804), χ2=39.718, P<0.001] were significantly higher in the roxadustat group than in the EPO group within the first 6 months and 12 months of treatment, and within 3 months after the first dialysis. However, there were no statistically significant differences observed in these outcomes between the two groups within 12 months of follow-up after the peri-dialysis period (all P>0.05). The incidences of cardiovascular and cerebrovascular events (log-rank test, χ2=84.243, P<0.001) and thrombotic events (log-rank test, χ2=7.123, P=0.008) in the roxadustat group were both lower than those in the EPO group. The change of average Hb levels in the EPO group was higher than that in the roxadustat group of the first month of treatment [5.00 (-3.70,14.70) g/L vs 1.00 (-8.30,9.00) g/L, Z=-3.700, P<0.001], but lower than that in the roxadustat group in the second month [8.20 (0, 18.00) g/L vs. 10.50 (2.50, 20.70) g/L, Z=2.807, P=0.005]; there was no statistically significant difference in average Hb change between the two groups in the third month (Z=0.972, P=0.331). The proportion of patients maintaining average Hb concentrations within the target range after 3 months of continuous administration in the EPO group was higher compared to the roxadustat group [10.9% (197/1 804) vs. 7.5% (41/545), χ2=5.305, P=0.021]. Conclusion For patients with CKD stage 5 and anemia during the peri-dialysis period, EPO demonstrates superior cardiovascular safety profile compared to roxadustat and is more effective in improving Hb level in the short term.

Objective To evaluate the short-term efficacy of sucroferric oxyhydroxide in treating hyperphosphatemia in patients with end-stage renal disease. Methods A self-controlled before-and-after study was performed. The clinical data of patients with end-stage renal disease complicated with hyperphosphatemia who received regular treatment and follow-up at the First Affiliated Hospital of Ningbo University and used sucroferric oxyhydroxide for phosphorus reduction treatment from May to August 2024 were retrospectively analyzed. Based on the quartiles of the initial serum phosphorus levels, patients were divided into 4 groups: 1.78-<1.91 mmol/L group (n=15), 1.91-<2.11 mmol/L group (n=15), 2.11-<2.35 mmol/L group (n=16), and ≥2.35 mmol/L group (n=15). The decrease in serum phosphorus levels before and after treatment in each group and the differences in the extent of decrease among the 4 groups were compared. The correlation between the degree of decrease in blood phosphorus and the pre-medication venous blood phosphorus level was analyzed using Pearson correlation analysis. Results A total of 61 patients were included, and the age was (51.89±12.29) years old. Among them, 40 patients were males (65.6%). There were 20 patients (32.8%) on maintenance hemodialysis, 39 patients (63.9%) on peritoneal dialysis, and 2 patients (3.3%) on combined dialysis. After one month of administration, the venous phosphorus level decreased from (2.19±0.37) mmol/L to (1.72±0.57) mmol/L (t=5.925, P<0.001). Meanwhile, the calcium-phosphorus product decreased from (61.87±12.34) mg²/dl² to (51.01±17.15) mg²/dl² (t=4.370, P<0.001). After one month of medication, 33 patients achieved the target blood phosphorus level, with an achievement rate of 54.1%. The reductions in serum phosphorus were (0.11±0.59) mmol/L in the 1.78-<1.91 mmol/L group, (0.32±0.54) mmol/L in the 1.91-<2.11 mmol/L group, (0.54±0.35) mmol/L in the 2.11-<2.35 mmol/L group, and (0.89±0.70) mmol/L in the ≥2.35 mmol/L group. A statistically significant difference was observed in the reduction of serum phosphorus among the 4 groups (F=5.343, P=0.003). Pearson correlation analysis revealed a positive correlation between the degree of decrease in serum phosphorus at one month of medication and the pre-medication venous blood phosphorus level (r=0.417, P=0.001). Conclusion Sucroferric oxyhydroxide effectively reduces serum phosphorus and calcium-phosphorus product in patients with end-stage renal disease and hyperphosphatemia within one month.

Objective To compare the differences in complications between 4-6 mm tapered arteriovenous graft (AVG) and 6 mm standard AVG and evaluate the patency rates of the two types of AVG. Methods This study was a single-center retrospective cohort study. The relevant data of patients who underwent upper arm AVG surgery in the Department of Nephrology, Beijing Haidian Hospital from January 2017 to July 2018 were analyzed. According to the type of graft, the patients were divided into 4 to 6 mm-tapered grafts (4-6 mm group) and 6 mm-standard grafts (6 mm group). The occurrence of hemodialysis access-induced distal ischemia (HAIDI), high-output heart failure, and access-related complications was recorded. Kaplan-Meier survival curve analysis was performed to analyze the patency rates of AVG in the two groups. Results A total of 116 patients were enrolled in this study, with 59 patients (50.9%) in the 4-6 mm group and 57 patients (49.1%) in the 6 mm group. There was no statistically significant difference in the baseline data, preoperative and postoperative 6-month and 12-month vascular ultrasound indicators between the two groups (all P>0.05). Three patients experienced fistula thrombosis within 30 days after the operation, including one in the 4-6 mm group and two in the 6 mm group. Two patients developed infections during the 6-month to 1-year follow-up period after surgery, both in the 6 mm group. One patient in the 4-6 mm group developed HAIDI and improved after conservative drug treatment. None of the patients in either group developed high-output heart failure. Kaplan-Meier survival analysis showed that the primary patency rates of patients in the 4-6 mm group at 1 (37.9% vs. 56.4%, log-rank test, χ²=3.996, P=0.046) and 2 (17.2% vs. 33.5%, log-rank test, χ²=5.193, P=0.023) years after surgery were significantly lower than those in the 6 mm group. There was no statistically significant difference in the primary patency rates of the two groups at 3 and 5 years after surgery (all P>0.05). After 1, 2, 3 and 5 years of the operation, there was no statistically significant difference in the secondary patency rates between the two groups (all P>0.05). Conclusions Compared with the 6 mm standard AVG, 4-6 mm tapered AVG does not reduce the risk of HAIDI, nor does it improve the patency rates. Therefore, tapered grafts are not recommended for routine use.

Objective To explore the related factors for the early occurrence of acute kidney disease (AKD) in patients with idiopathic membranous nephropathy (IMN) and to establish a scoring prediction system. Methods It was a retrospective cohort study. The clinical data were collected from patients diagnosed with IMN through renal biopsy and undergoing regular follow-up ≥3 months at the Nephrology Department of Beijing Anzhen Hospital, Capital Medical University from January 2010 to March 2023. Based on whether AKD occurred within 3 months after diagnosis, the patients were divided into AKD group and non-AKD group. The clinical, pathological, treatment, and prognosis were compared between the two groups. Multivariate logistic regression analysis was used to identify influencing factors of AKD. Based on the odds ratios (OR) of the independent correlated factors and clinical considerations, each factor was assigned a score to develop a risk scoring system. Receiver operating characteristic curve was used to evaluate the calibration ability of this risk scoring system. The Hosmer-Lemeshow goodness-of-fit test was used to evaluate the calibration ability of this risk scoring system. Results A total of 372 patients with IMN were included in this study, with age of (52.4±14.1) years, including 151 females (40.6%). Among the 372 patients, 63 patients (16.9%) were in the AKD group and 309 patients (83.1%) were in the non-AKD group. Compared with the non-AKD group, the AKD group had older age (Z=4.709, P<0.001), and higher proportion of females (χ²=5.628, P=0.018), proportion of hypertension (χ²=13.608, P<0.001), proportion of anemia (χ²=22.344, P<0.001), serum anti-phospholipase A2 receptor antibody titer (Z=2.781, P=0.005), proportion of diuretic use (χ²=11.631, P=0.001), proportion of ischemic glomeruli (t=3.839, P=0.001), proportion of sclerotic glomeruli (t=3.958, P<0.001), and proportion of complement C3 positivity in renal tissues (χ²=11.341, P=0.001). Additionally, serum albumin (Z=-3.553, P<0.001), dosage of used cyclosporine (t=-3.060, P=0.002) and estimated glomerular filtration rate (eGFR, Z=-3.842, P<0.001) in the AKD group were lower than those in the non-AKD group. Multivariate logistic regression analysis showed that, after adjusting for eGFR, serum anti-phospholipase A2 receptor antibody titer, use of diuretics, and the proportion of ischemic glomeruli, females [OR=0.375, 95% confidence interval (CI) 0.187-0.750, P=0.006], increase age (OR=1.352, 95% CI 0.999-1.830, P=0.050), hypertension (OR=2.661, 95% CI 1.091-6.489, P=0.031), decreased serum albumin (<30 g/L, OR=0.650, 95% CI 0.406-0.901, P=0.013), anemia (OR=2.050, 95% CI 1.059-3.970, P=0.033), and complement C3 positivity of renal tissues (OR=2.793, 95% CI 0.998-7.818, P=0.050) were independent factors correlated with AKD in IMN patients. Based on these correlated factors, a risk scoring system was established for AKD in IMN patients. The area under the receiver operating characteristic curve was 0.787 (95% CI 0.730-0.844), indicating good discriminative ability. The Hosmer-Lemeshow goodness-of-fit test demonstrated good calibration ability (χ² =7.752, P=0.458). The risk of AKD for IMN patients with low-risk (≤8 points), moderate-risk (9-14 points), and high-risk (≥15 points) was 5.9%, 24.9%, and 63.5%, respectively, based on the established risk scoring system. In terms of prognosis, there was no statistically significant difference in the 6-month disease remission rate between AKD and non-AKD groups (χ²=1.931, P=0.165). However, the proportion of eGFR decline ≥ 30% at 1 year in the AKD group was higher than that in the non-AKD group (χ²=27.481, P<0.001), and both AKD group with short-term renal function recovery and AKD group without short-term renal function recovery had higher proportions of eGFR decline ≥ 30% at 1 year than that of the non-AKD group (all P<0.05). Conclusions IMN patients with AKD in the early stage have poorer long-term renal outcomes. Females, increasing age, hypertension, hypoalbuminemia, anemia, and positive complement C3 in renal tissues are independent related factors for the occurrence of AKD in IMN patients. The established risk scoring system may assist clinicians in identifying high-risk AKD patients early and implementing preventive interventions may help improve long-term renal prognosis.

Objective To discuss the effect of methyltransferase- like 3 (METTL3) on vascular calcification in chronic kidney disease (CKD) rats by regulating histone deacetylase 1 (HDAC1). Methods Thirty-six healthy male SD rats aged 7?8 weeks were randomly divided into control group, CKD model group (CKD group) and METTL3 inhibitor group (SAH group) by random sampling method. Except for the control group, all other groups were constructed with CKD rat models. The rats in the control group were fed with normal chow, while the rats in the CKD group and the SAH group were given 250 mg/kg of adenine by gavage and fed with a high-phosphorus diet containing 1.8% phosphorus for 4 consecutive weeks. From the 5th to 8th week, adenine was administered by gavage every other day. During the 5th to 8th weeks of the model establishment, rats in the SAH group were intraperitoneally injected with 5 mg/kg SAH twice a week, while rats in the control group and the CKD group were intraperitoneally injected with the same volume of 0.9% sodium chloride solution. Fully automated biochemical analyzer was used to measure serum creatinine (Scr), blood urea nitrogen (BUN), serum calcium and serum phosphorus. HE staining was used to observe pathological changes in renal tissues and thoracic aortic tissues. Von Kossa staining was performed to observe the calcification status of the thoracic aorta. Immunohistochemistry was performed to measure the protein expression levels of bone morphogenetic protein 2 (BMP2) and runt-related transcription factor 2 (Runx2) in the thoracic aorta. Western blotting was used to measure the protein expression levels of METTL3, HDAC1, light chain 3 protein (LC3Ⅱ), and p62 in the thoracic aorta. Colorimetric method was used to detect the level of m6A methylation of total RNA. Results Compared with the control group, the structure of the renal tissues in the CKD group was damaged with clear enlargement of renal tubular lumens, extensive proliferation of renal interstitial fibroblasts, and clear infiltration of inflammatory cells (all P<0.05). Compared with the control group, a large amount of black adenine metabolites were deposited, the aortic vascular structure was severely damaged with obvious calcified nodules, and the middle layer of the aortic vascular tissue showed large areas of black or brownish black color, with severe calcification in the CKD group. The serum calcium level, and the protein expression levels of HDAC1 and LC3Ⅱ were lower, while serum phosphorus, Scr, BUN and m6A methylation levels, and the protein expression levels of BMP2, Runx2, METTL3 and p62 were higher in the CKD group than those in the control group (all P<0.05). The SAH group showed less pathological damage of renal tissues compared to the CKD group, with a relatively normal structure and reduced adenine crystals. The pathological damage of aortic vascular tissues was also reduced, with a relatively normal structure and fewer calcified nodules in SAH group. Compared with the CKD group, the black or brownish black color of aortic vascular tissues was decreased, and the degree of calcification was reduced in SAH group. Compared with the CKD group, the serum calcium level, and the protein expression levels of HDAC1 and LC3Ⅱ were raised, while serum phosphorus, Scr, BUN and m6A methylation levels, and the protein expression levels of BMP2, Runx2, METTL3 and p62 were reduced in SAH group (all P<0.05). Conclusion Inhibition of METTL3 can alleviate vascular calcification by inhibiting m6A methylation modification of HDAC1 in CKD rats.

This article reports a case of exercise-related acute kidney injury without renal hypouricemia. The patient was a 20-year-old male who experienced abdominal pain following a 1 000-meter sprint, accompanied by muscle soreness in the lower limbs. There was no decrease in urine output or presence of brown urine. However, the patient exhibited mild proteinuria, no microscopic hematuria, markedly elevated serum creatinine, hyperuricemia and mildly elevated creatine kinase. Renal biopsy indicated acute tubular interstitial injury. Renal function recovered after treatment with glucocorticoids, hydration, uric acid reduction, and blood pressure control. Further testing demonstrated a normal uric acid excretion fraction, and genetic testing did not identify any mutations associated with renal hypouricemia genes. Based on the clinical and pathological findings, the patient was diagnosed without renal hypouricemia-induced acute renal failure with severe loin pain and patchy renal ischemia after anaerobic exercise. By reporting this rare case, we aim to enhance clinicians' awareness of the diagnosis and treatment of this disease.

This article reports the diagnosis and treatment of interstitial lung disease (ILD) in a 42-year-old male patient with phospholipase A2 receptor antibody-positive membranous nephropathy following rituximab therapy. The patient received intensive treatment with a single 1 g dose of rituximab for his primary renal condition. Two days later, he developed a perianal abscess, which was resolved after surgical drainage. Ten days post-rituximab infusion, he presented with cough and productive sputum. A chest CT scan revealed newly developed multiple patchy opacities in both lungs, accompanied by pleural effusion. Despite treatment with broad-spectrum antibiotics (meropenem) and antiviral therapy (ganciclovir), his pulmonary infiltrates showed no improvement. Extensive investigations, including pathogen metagenomic next-generation sequencing of bronchoalveolar lavage fluid, identified no definite infectious etiology. Based on the temporal relationship to drug administration and after excluding alternative causes, a diagnosis of rituximab-induced ILD (RTX-ILD) was established. Rituximab was discontinued, and the immunosuppressive regimen was switched to intravenous methylprednisolone (40 mg daily). After one week of glucocorticoid therapy, the patient's respiratory symptoms and radiological findings significantly improved. This case highlights that RTX-ILD should be suspected in patients receiving rituximab who develop new pulmonary lesions refractory to broad-spectrum antibiotics. Early diagnosis, prompt withdrawal of rituximab, and timely initiation of corticosteroid therapy are crucial for improving clinical outcomes.

This case report describes the development of Kaposi sarcoma (KS) in a patient with membranous nephropathy (MN) following immunosuppressive therapy. A 58-year-old man was admitted with a 1-year history of intermittent edema of bilateral lower extremities, and MN was confirmed via renal biopsy. Five months after treatment with glucocorticoids and cyclophosphamide, the patient developed cutaneous lesions on the medial side of the left lower extremity and foot. Skin biopsy results indicated a vascular endothelial-derived tumor, with immunohistochemical positivity for CD31, CD34, ETS-related gene, friend leukemia integration 1 transcription factor and human herpes virus-8, which supported the diagnosis of KS. Based on patient' immunosuppressive medication history, iatrogenic KS was considered. Notably, the lesions showed no clinical remission despite reduction in immunosuppressive therapy intensity, and the patient eventually died of disease progression. By reviewing and summarizing the clinical manifestations and outcomes of relevant cases of glomerular diseases complicated with KS, this case report aims to improve clinicians' awareness of the diagnosis and management of KS complicating MN.

Vacuole, ubiquitin-activating enzyme (E1), X-linked, autoinflammatory, somatic (VEXAS) syndrome is a newly recognized disease featured by somatic mutation of UBA1 gene. Patients present with late-onset inflammatory status and hematological abnormalities, while renal injuries are not commonly seen. This paper reports a 62-year-old male patient with VEXAS syndrome presenting with recurrent fever and anemia. He experienced a gradual onset of relapsing polyarthritis and acute kidney injury. Further laboratory tests showed elevation of serum C reactive protein, as well as erythrocyte sedimentation rate. Bone marrow smear showed vacuoles in myeloid precursor cells. Kidney biopsy showed tubulointerstitial nephritis. The genetic test revealed UBA1 mutation. The patient was diagnosed with VEXAS syndrome with tubulointerstitial nephritis, and received glucocorticoids and cyclophosphamide. Roxadustat was prescribed for anemia. His general condition, renal function as well as anemia significantly improved after treatment follow-up. The case contributes to enhancing clinician's awareness and understanding of VEXAS syndrome.

Autosomal dominant tubulointerstitial kidney disease (ADTKD) is a rare group of inherited tubulointerstitial kidney disorders. To date, pathogenic variants in at least 5 genes—UMOD, MUC1, REN, HNF1B, and SEC61A1—have been identified as associated ADTKD, with SEC61A1-related cases being extremely rare. This article reports the first confirmed case of ADTKD caused by a novel pathogenic variant in the SEC61A1 gene (ADTKD5), c.544T>C (p.F182L) in China. The patient was a young girl whose initial manifestations included congenital anemia and impaired renal tubular concentrating function, which were not initially recognized as significant. She later came to medical attention due to unexplained elevated serum creatinine accompanied by hyperuricemia. The diagnosis of ADTKD was confirmed by whole-exome sequencing. Recombinant human erythropoietin was administered subcutaneously to treat renal anemia, and febuxostat was prescribed orally for the management of hyperuricemia. This case can help to enhance awareness of ADTKD among clinicians, particularly pediatric nephrologists.

Atypical hemolytic uremic syndrome (aHUS) is a rare and severe thrombotic microangiopathy. This study retrospectively analyzed the clinical data of 15 adult aHUS patients treated with eculizumab, aiming to evaluate its therapeutic efficacy and investigate the impact of treatment timing on patient outcomes, prognosis, and safety, so as to provide evidence for optimizing the clinical management of aHUS. The cohort included 12 females and 3 males, who received 4 to 20 doses of eculizumab. The patient's age was (43.4±20.2) years old. At the last follow-up, serum creatinine and lactate dehydrogenase levels were significantly decreased compared to pre-treatment values, while estimated glomerular filtration rate, hemoglobin, and platelet counts were significantly increased. Hematological remission was achieved in 8 patients, and renal remission was achieved in 8 patients. Among the 9 patients who required dialysis at the onset of the disease, 3 patients were able to discontinue dialysis, 1 patient died of heart disease, and the rest progressed to chronic renal failure. The median time from the onset of aHUS to the initiation of eculizumab treatment was 7 (7, 30) days. The patients were divided into group 1 (≤7 d, n=8) and group 2 (>7 d, n=7) based on the median. At the last follow-up, the renal and hematological remission rates of patients in group 1 were significantly higher than those in group 2 (7/8 vs. 1/7, P=0.010; 8/8 vs. 0/7, P<0.001), and the proportion of patients without dialysis in group 1 was significantly higher than that in group 2 (8/8 vs. 2/7, P=0.007). The results indicate that eculizumab treatment can significantly improve hematological parameters and renal function in aHUS patients with a favorable safety profile. Furthermore, initiation of treatment within 7 days of disease onset is associated with a more pronounced therapeutic response.

Acute kidney injury (AKI) is a clinical syndrome characterized by high morbidity and mortality, yet effective treatment options remain limited. Sodium-glucose transporter 2 inhibitors (SGLT2i) have been extensively utilized in the management of chronic kidney disease. Although their pharmacological mechanisms may theoretically predispose people to AKI, a growing body of clinical studies and experimental evidences suggest that SGLT2i may confer protective effects against AKI through multiple pathways. However, the use of SGLT2i in the specific populations may elevate the risk of AKI. This review summarizes the dual roles of SGLT2i and the underlying mechanisms on AKI and discusses the potential applications and controversies in clinical practice, with the aim of providing new strategies for the prevention and treatment of AKI.

Antiplatelet drugs are widely used in the prevention and treatment of cardiovascular diseases in the general population. However, people with chronic kidney disease (CKD) face tendencies of thrombosis and bleeding, as well as significantly increasing risk of cardiovascular events. Owing to the lack of results of large-scale clinical randomized controlled trials, there is no definite conclusion on how to choose appropriate antiplatelet drugs to prevent cardiovascular complications, or how to balance the antiplatelet effects with bleeding risks. This article will overview the pathogenesis of cardiovascular complications in patients with CKD, the effects and mechanisms of commonly used antiplatelet drugs and their application in preventing cardiovascular complications, to better understand and prevent the cardiovascular complications of CKD and help improve the prognosis of patients.

Patients with end-stage renal disease undergoing peritoneal dialysis (PD) often experience multiple complications that require medication. The PD process can influence the pharmacokinetic characteristics of certain drugs, including absorption, distribution, metabolism and excretion, presenting challenges for clinical drug use. This paper summarizes the factors affecting pharmacokinetic characteristics in PD patients, including systemic conditions, dialysis-related variables, and drug-specific properties, and also examines the pharmacokinetics of antibiotics for PD-related peritonitis and medications for chronic kidney disease complications, along with clinical considerations for their use, aiming to provide a reference for guiding the clinical medication of PD patients and inform future research.

Perigraft seroma is a relatively rare complication after arteriovenous polytetrafluoroethylene graft implantation, and its exact etiology remains unclear. Currently, it is believed that the pathogenesis may be related to factors such as destruction of porosity, imbalance pressure of porosity, and poor connective tissue incorporated into the graft. Clinically, it often manifests as a non-pulsatile mass occurring at the arterial anastomosis, which may lead to thrombosis, loss of available puncture sites, secondary infection, skin erosion, etc. Simple excision of the seroma is associated with a high risk of recurrence; therefore, concurrent management of the involved segment of the prosthetic graft is required, including creating a new graft bypass, local application of medical adhesive or fibrin glue, or implantation of a covered stent. Delayed treatment of graft thrombosis to assist in the treatment of seroma may be a relatively ideal therapeutic approach. In addition, prevention of seroma is also critical.

Objective To compare the efficacy and safety of obinutuzumab with glucocorticoids combined with cyclophosphamide (CTX) in the treatment of primary membranous nephropathy (PMN). Methods This was a retrospective cohort study. Patients with PMN who received glucocorticoid combined with CTX or obinutuzumab therapy at Huashan Hospital Affiliated to Fudan University from January 2012 to July 2024 were enrolled. The primary endpoint was the overall remission rate, including complete remission (CR) and partial remission (PR). Patients were divided into the obinutuzumab group and glucocorticoid combined with CTX group according to the therapeutic regimen. The differences in overall remission rate and CR rate between the two groups at 3, 6 and 12 months after treatment were compared. Kaplan-Meier survival curve was used to compare the cumulative overall remission rate between the two treatment regimens, and univariate Cox regression analysis was performed to evaluate whether different immunosuppressive regimens were influencing factors for the remission of PMN. Meanwhile, adverse events (AEs) occurring within 12 months after the initiation of treatment were collected, and the differences in AEs between the two groups were compared. Results A total of 61 patients with PMN were enrolled, with an age of (54.3±10.7) years, including 50 males (82.0%). The baseline indicators included an estimated glomerular filtration rate of (85.1±19.6) ml·min?1·(1.73 m2)?1, a serum albumin level of (21.6±5.0) g/L, 24-hour urinary protein excretion of (9.2±3.4) g, and an anti-phospholipase A2 receptor antibody level of 114.0 (46.0, 247.2) RU/ml. Among them, 31 patients (50.8%) received obinutuzumab with a follow-up duration of 12.0(11.0, 20.0) months, and 30 patients (49.2%) received glucocorticoid combined with CTX with a follow-up duration of 18.5 (12.0, 32.3) months. There were no statistically significant differences in baseline estimated glomerular filtration rate, serum albumin or 24-hour urinary protein excretion between the two groups (all P>0.05). At 6 months and 12 months after treatment, the overall remission rates were 67.7% and 80.8% in the obinutuzumab group, and 56.7% and 63.3% in the glucocorticoid combined with CTX group, respectively, with no statistically significant differences between the two group (all P>0.05). However, the 6-month immunological remission rate in the obinutuzumab group was significantly higher than that in the glucocorticoid combined with CTX group (80.0% vs. 50.0%, χ²=4.713, P=0.030). Kaplan-Meier survival analysis showed no statistically significant difference in the cumulative overall remission rate between the two groups during the follow-up period (Log-rank test, χ²=1.656, P=0.198). Univariate Cox regression analysis indicated that age was associated with overall remission in PMN (hazard ratio=0.97, 95% confidence interval 0.94-0.99, P=0.006). Within 12 months after treatment initiation, there was no statistically significant difference in the incidence of AEs between the two groups (50.0% vs. 32.3%, χ²=1.984, P=0.159). Conclusions The efficacy and safety of obinutuzumab in the treatment of PMN may be non-inferior to those of glucocorticoid combined with CTX regimen.

Objective To investigate the impact of different bed rest time on the safety and comfort of low bleeding risk patients after ultrasound-guided percutaneous renal biopsy, and to evaluate the safety and feasibility of shortening the bed rest time. Methods This was a single-center retrospective cohort study. Patients at low risk of bleeding who underwent ultrasound-guided percutaneous renal biopsy in the Department of Nephrology, Peking University First Hospital between August 17, 2023, and September 29, 2024, were included, and their relevant data were collected. Patients were divided into two groups based on post-procedure bed rest time: an 8-hour group and a 24-hour group. Propensity score matching (PSM) was performed with a caliper value of 0.2 at a 1:1 ratio. The incidence of bleeding events, maximum postoperative pain scores, comfort scores, and the incidence of bleeding-related complications (low back pain, hematuria, infection) within 30 days post-biopsy were compared between the two groups. Univariate logistic regression analysis was used to assess the risk of shortened bed rest time on bleeding events after renal biopsy. Inverse probability of treatment weighting (IPTW) was used for sensitivity analysis. Results A total of 513 low bleeding risk patients were included in the analysis. After PSM, a total of 308 patients were included, with 154 patients in the 8-hour bed rest group and 154 patients in the 24-hour bed rest group. There were no statistically significant differences in baseline characteristics between the 8-hour and 24-hour bed rest groups (all P>0.05). The incidence of bleeding events showed no significant difference between the two groups (21.43% vs. 24.68%, χ2=0.458, P=0.499). Compared to the 24-hour group, patients in the 8-hour group had significantly lower maximum postoperative pain scores [1(0, 1) vs. 1(0,2), Z=3.868, P<0.001] and higher comfort scores [(92.7±11.2) vs. (87.8±10.0), t=-4.027, P<0.001]. The incidence of bleeding-related complications within 30 days post-biopsy was not statistically different between the two groups (all P>0.05). Logistic regression analysis indicated that shortened bed rest time was not a relevant factor for bleeding events after renal biopsy [odds ratio (OR)=0.833, 95% confidence interval (CI) 0.488-1.416, P=0.499]. IPTW-weighted univariate logistic regression analysis also showed no significant association between shortened bed rest time and bleeding events (OR=0.914, 95% CI 0.664-1.269, P=0.586). Conclusion Shortening post-renal-biopsy bed rest to 8 hours demonstrates no significant increase in bleeding risk among low-bleeding-risk patients, and can improved patient pain scores and comfort levels.

Objective To investigate the gene mutation spectrum in patients with autosomal dominant polycystic kidney disease (ADPKD), analyze the correlation between clinical phenotypes and disease progression indicators, evaluate the relationship between gene mutation types and the estimated age of end-stage renal disease (ESRD), and provide a comprehensive genetic basis for expanding the ADPKD variant database, precise diagnosis, prognosis assessment, and individualized management. Methods It was a single-center retrospective study. This retrospective study included 120 ADPKD patients followed at the Department of Nephrology, the Second Affiliated Hospital of Dalian Medical University, from June 2017 to December 2024. Demographic, clinical phenotype, and genetic data were collected. Estimated glomerular filtration rate (eGFR), total kidney volume (TKV), and estimated ESRD age were served as primary outcome indicators for disease progression. TKV was measured by magnetic resonance imaging, and eGFR was calculated using the Chronic Kidney Disease Epidemiology Collaboration equation. Spearman correlation analysis was used to assess the associations between eGFR, TKV, and estimated ESRD age and clinical indicators. Patients were stratified into truncating and non-truncating mutation groups based on PKD1 mutation type, and into single-site and multi-site mutation groups based on the number of PKD1 mutation sites. Differences in estimated ESRD age between the groups were compared. Results Among 120 patients (53 males, 44.2%; 67 females, 55.8%), 84 of 110 (76.4%) had a family history of ADPKD, 53 of 115 (46.1%) reported renal pain, 64 of 86 (74.4%) had polycystic liver disease, 79 of 116 (68.1%) had hypertension, and 11 of 97 (11.3%) had proteinuria. Genetic testing in 78 patients identified PKD1 mutations in 67 (85.9%), PKD2 mutations in 6 (7.7%), and both in 5 (6.4%). Among PKD1 mutations, 45 of 67 (67.2%) were truncating and 22 of 67 (32.8%) were non-truncating. A total of 97 mutation sites were detected: 89.7% in PKD1 and 10.3% in PKD2. Missense mutations were the most common PKD1 variant (34.5%). Compared with the ADPKD variant database, 52 novel and 45 known mutation sites were identified. eGFR correlated negatively with TKV (r_s =-0.526, P<0.001), age (r_s =-0.706, P<0.001), hypertension (r_s =-0.496, P<0.001), polycystic liver disease (r_s =-0.268, P=0.013), serum uric acid (r_s =-0.350, P<0.001), blood urea nitrogen (r_s =-0.646, P<0.001), triglycerides (r_s =-0.208, P=0.040), and male (r_s =-0.188, P=0.041), and positively with hemoglobin (r_s =0.268, P=0.013) and blood platelet count (r_s =0.231, P=0.033). TKV correlated positively with age (r_s =0.391, P<0.001), hypertension (r_s =0.312, P=0.005), serum creatinine (r_s =0.506, P<0.001), uric acid (r_s =0.222, P=0.044), and blood urea nitrogen (r_s =0.357, P<0.001), and negatively with eGFR (r_s =-0.526, P<0.001) and blood platelet count (r_s =-0.247, P=0.049). Estimated ESRD age correlated negatively with hypertension (r_s =-0.248, P=0.026), body weight (r_s =-0.227, P=0.040), uric acid (r_s =-0.402, P<0.001), and blood urea nitrogen (r_s =-0.320, P=0.003), and positively with eGFR (r_s =0.462, P<0.001). The estimated ESRD age was significantly earlier in the PKD1 truncating mutation group than that in the non-truncating group [(59.40±12.46) years vs. (71.44±14.71) years, t=-3.147, P=0.003], and no significant difference was found between single-site and multi-site mutation groups [(64.80±12.90) years vs. (64.03±15.09) years, t=-0.149, P=0.883]. Conclusions This study identified 52 novel ADPKD mutation sites. Hypertension and elevated serum uric acid are the key clinical indicators associated with disease progression. Patients with PKD1 truncating mutations have an earlier estimated ESRD onset than those with non-truncating mutations.

Objective To analyze the application effect of the information-based management model in patients undergoing peritoneal dialysis (PD), clarify the impact of this model on the core indicators related to patients' treatment; to explore the incidence rate and main causes of technical failure in PD patients under the information-based management model, so as to provide a new management model for improving the quality of clinical treatment. Method This was a single-center, prospective study. A total of 409 PD patients who underwent regular follow-up at Foshan First People's Hospital in 2022 were enrolled as research subjects, and an information-based intensive management model was adopted to strengthen patient management. General patient data, biochemical indicators, follow-up data, and other relevant information were collected, with follow-up conducted until December 31, 2024. PD technical failure was defined as catheter removal followed by transfer to hemodialysis or patient death. Changes in the quality of treatment and the occurrence of PD technical failure in PD patients under the information-based management model were analyzed. A Cox regression model was used to explore the factors affecting the prognosis of PD patients. Patients were divided into a low N?terminal proB?type natriuretic peptide (NT?proBNP) group and a high NT?proBNP group based on the mean NT‐proBNP value at enrollment; they were also divided into a low hypersensitive C-reactive protein (hsCRP) group and a high hsCRP group according to the mean hsCRP value at enrollment. The Kaplan-Meier method was applied to compare differences in PD technical survival rates between the two groups (for NT?proBNP and hsCRP classifications, respectively). Result A total of 329 peritoneal dialysis (PD) patients were enrolled in the study, with a median age of 47.0 (37.0, 57.5) years, including 153 males (46.5%). By December 31, 2024, 25 PD patients had died, 53 had switched to hemodialysis, and there were 78 cases of technical failure (23.7%). Compared with 2022, PD patients had higher hemoglobin levels in 2024 (t=-3.550, P<0.001). Compared with the continuous peritoneal dialysis group (n=251), the technical failure group (n=78) had significantly higher age (Z=-2.410, P=0.016), NT?proBNP (Z=-3.819, P<0.001), TyG index (t=2.508, P=0.013), and hypersensitive C-reactive protein (hsCRP) (Z=-4.315, P<0.001) at enrollment. Cox regression analysis showed that male sex [hazard ratio (HR)=1.653, 95% confidence interval (CI) 1.041-2.624, P=0.033), age (HR=1.031, 95% CI 1.011-1.052, P=0.002), NT?proBNP >4 164.3 ng/L (HR=2.286, 95% CI 1.405-3.720, P=0.001), and hsCRP >3.6 mg/L (HR=1.868, 95% CI 1.147-3.041, P=0.012) were the relevant factors for technical failure in PD patients. Conclusion Under the information-based management model, hemoglobin levels in PD patients are improved. Male, increasing age, NT?proBNP >4 164.3 ng/L, and hsCRP >3.6 mg/L are the relevant factors for technical failure in PD patients.

Objective To investigate the role and mechanism of budding uninhibited by benzimidazole 1 (BUB1) protein kinase in renal fibrosis in mice, and to provide new theoretical basis and treatment ideas for chronic renal fibrosis treatment. Methods (1) The expression level of BUB1 gene in unilateral ischemia-reperfusion (UIR) renal tissues was queried through the RNA-seq results of the UIR model and analyzed by the Kidney Interactive Transcriptomics online. (2) Eight-week-old 20-25 g male C57BL/6J mice were used to establish the UIR model. The mice were divided into sham-operated group (sham group), UIR model group (UIR group), and UIR combined with BAY-1816032 treatment group (UIR+BAY group). Western blotting and real-time quantitative PCR were used to detect the protein and mRNA expression levels of renal fibrosis-related factors. Sirius Red staining and Masson staining were used to assess the renal pathological changes. mRNA transcriptome sequencing analysis was performed to screen for differentially expressed genes between the UIR group and the UIR+BAY group. (3) An in vitro partial epithelial mesenchymal transition (pEMT) model was established in mouse TKPT cells. The gene knockdown experiments set up negative control group, BUB1 knockdown group (shBUB1 group), transforming growth factor-β1 (TGF-β1) group, and TGF-β1+shBUB1 group. The gene overexpression experiments set up control group, BUB1 overexpression group (BUB1 group), TGF-β1 group, TGF-β1+BUB1 group, and TGF-β1+BUB1+FBJ murine osteosarcoma viral oncogene homolog (c-Fos) inhibitor T-5224 group. The expression of fibrosis-related indicators was observed. Results (1) RNA-seq and single cell transcriptome database analysis of kidney showed that the expression of BUB1 was significantly increased in the UIR model (all P<0.05), and it was expressed in the cytoplasm and nucleus of various cells in kidney tissue. (2) Compared with the sham group, the mRNA and protein expression of BUB1 in the UIR group was significantly increased (all P<0.05). Compared with the UIR group, the UIR+BAY group showed downregulated mRNA and protein expression of fibrosis-related factors fibronectin and α-SMA, as well as downregulated mRNA expression of collagenⅠ and collagenⅢ in renal tissues. Pathological examination revealed significantly alleviated renal tubular epithelial cell injury and extracellular matrix deposition (all P<0.05). (3) In TKPT cells, compared with the TGF-β1 group, the expression of the fibrosis-related factors was significantly downregulated in the TGF-β1+shBUB1 and TGF-β1+BAY groups (all P<0.05). (4) RNA transcriptome sequencing analysis of differentially expressed genes between the UIR and UIR+BAY groups identified c?Fos gene as the most significantly altered (P<0.05). Validation in vivo and in vitro showed that c?Fos protein levels were significantly upregulated after UIR and TGF-β1 induction but markedly decreased after BAY treatment (all P<0.05). Overexpression of BUB1 significantly upregulated c?Fos expression level, while knockdown of BUB1 significantly reduced c-Fos expression level (both P<0.05). Overexpression of BUB1 exacerbated TGF-β1-induced fibrotic injury in mice, whereas treatment with the c?Fos inhibitor T-5224 significantly ameliorated this process (all P<0.05). Conclusions BUB1 is significantly upregulated in renal fibrosis injury in mice. Inhibiting BUB1 can reduce pEMT of renal proximal tubular epithelial cells and alleviate the level of renal fibrosis, and this effect may be achieved by regulating the c?Fos signaling pathway.

The patients newly diagnosed with maintenance hemodialysis (MHD) were retrospectively enrolled in this study from April 2023 to March 2024 at Haihe Hospital, Tianjin University, and were followed up for one year, to investigate the relationship between serum free triiodothyronine (T3) and major adverse cardiovascular events (MACE) in patients undergoing MHD. During the follow-up period, the patients were divided into the MACE group and the non-MACE group based on whether new MACE occurred. The differences in clinical data between the two groups were compared.The results showed that a total of 188 patients were included, with age of (57.98±11.87） years old, and 114 males (60.64%). During the follow-up period, 82 patients (43.62%) developed MACE. The age (t=4.753, P<0.001), proportion of diabetes mellitus (χ ²=15.623, P<0.001), proportion of low T3 syndrome (χ ²=5.040, P=0.025), parathyroid hormone (t=4.101, P<0.001), and low-density lipoprotein cholesterol (t=2.713, P=0.007) in the MACE group were all higher than those in the non-MACE group, and the left ventricular ejection fraction (Z=-2.420, P=0.016) and free T3 (t=-5.745, P<0.001) were lower than those in the non-MACE group. Multivariate logistic regression analysis results showed that age [odds ratio (OR)=1.063, 95% confidence interval (CI) 1.024-1.103], diabetes mellitus (OR=4.262, 95% CI 1.941-9.357), parathyroid hormone (OR=1.019, 95% CI 1.010-1.029), left ventricular ejection fraction (OR=0.957, 95% CI 0.918-0.996), and free T3 (OR=0.334, 95% CI 0.207-0.538) were the independent correlated factors of MACE in MHD patients. Receiver operating characteristic curve analysis indicated that free T3 level had predictive value for MACE. The area under the curve was 0.743 (95% CI 0.672-0.814), and the optimal cut-off value was 3.21 pmol/L with the sensitivity of 76.83% and the specificity of 66.04%. The study suggests that reduced free T3 is closely associated with the occurrence of MACE in MHD patients, and diabetes mellitus, increased age, elevated parathyroid hormone, decreased left ventricular ejection fraction, and decreased free T3 are the independent related factors of MACE in MHD patients.

This article reports a case of myosin heavy chain 9-related disease (MYH9-RD) accompanied by kidney damage. A 25-year-old female presented with thrombocytopenia and was initially diagnosed with immune thrombocytopenic purpura at another hospital. She was treated with glucocorticoids and human immunoglobulin but showed poor response. During the disease course, she developed renal impairment, hearing loss, and cataracts. Renal biopsy revealed focal segmental glomerulosclerosis. Genetic testing identified a heterozygous mutation in the MYH9 gene, leading to a final diagnosis of MYH9-RD. After a definitive diagnosis, treatment involved tapering prednisone and administering eltrombopag to increase the platelet count. However, the patient independently discontinued all medications following discharge and ultimately progressed to end-stage renal disease, necessitating maintenance hemodialysis. As MYH9-RD is a rare disorder, this case underscores the importance of enhancing clinicians' awareness to avoid misdiagnosis.

IgA nephropathy is a common primary glomerulonephritis, and currently there is no definitively effective and safe therapeutic strategy. Budesonide enteric-coated capsule is a causal treatment for IgA nephropathy. This patient mainly presented gross hematuria and proteinuria, accompanied by abnormal renal function. Based on renal biopsy pathology, the diagnosis was made as mild to moderate mesangial proliferative IgA nephropathy with acute kidney injury. After treatment with budesonide enteric-coated capsule and angiotensinⅡreceptor blocker, the patient's urine protein gradually decreased and eventually disappeared, and the renal function was significantly improved. This case demonstrates the favorable efficacy of budesonide enteric- coated capsule in the treatment of IgA nephropathy, and underscores the crucial importance of timely treatment for improving prognosis, providing a reference for clinical practice.

Peritoneal dialysis (PD)-associated peritonitis remains the most common and serious infectious complication in PD patients, increasing the risk of hospitalization, technique failure, and mortality. Although empirical antibiotic regimens are widely adopted, their comparative effectiveness is inconclusive, and management strategies differ considerably among centres. This paper systematically reviewed publications from the past 20 years that compared empirical antibiotic therapies for PD-related peritonitis. The results indicated that: (1) For Gram-positive bacterial infections, no significant difference in clinical outcomes was found between cefazolin- and vancomycin-based regimens. (2) Multiple classes of anti-Gram-negative agents (third-generation cephalosporins, aminoglycosides, and fluoroquinolones) had been used, but current evidence did not demonstrate the superiority of any single option. (3) Prophylactic anti-fungal therapy appeared to reduce the incidence of secondary fungal peritonitis; however, supporting data was limited. This synthesis summarises the best available evidence to guide the selection of empirical antibiotics and to improve the prognosis of patients with PD-associated peritonitis.

Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease. In China, approximately 700,000 individuals are affected by ADPKD, with about half progressing to end-stage kidney disease (ESKD) between the ages of 50 and 60 years. ADPKD is the fourth leading cause of ESKD. In addition to causing renal lesions, the disease also involves multiple extrarenal organs, including liver cysts, intracranial aneurysms, valvular heart disease, etc., bringing heavy disease burden to individuals, families and society. Therefore, ADPKD has always been a research hotspot in the field of nephrology worldwide. In recent years, the basic and clinical research of ADPKD has made continuous progress, which has brought new theories, new technologies and new therapies to the clinical management of ADPKD. In order to improve the understanding and management of ADPKD among medical staff in China, the Clinical Practice Guidelines Working Group, Nephrology and Dialysis Association of Chinese Non-government Medical Institution Association has developed this Clinical practice guideline for ADPKD in China (2026). Based on evidence-based medicine evidence and clinical experience, the guideline systematically expounds the diagnosis and evaluation of ADPKD, measures to delay disease progression, treatment of renal and extrarenal complications, management of special ADPKD patients and other contents, comprehensively reflecting the forefront of clinical diagnosis and treatment of ADPKD and patient management strategies. This will serve as an important reference for standardizing the diagnosis, evaluation and treatment of ADPKD.