Objective To analyze the clinical characteristics and evolution in the diagnosis and management of acute kidney injury (AKI) among hospitalized patients, identify existing problems, and provide a basis for improving clinical practice. Methods A single-center repeated cross-sectional study was conducted to enroll hospitalized patients with AKI at Peking University First Hospital in January and July, 2013 and January and July, 2018—2020. The demographic characteristics, AKI severity, etiologies, clinical phenotypes, recognition patterns, and outcomes were compared between the two groups. Stacked bar charts and network analysis were used to explore patterns of nephrotoxic drug use, and chord diagram was applied to illustrate the association between initial AKI stage and renal function recovery. Results A total of 668 hospitalized patients with AKI were included. There were 196 patients, with age of (63.6±17.5) years, and 116 males (59.2%) in the 2013 group. There were 472 patients, with age of (64.0±17.7) years and 278 males (58.9%) in the 2018—2020 group. Compared with the 2013 cohort, the proportion of hospitalized patients who underwent serum creatinine testing at least twice in the 2018—2020 cohort increased significantly [35.5% (13 169/37 094) vs. 25.3% (562 191/2 223 230)]. The proportion of the highest AKI stage classified as stage 1 increased, accompanied by a reduction in stage 2 and stage 3, and the difference did not reach statistical significance (χ2=4.516, P=0.105). The timely recognition rate of stage 1 AKI showed a slight increase [52.7% (202/472) vs. 44.2% (65/196)], but the difference was not statistically significant (χ2=2.012, P=0.156). The overall non-recognition rate of AKI remained unchanged [33.3% (157/472) vs. 33.5% (64/191), χ2=0.762, P=0.683]. Among common etiologies, hypoperfusion remained highly prevalent in both groups, with no statistically significant difference [84.3% (398/472) vs. 84.2% (165/196), χ2=0.002, P=0.964]. The overall rate of nephrotoxic drug use remained stable [ 83.9% (396/472) vs. 85.2% (167/196), χ2=0.178, P=0.673], whereas the proportion of patients exposed to multiple nephrotoxic agents (>3 drugs) increased significantly [28.0% (132/472) vs. 11.7% (23/196), χ2=20.476, P<0.001]. β?lactam antibiotics, other antimicrobial agents, diuretics, and antipyretic and analgesic drugs were the most commonly used combinations. In terms of clinical classification, the proportions of prerenal and postrenal AKI were significantly higher, while the proportion of intrinsic renal AKI decreased, with a statistically significant difference (χ2=22.357, P<0.001). In terms of clinical outcomes, the proportions of dialysis [6.8% (32/472) vs. 15.3% (30/196), χ2=11.958, P<0.001], in-hospital mortality [17.2% (81/472) vs. 28.6% (56/196), χ2=11.060, P<0.001], and non-recovery rate of renal function at discharge [31.4% (106/337) vs. 42.1% (59/140), χ2=4.995, P=0.025] all decreased significantly. The chord diagram showed that non-recovery rate of renal function in patients with AKI stage 1 to 3 all presented a downward trend in the 2018—2020 cohort compared with the 2013 cohort. Conclusions Compared with the 2013 cohort, hypoperfusion and exposure to nephrotoxic drugs remain common among hospitalized patients with AKI, with a marked increase in polypharmacy in the 2018—2020 cohort. Meanwhile the patients have more frequent monitoring of serum creatinine, and the ability to identify mild AKI has slightly improved, and the overall prognosis has also improved. This suggests that early identification of AKI still faces challenges, and the management of AKI still requires strengthened monitoring and control of drug risks.
Objective To investigate the expression profiles of renal injury markers, metabolic and inflammation-related factors in patients with diabetic kidney disease (DKD), and to analyze their correlation with serum leptin, in order to provide more reference data for clinical practice. Methods It was a retrospective case-control study. The patients diagnosed with DKD in the Department of Nephrology, Guizhou Provincial People's Hospital from July 2017 to July 2018 were enrolled as the DKD group. Age- and gender-matched healthy individuals undergoing routine health check-ups during the same period were enrolled as the healthy group. Clinical data of study subjects were collected. Antibody microarray was used to measure the urinary kidney injury markers and serum metabolic and inflammation-related factors. Spearman correlation method was used to analyze the correlations between serum leptin and kidney injury markers, metabolic and inflammation-related factors. Benjamini-Hochberg method was applied to perform multiple comparisons. Results Compared with the healthy group, the DKD group showed significantly higher levels of fasting blood glucose [7.73 (6.21, 9.54) mmol/L vs. 3.80 (2.89, 4.79) mmol/L, Z=6.283, P<0.001], glycosylated hemoglobin [9.75% (7.17%, 12.04%) vs. 4.32% (3.44%, 5.14%), Z=6.068, P<0.001], serum creatinine [129.08 (112.84, 143.61) μmol/L vs. 88.55 (78.03, 98.16) μmol/L, Z=6.319, P<0.001], blood urea nitrogen [10.73 (8.99, 12.38) mmol/L vs. 6.28 (5.34, 6.86) mmol/L, Z=6.594, P<0.001] and 24-hour urinary protein quantity [0.301 (0.278,0.328) g vs. 0.020 (0.019, 0.022) g, Z=6.881, P<0.001], and lower estimated glomerular filtration rate [46.25 (43.75, 49.95) ml·min?1·(1.73 m2)?1 vs. 89.23 (83.22, 94.25) ml·min?1·(1.73 m2)?1, Z=-6.367, P<0.001]. In terms of kidney injury markers, levels of urinary cystatin C, urinary kidney injury molecule-1, urinary neutrophil gelatinase- associated lipocalin, urinary fatty acid-binding protein, urinary adiponectin and serum cystatin C in the DKD group were significantly higher than those in the healthy group (all q<0.05). In terms of metabolic factors, serum leptin, growth differentiation factor-15 and fibroblast growth factor-19 in the DKD group were significantly higher than those in the healthy group (all q<0.05). In terms of inflammation-related cytokines, serum CXC chemokine ligand 1, urinary CXC chemokine ligand 1, urinary vascular cell adhesion molecule-1, interleukin (IL)-1α, IL-2, IL-3, IL-10, IL-11, IL-16, IL-18-binding protein α, IL-22, IL-27 and IL-31 in the DKD group were significantly higher, while IL-17A level was significantly lower than that in the healthy group (all q<0.05). Spearman correlation analysis showed that serum leptin was positively correlated with serum cystatin C (r=0.762, q=0.038), serum growth differentiation factor-15 (r=0.673, q=0.039), IL-2 (r=0.929, q=0.006), IL-16 (r=0.762, q=0.038), IL-18-binding protein α (r=0.786, q=0.032) and IL-22 (r=0.762, q=0.038), and negatively correlated with IL-17A (r=-0.857, q=0.021). Conclusions The expression profile of DKD patients is mainly characterized by elevated kidney injury markers, metabolic dysregulation, and unbalanced inflammation-related factors. Serum leptin level is significantly increased in DKD patients and closely associated with kidney injury markers as well as metabolic and inflammation-related factors. Leptin may participate in the progression of DKD through activation of renal inflammatory pathways and represent a potential target for clinical intervention.
Objective To identify differentially expressed genes (DEG) and potential regulatory pathways in B cells associated with galactose-deficient IgA1 (Gd-IgA1) level in patients with IgA nephropathy (IgAN) through transcriptomic analysis, and to elucidate the underlying molecular mechanism of Gd-IgA1 in the pathogenesis of IgAN. Methods It was a prospective exploratory study. The study subjects were patients with primary IgAN diagnosed through renal biopsy in the Nephrology Department of Tianjin Medical University General Hospital. IgAN patients were divided into high Gd-IgA1 group (>10 mg/L, n=6) and low Gd-IgA1 group (<5 mg/L, n=5) based on plasma Gd-IgA1 level. Peripheral blood B cells were isolated for RNA sequencing. Gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) analysis were used to conduct the functional and pathway annotations and enrichment analyses of DEG. Flow cytometry was used to verify the expression of platelet activation marker CD62P in an independent cohort of IgAN patients (n=20). In vitro co-culture experiments were applied to evaluate the effect of platelets on Gd-IgA1 production by incubating activated platelets with peripheral blood mononuclear cells at a ratio of 10∶1 for 5 days. Overlap analysis of DEG was performed by integrating published genome-wide association study data on IgA1 glycosylation and IgAN. Results A total of 40 patients with primary IgAN were enrolled in this study. The Gd-IgA1 level in the high and low groups was 11.44 (10.72, 14.99) mg/L and 4.46 (3.69, 4.72) mg/L, respectively. A total of 1 445 DEG were identified, with 1 277 upregulated genes and 168 downregulated genes. GO analysis highlighted that upregulated genes were significantly enriched in biological processes related to platelet degranulation, activation, and coagulation. KEGG analysis highlighted the enrichment of pathways such as platelet activation and cell adhesion. In clinical samples, CD62P expression level was positively correlated with Gd-IgA1 level (r=0.54, P=0.011). In vitro experiments confirmed that activated platelets promoted Gd-IgA1 production by peripheral blood mononuclear cells (P<0.001). Genome-wide association study integration analysis revealed overlaps between multiple IgAN susceptibility genes (e.g., tumor necrosis factor receptor superfamily member 13B, platelet factor 4 variant 1) and the identified DEG, suggesting an association between genetic susceptibility and platelet-related pathways. Conclusions High Gd-IgA1 level in IgAN patients is closely associated with the enrichment of platelet activation pathways in the B cell transcriptome. Activated platelets may promote Gd-IgA1 production. This study provides a new perspective for understanding the pathogenesis of IgAN and suggests that platelets may serve as a potential therapeutic target.
Objective To explore the effects of different surgical techniques on the peritoneal dialysis (PD) catheter patency rate as well as the risk factors of catheter dysfunction. Methods It was a retrospective cohort study. Clinical data of patients who underwent initial PD catheter placement and follow-up at Beijing Haidian Hospital from January 1, 2019 to October 1, 2024 were collected. Patients were divided into open surgery group and laparoscopic surgery group according to the catheter placement technique, and clinical data between the two groups were compared. The endpoint event was catheter dysfunction and patient withdrawal from PD, including death, transfer to hemodialysis, renal transplantation, and loss to follow-up. The follow-up period ended on April 1, 2025. Kaplan-Meier method was used to plot the survival curve of cumulative PD catheter patency rate, and the log-rank test was used to compare the differences of patency rates between the two groups. Cox regression model was used to analyze the influencing factors of PD catheter dysfunction, and receiver-operating characteristic curves were plotted. Results A total of 493 PD patients were enrolled in this study, with age of (54.83±15.48) years and 257 males (52.1%), including 257 patients in the open surgery group and 236 patients in the laparoscopic surgery group. Compared with the open surgery group, the laparoscopic surgery group had higher body mass index [(24.960±4.613) kg/m2 vs. (23.051±4.501) kg/m2, t=4.648, P<0.001], proportion of a history of abdominal surgery [37.7% (89/236) vs. 12.8% (33/257), χ2=40.866, P<0.001], proportion of diabetes mellitus [46.2% (109/236) vs. 37.0% (95/257), χ2=4.313, P=0.038] and proportion of receiving automated PD after surgery [39.4% (93/236) vs. 26.8% (69/257), χ2=8.795, P=0.003], and better residual renal function [24-hour urine output: 700 (400,1 200) ml vs. 550 (250,1 100) ml, Z=2.378, P=0.018]. In contrast, the laparoscopic surgery group had lower age [(52.770±15.013) years vs. (56.720±15.697) years, t=2.852, P=0.005], and lower proportions of coronary heart disease [33.1% (78/236) vs. 46.3% (119/257), χ2=9.006, P=0.003], cardiovascular events [31.4% (74/236) vs. 44.4% (114/257), χ2=8.816, P=0.003], and cerebrovascular disease [7.2% (17/236) vs. 19.8% (51/257), χ2=16.533, P<0.001]. Kaplan-Meier survival analysis showed that the follow-up period was 31 (26, 41) months, and the overall catheter patency rate in the cohort was 72.76%. Compared with the open surgery group, the laparoscopic group had a significantly higher catheter patency rate (87.47% vs. 72.37%, Log-rank test, χ2=17.035, P<0.001]. Multivariate Cox regression analysis showed that catheterization surgery method [laparoscopic surgery/open surgery, HR=0.355, 95% confidence interval (CI)0.219-0.576, P<0.001], serum potassium (HR=0.674,95% CI 0.508-0.895, P=0.006), serum albumin (HR=0.852, 95% CI 0.826-0.880, P<0.001), constipation (HR=1.946, 95% CI 1.216-3.112, P=0.006), history of abdominal surgery (HR=8.038, 95% CI 4.743-13.623, P<0.001), and history of diabetes mellitus (HR=2.485,95% CI 1.525-4.049, P<0.001) were independent factors correlated with catheter dysfunction. Receiver-operating characteristic curve analysis showed that the combined model of the above independent factors including low serum albumin (< 25.15 g/L), low serum potassium (<3.465 mmol/L), history of diabetes mellitus, laparoscopic catheterization procedure, history of abdominal surgery, and history of constipation achieved an area under the curve of 0.941 (95% CI 0.921-0.961, P<0.001). Conclusions Laparoscopic catheterization may significantly increase the long-term patency rate of PD catheters. Serum albumin level, serum potassium level, history of diabetes mellitus, laparoscopic catheterization method, history of abdominal surgery and history of constipation are independent factors associated with PD catheter dysfunction. The constructed predictive model based on serum albumin <25.15 g/L, serum potassium <3.465 mmol/L, history of diabetes mellitus, laparoscopic surgery, history of abdominal surgery, and history of constipation has good discriminative efficacy.
Anti-neutrophil cytoplasmic antibody-associated vasculitis (AAV) is an autoimmune disease characterized by necrotizing small-vessel vasculitis and is often accompanied by severe complications such as diffuse alveolar hemorrhage (DAH) and rapidly progressive glomerulonephritis, making management challenging. The paper reports a critically ill patient with AAV involving both the lungs and kidneys, with initial presentation of rapidly progressive glomerulonephritis. Despite methylprednisolone pulse combined with cyclophosphamide and rituximab, DAH still developed. After reduced-dose methylprednisolone pulse combined with eculizumab for another treatment, the alveolar bleeding resolved rapidly. Subsequently, glucocorticoids were tapered quickly, and intermittent rituximab was given as maintenance therapy. The patient achieved disease remission and a stable recovery in renal function. This case may provide reference for managing similarly severe AAV patients.
Scleroderma renal crisis (SRC) is a clinical emergency but has challenging outcomes, especially when complicated with thrombotic microangiopathy (TMA). Here the paper reports a 58-year-old male who presented with systemic sclerosis complicated with pulmonary interstitial fibrosis, esophageal dysfunction and TMA. He experienced new-onset hypertension and acute kidney failure after glucocorticoids treatment, and required hemodialysis despite immediate use of angiotensin-converting enzyme inhibitor for blood control. Serum laboratory tests revealed low complement 3, elevated C5b?9, and positive anti-complement factor H antibody. Renal biopsy pathology showed TMA and glomerular ischemia. Diagnosis of anti-complement factor H antibody-positive atypical hemolytic uremic syndrome secondary to scleroderma renal crisis was made. In addition to mycophenolate mofetil and rapid decline of glucocorticoids, he received eculizumab 900 mg per week for four weeks, followed by 1 200 mg at an extended interval of three weeks with careful monitoring of serum C5b?9 level for six months. He stopped hemodialysis four months after treatment, with serum creatinine dropping from 703 μmol/L to 296 μmol/L after one year of follow-up. Early use of eculizumab may reverse renal function impairment in patients with SRC- atypical hemolytic uremic syndrome. Moreover, even under economic constraint, an individually extended dosing interval based on C5b?9 monitoring may still be effective.
This article reports a case of complement-mediated atypical hemolytic uremic syndrome (aHUS) with anti-neutrophil cytoplasmic antibody (ANCA) positivity. A 63-year-old male presented with a 1-month history of fever. At admission, the patient's platelet count was 48×109/L, hemoglobin was 67 g/L, and schistocyte was 2.3%. Myeloperoxidase-ANCA titer was > 400 RU/ml. Complement C3 was 0.51 g/L, and complement factor B was < 12.00 mg/dl. A disintegrin and metalloproteinase with thrombospondin type 1 motif member 13 (ADAMTS13) activity was normal. Shiga toxin infection, drug-induced injury, and malignant hypertension were excluded. Renal biopsy showed acute thrombotic microangiopathy and negative immunofluorescence. The diagnosis of aHUS with ANCA positivity was established. Initial treatment with methylprednisolone 125 mg/d for 3 days followed by prednisone 80 mg/d with taper was given. Persistent thrombocytopenia delayed renal biopsy. Serum creatinine rose to 422 μmol/L, and the patient required platelet transfusion and hemodialysis. After pathological confirmation, eculizumab was administered (900 mg weekly for 4 weeks, then 1 200 mg every 2 weeks). Two weeks later, platelet count increased to 151×109/L and serum creatinine decreased to 195 μmol/L. At 12-month follow-up, the patient's renal function was stable, myeloperoxidase-ANCA became negative, and complement C3 and factor B were normalized. In patients with ANCA positivity and thrombotic microangiopathy, complement and ADAMTS13 assessment should be performed simultaneously for diagnosis. ANCA positivity may precede or coexist with aHUS. Early recognition of complement abnormality and timely eculizumab initiation may significantly improve prognosis of patients.
This paper describes a rare case of pyoderma gangrenosum (PG) complicated by Cryptococcus neoformans infection induced by obinutuzumab in a patient with refractory nephrotic syndrome. The patient was a 43-year-old man with relapsing and refractory nephrotic syndrome, and had a history of elevated serum creatinine during previous therapies. After disease relapsed, obinutuzumab was administered. Within 48 hours of infusion, the patient developed redness, swelling, pain and increased skin tension on the left elbow, which progressed rapidly into ulcers. A multidisciplinary evaluation, combined with laboratory, imaging, and pathogen detection, led to the diagnosis of obinutuzumab-induced PG complicated with secondary Cryptococcus neoformans infection. The patient was successfully managed with comprehensive therapy including surgical debridement and skin grafting, glucocorticoid-based immunomodulation, and antifungal treatment with amphotericin B plus flucytosine. Obinutuzumab-associated PG concurrent with cryptococcal infection is clinically rare. This case highlights the need for vigilance regarding complex complications during treatment with novel anti-CD20 monoclonal antibodies, which may induce autoimmune skin damage and severe opportunistic infection secondary to profound immunosuppression, and may provide insights into the diagnosis and management of similar cases.
This article reports a rare case of hemoglobin cast nephropathy caused by an immune checkpoint inhibitor. The patient, a 59-year-old male, developed acute kidney injury accompanied by anemia and thrombocytopenia after receiving immune checkpoint inhibitor therapy for gastric cancer. After empirical treatment with glucocorticoids, the patient's renal function showed poor recovery. Then renal biopsy was performed. The biopsy indicated acute tubular necrosis and hemoglobin cast nephropathy. After fluid support therapy, renal function returned to normal. This case suggests that a rigorous diagnostic and differential approach is required to identify the underlying etiology for immune checkpoint inhibitor-associated acute kidney injury. When necessary, renal biopsy can be used to guide diagnosis and treatment.
In recent years, artificial intelligence (AI) has been increasingly applied in nephrology, demonstrating significant potential across both clinical practice and research. The paper systematically reviews the current applications and challenges of AI in precision diagnosis, treatment decision-making, disease prediction, drug discovery, and scientific research in kidney diseases. In precision diagnosis, AI facilitates medical data management via natural language processing and clinical decision support systems, and enables automated segmentation and quantitative analysis of renal pathology and multimodal imaging, thereby improving diagnostic consistency and efficiency. In therapeutic decision-making, AI supports fundus image-based screening, individualized immunosuppressive therapy, complication management, and dialysis optimization, promoting a shift from empirical medicine to precision medicine. For disease prediction, AI models enable early warning of acute kidney injury, prediction of chronic kidney disease progression and end-stage kidney disease risk, and prognostication of kidney transplantation outcomes, while also uncovering novel molecular subtypes. In drug development, AI accelerates target identification, lead compound design, and safety profiling. In scientific research, generative AI enhances data processing and medical writing efficiency. Despite these advances, challenges remain, including insufficient data standardization, lack of interdisciplinary collaboration, poor model interpretability, and difficulties in clinical translation. Future efforts should focus on building high-quality data platforms, fostering cross-disciplinary talents, and advancing multimodal and semi-supervised learning techniques to drive nephrology toward digitalized, precise, and standardized care.
The development of retinal vessel quantitative analysis techniques and breakthroughs in artificial intelligence algorithms have made fundus images an important tool for non-invasive screening and dynamic monitoring of kidney diseases. Fundus image diagnosis, as a non-invasive method, is highly correlated with renal vascular lesions. Its convenience, repeatability, and high sensitivity to early microvascular abnormalities have opened up new avenues for the precise diagnosis and treatment of kidney diseases. This review summarizes the research and application progress of fundus images in the diagnosis and treatment of kidney diseases, including the biological basis of fundus images and renal pathophysiology, the development of common fundus imaging techniques, the research status of fundus images and retinal features in the diagnosis and treatment of common kidney diseases, the construction of diagnostic prediction models, and the research progress of cutting-edge directions such as artificial intelligence multimodal fusion and clinical applications of microvascular parameters. This article aims to systematically review the research progress of fundus image technology in the diagnosis and treatment of kidney diseases, promote the translational application of fundus image diagnosis technology in the clinical practice of precise diagnosis and treatment of kidney diseases, and provide multidimensional evidence for optimizing treatment strategies and research layout.
In recent years, super-resolution microscopy imaging techniques representing by three- dimensional electron microscopy, cryo-electron microscopy, correlative light and electron microscopy, low-vacuum scanning electron microscopy, super-resolution microscopy, expansion microscopy, and multiphoton microscopy have developed rapidly, providing high-resolution and multidimensional observational approaches for kidney disease research. This review summarizes the latest advances in the nanoscale imaging and three-dimensional visualization of key renal structures, including podocytes, glomerular basement membrane, glomerular filtration barrier, and renal tubules; the conformational analysis and assembly mechanisms of biomacromolecules; dynamic structure-function association analysis; and the emerging applications of these cutting-edge super-resolution microscopy imaging technologies in disease diagnosis, with the aim of offering new technical perspectives and methodological insights for basic research and clinical diagnosis and treatment of kidney diseases.
Chronic kidney disease (CKD) has become a global public health issue. In May 2025, the World Health Assembly officially approved the world's first resolution on kidney health, recognizing kidney disease as a major non-communicable disease of global priority. To improve the diagnosis and treatment of CKD in China, expert group on kidney clinical quality control center in Shanghai developed and released the "Guidelines for screening, diagnosis, prevention and treatment of CKD" in 2017, which was revised and updated in 2022. These guidelines have significantly enhanced the awareness and management of CKD among general practitioners and nephrology specialists at all levels in China. Based on emerging clinical evidence on CKD in recent years, as well as the development and application of new medications, the clinical practice guidelines working group of the Kidney Disease Dialysis Special Committee of the China Association of Non-Public Medical Institutions has developed the "Chinese clinical practice guideline for screening, diagnosis, and treatment of chronic kidney disease (2026)" building upon the original guidelines. Key revisions and updates include diagnostic criteria for CKD, etiology diagnosis, screening subjects and indicators, progression assessment and risk prediction models for kidney failure, and management of risk factors and complications. These guidelines are intended to provide reference for improving China's CKD screening system and standardizing the diagnosis and treatment of CKD by clinical nephrologist.
