Introduction:Diabetic kidney disease (DKD) remains a leading cause of end-stage kidney disease despite advances with renin-angiotensin system blockade, sodium-glucose cotransporter 2 inhibitors, finerenone, and glucagon-like peptide-1 receptor agonists. Therapeutic monoclonal antibodies may offer a targeted strategy to modulate inflammatory, fibrotic, metabolic, and vascular pathways involved in DKD. This review summarizes the mechanistic rationale, clinical evidence, translational barriers, and future prospects of antibody-based therapies for DKD. Methods:We conducted a narrative literature review using PubMed, the Cochrane Library, and ClinicalTrials.gov from database inception to March 31, 2026. We prioritized peer-reviewed preclinical studies, clinical trials, and high-quality reviews addressing mAb-based strategies targeting DKD-related pathways, including TGF-β1, VEGF-B, CTGF, suPAR, integrin αvβ8, signal regulatory protein α, and PCSK9. Results:Phase II studies of anti-TGF-β1 and anti-VEGF-B antibodies failed to show meaningful renal benefit, highlighting challenges such as pathway redundancy, delayed intervention, insufficient intrarenal target engagement, and off-kidney toxicity. Anti-CTGF therapy showed an early signal of albuminuria, whereas anti-suPAR remains under clinical evaluation. Emerging preclinical targets, including integrin αvβ8 and signal regulatory protein α, may provide more kidney-focused modulation of fibrotic and inflammatory pathways. PCSK9 monoclonal antibodies, particularly evolocumab and alirocumab, appear promising because they may confer renal benefit through lipid lowering and kidney-intrinsic effects on lipotoxicity, oxidative stress, AMPK signaling, and profibrotic pathways. Conclusion:Monoclonal antibodies represent a biologically compelling but clinically underdeveloped strategy for DKD. Future progress will require earlier biomarker-informed patient selection, confirmation of intrarenal target engagement, appropriate renal endpoints, and rational combination with established kidney-protective therapies.

During acute gout flares, serum uric acid (SUA) levels may remain within the normal range, making diagnosis based solely on SUA unreliable. A systematic evaluation incorporating clinical symptoms and imaging (ultrasound, dual-source CT) is essential to detect monosodium urate (MSU) crystal deposition. Normal-SUA gout often presents with more pronounced inflammation, fever, elevated white blood cell count and C-reactive protein, and may occur after surgery or hemodialysis. Tophi can appear at typical or atypical sites (e.g., face, neck). No specific treatment guidelines exist, but lowering SUA to <360 μmol/L (6 mg/dl) reduces gout flares and promotes MSU dissolution. Emerging therapies—including anti-IL-1β monoclonal antibodies, NLRP3 inhibitors, uricases, and green tea components—show promise in controlling attacks and dissolving crystals without affecting SUA levels.

AIMS:Microalbuminuria, common in diabetes, lacks clarity as a predictor of diabetes onset. This study examines its association with incident type 2 diabetes (T2DM) and clinical implications. METHODS:This prospective cohort analysis utilized data from 411,389 UK Biobank participants with baseline urine albumin-to-creatinine ratio (UACR) measurements. Cox proportional hazards regression models, supplemented by restricted cubic spline analyses, were implemented to longitudinally evaluate the association between UACR levels and incident T2DM risk. RESULTS:Over an average follow-up duration of 13.8 years (range: 13.1-14.6 years), 15,942 new cases of diabetes were identified. After adjusting for potential confounders, the hazard ratios for incident T2DM were 1.31 (95% CI: 1.17-1.45) for UACR between 3-30 mg/mmol and 2.20 (95% CI: 1.58-3.06) for UACR > 30 mg/mmol, when compared to a reference UACR of <3 mg/mmol. These results remained stable across multiple sensitivity analyses, including those addressing potential confounding factors such as body mass index, insulin resistance, uric acid levels, and estimated glomerular filtration rate using the creatinine-cystatin C equation (eGFRcr-cys). CONCLUSION:This large-scale cohort study demonstrates that microalbuminuria serves as a clinical predictor of elevated risk for incident T2DM in adults. Routine UACR screening in high-risk populations may enhance early detection and intervention.

Background: It is well-established that reduced kidney function and large amounts of proteinuria are associated with thrombotic and embolic events. However, the relationship between urine albumin-to-creatinine ratio (UACR) and the risk of incident arterial thromboembolism (ATE) and pulmonary embolism (PE) remains unclear. Objectives: This study aims to clarify the relationship between UACR and the incidence of ATE and PE. We sought to determine whether UACR is a risk factor for these events. Methods: A total of 419,282 participants from the UK Biobank with available UACR data were included in the analysis. Cox proportional hazards regression models and restricted cubic spline analyses were used to examine the relationship between UACR and the risk of ATE and PE. Results: Over an average follow-up period of 13.9 years (range, 12.7-15.0 years), we identified 1220 incident ATE cases and 6879 PE events. Compared with a UACR of < 3 mg/mmol, the multivariable-adjusted hazard ratios for UACR of 3 to 30 mg/mmol and UACR of > 30 mg/mmol were as follows: 1.36 (95% CI, 1.00-1.85) and 2.48 (95% CI, 1.14-5.42) for incident ATE; 0.95 (95% CI, 0.82-1.09) and 1.70 (95% CI, 1.11-2.61) for PE, respectively. These associations remained consistent across various sensitivity analyses designed to address potential confounding factors. The findings were also robust in joint analyses considering both UACR and estimated glomerular filtration rate creatinine-cystatin C equation or serum albumin levels. Conclusion: This large cohort study demonstrates that moderately or severely increased albuminuria is associated with an increased risk of incident ATE and PE in adults. These findings highlight the importance of early identification and management of albuminuria as a potential strategy for the prevention of arterial and pulmonary thromboembolic events.

INTRODUCTION:The objective of this study is to investigate the dynamic changes in serum albumin and ferritin as potential predictors for early-onset peritoneal dialysis-related peritonitis (PDRP) in patients undergoing peritoneal dialysis (PD). METHODS:This retrospective study included 215 patients with end-stage renal disease who initiated PD at Huadong Hospital. Patients were followed up to 24 months, during which episodes of PDRP were recorded. The dynamic changes in serum albumin and ferritin levels were evaluated within the first 6 months of PD initiation. Data were analyzed to assess the relationship between these biomarkers and early-onset PDRP. RESULTS:Among the 215 patients, 33.49% developed PDRP, and 28.93% experienced early-onset PDRP. Patients with lower baseline serum albumin levels (<35 g/L) and higher baseline ferritin levels (≥400 μg/L) had an increased risk of developing early-onset PDRP. Importantly, the risk associated with low initial albumin was not significant when serum albumin levels remained stable within the first 6 months (-5% to 5% change). Similarly, although higher baseline ferritin was associated with a higher risk of early-onset PDRP, patients with fluctuating ferritin levels (more than 35% change) showed no significant increase in the risk. Kaplan-Meier analysis revealed a lower cumulative technical survival rate in patients with early-onset PDRP. CONCLUSION:Dynamic changes in serum albumin and ferritin levels within the first 6 months of PD can serve as significant predictors of early-onset PDRP, but stable levels of these markers mitigate their predictive value. Close monitoring of these biomarkers may help in identifying high-risk patients and improving PD outcomes.

AIMS:To explore the link between daytime napping and the risk of major adverse cardiovascular events (MACE) and mortality in individuals with type 2 diabetes. METHODS:This prospective study included 21,129 participants with diabetes from the UK Biobank, all of whom were free of MACE and cancer at baseline. Data on habitual daytime napping and sleep duration were collected via a baseline questionnaire. Cox proportional hazards regression models were employed to assess the relationship between daytime napping and MACE, all-cause mortality, and cardiovascular disease (CVD) specific mortality. MACE was defined as a composite of myocardial infarction, heart failure, and stroke. RESULTS:Over an average 11.9-year follow-up, 5,611 MACE cases, 3,854 all-cause deaths, and 1,839 CVD deaths were identified. Compared to those who never/rarely napped, the multivariable-adjusted hazard ratios for usually napping were: 1.39 (1.08, 1.65) for MACE; 1.44 (1.01, 1.92) for myocardial infarction; 1.33 (1.07, 1.64) for heart failure; 1.57 (1.06, 2.33) for stroke; 1.28 (1.01, 1.60) for all-cause mortality; 1.33 (0.97, 1.94) for CVD mortality. CONCLUSIONS:Frequent daytime napping is significantly associated with an increased risk of MACE and mortality among individuals with diabetes, particularly those who have extended sleep durations of more than 10 h and severe diabetes.

Decreased renal uric acid excretion is a major contributor to hyperuricemia (HUA), but its underlying mechanism remains unclear. Here, we identify cathepsin B (CTSB) as a key regulator of urate handling in HUA. Urinary CTSB levels were elevated in HUA patients, and renal CTSB expression was increased in HUA mice. In CTSBtecKOmice, the expression of reabsorptive urate transporters URAT1 and GLUT9 was decreased, while the secretory transporter ABCG2 was upregulated, leading to enhanced renal uric acid excretion and reduced serum uric acid (SUA). CTSB deficiency also reduced serum IL-1β, IL-6, and TNF-α levels. In vitro and transcriptomic analyses revealed that CTSB inhibition suppressed glycolysis-marked by reduced HK2 and PKM2 expression-downregulated URAT1 and GLUT9, and upregulated ABCG2. Conversely, CTSB overexpression enhanced glycolysis and reversed these effects. These findings suggest that CTSB promotes urate retention via glycolysis and may serve as a novel target for HUA treatment.

ObjectiveTo assess cardiac function using two-dimensional speckle-tracking echocardiography (2D-STI) in diabetic nephropathy (DN) patients and investigate the relationship between albuminuria and early cardiac systolic and diastolic dysfunction, along with associated risk factors based on clinical indicators.MethodsA total of 75 patients with DN, 100 patients with diabetes mellitus (DM), and 37 healthy controls were recruited. Clinical data were collected, and conventional echocardiography as well as 2D-STI were performed on all participants.Results2D-STI findings revealed a significant increased occurrence rate of subclinical left ventricular systolic dysfunction [global longitudinal strain values (GLS) <18%], among diabetic patients compared to healthy controls. Furthermore, the proportion of GLS<18% occurrence was higher in the DN group compared to the DM group (p<0.001) and especially higher in the massive albuminuria group than that in the microalbuminuria group (p<0.001). The results demonstrated that albuminuria, eGFR<60 ml/min/1.73 m2, and total cholesterol were identified as significant risk factors for the development of subclinical left ventricular systolic insufficiency in diabetic patients. However, when considering only patients with DN and adjusting for covariates, it was found that only total cholesterol remained statistically significant (p< 0.05).ConclusionThe higher cholesterol levels in patients with DN are associated with a greater risk of subclinical left ventricular systolic dysfunction reflected by a decrease in GLS assayed with 2D-STI.Critical relevance statementGLS measured by 2D-STI combined with clinical indexes to evaluate and predict subclinical left ventricular systolic function in patients with DM, providing reference for early prevention and treatment of cardiac dysfunction in patients with DN.

Objective:This study evaluates cardiac function in older adults with T2DM and preserved LVEF using two-dimensional speckle-tracking echocardiography to explore the risk factors associated with subclinical left ventricular systolic dysfunction (GLS <18%) in this population. Methods:All patients (n = 87, aged 60 years and above) and controls (n = 20) underwent clinical assessment and echocardiography, including GLS assessment. Results:Univariate analysis identified gender (OR 3.368, p=0.008), proteinuria (OR 5.918, p=0.003), eGFR (OR 0.971, p=0.003), HDL (OR 0.201, p=0.013), triglycerides (OR 3.379, p=0.005), and HOMA-IR (OR 1.173, p=0.049) as potential risk factors for subclinical LV systolic insufficiency in older T2DM patients with preserved LVEF. Following adjustment for age and clinical covariates, multivariate logistic regression confirmed proteinuria (OR 4.063, p=0.030), eGFR (OR 0.974, p=0.049), hypertriglyceridemia (OR 3.069, p=0.050), and HOMA-IR (OR 1.249, p=0.026) as independent predictors. Conclusion:Despite normal global LVEF, proteinuria, hypertriglyceridemia, reduced eGFR, and insulin resistance are closely associated with the development of subclinical left ventricular systolic insufficiency in asymptomatic older adults with T2DM. Trial Registration:This study adheres to the principles outlined in the Declaration of Helsinki and received approval from the Ethics Review Committee of Huadong Hospital, affiliated with Fudan University (Approval No. 2022K150). Written informed consent was obtained from all participants. The registration number of this study at the Chinese Clinical Trial Center is ChiCTR2200062070.

Rationale & Objective:Chronic kidney disease (CKD) is a global health issue, potentially arising from rapid kidney function decline (RKFD). Although body composition influences various metabolic disorders, its relationship with kidney outcomes remains unclear. This study aimed to investigate the impact of body composition on RKFD and CKD risk. Study Design:A cohort study assessed the relationship between body composition and RKFD. A 2-sample Mendelian randomization approach investigated genetic evidence linking body composition to CKD risk. Setting & Participants:In total, 229 adults aged 50-70 years with normal kidney function were recruited from Huadong Hospital in Shanghai, China. Predictors:Body composition indicators include fat mass, lean mass, appendicular lean mass index, fat mass index, total and regional body fat percentages, and sarcopenic obesity, defined by high body fat percentages (>27% in men, >38% in women) and low lean mass (appendicular lean mass index <7.26 kg/m2 in men, <5.45 kg/m2 in women). Outcomes:The primary outcome was RKFD. The second was genetically predicted CKD risk. Analytical Approach:Cox regression and subgroup analyses assessed observational associations. The Mendelian randomization study used two-sample Mendelian randomization, multivariable, and bidirectional Mendelian randomization. Results:RKFD occurred in 9.9% of participants. Lower appendicular lean mass index and the presence of sarcopenic obesity were associated with higher RKFD risk. In overweight participants and those with baseline estimated glomerular filtration rate >90 mL/min/1.73 m2, the negative association between appendicular lean mass index and RKFD remained significant. Mendelian randomization analysis revealed that genetically predicted legs and whole-body fat percentages increased CKD risk, whereas appendicular muscle mass was negatively associated with CKD. Limitations:Differences between the outcomes require further validation. Some sample overlap in the Mendelian randomization analysis may introduce bias. Conclusions:Lower appendicular lean mass index and sarcopenic obesity were associated with RKFD. Higher leg and whole-body fat percentages and lower appendicular muscle mass significantly contribute to CKD risk, highlighting the importance of body composition in kidney health.

This meta-analysis aims to investigate the impact of abnormalities in mineral metabolic markers, including serum phosphate and calcium, intact parathyroid hormone (iPTH), and fibroblast growth factor 23 (FGF23) on the risk of fractures in patients with chronic kidney disease (CKD). A systematic search was conducted across MEDLINE, Web of Science, EMBASE, ClinicalTrials.gov, and the Cochrane Central Register for Controlled Trials. The outcomes were association of mineral metabolic markers with the risk of fractures in patients with chronic kidney disease. Pooled risk estimates and 95

Background. Lack of evaluations of the dietary phosphorus and dialysis phosphorus removal in daily clinical practice are common obstacles to assessing phosphorus balance and controlling phosphorus in hemodialysis patients. We aimed to investigate whether individualized therapy using a phosphorus balance calculator improves phosphorus control.Methods. A randomized, open-label, multicenter, 4-week clinical trial was conducted. A total of 119 maintenance hemodialysis patients aged 18-85 years old and with serum phosphorus level >1.45 mmol/L from three university teaching hospitals in Shanghai were enrolled. Patients were randomized in a 1:1 ratio to individualized therapy (n = 60) or conventional therapy (n = 59). The primary outcome was the serum phosphorus concentration after 4-week treatment. Secondary outcomes included the serum calcium and parathyroid hormone (PTH) concentrations, changes in serum phosphorus, calcium and PTH concentrations, and the proportion of patients achieving target ranges of serum phosphorus, calcium and PTH after 4-week treatment.Results. Among 119 randomized participants [mean age 62 years; 68 male (57%)], 116 completed the trial. Using the phosphorus balance calculator, the individualized group achieved a better phosphorus balance state and significantly reduced serum phosphorus (1.62 +/- 0.45 mmol/L versus 1.85 +/- 0.45 mmol/L, P = .006), increased the proportions of patients achieving target serum phosphorus range (41% versus 18%, P = .006) and had greater adjusted mean difference in change in serum phosphorus over the 4 weeks (-0.47 versus -0.23 mmol/L, P = .010) when compared with conventional therapy. No significant changes were observed in serum calcium and PTH levels, the proportion of patients achieving target serum calcium or PTH levels, or the adjusted mean difference of serum calcium and PTH levels over the treatment period.Conclusion. Phosphorus balance calculator was proved to improve serum phosphorus control in patients undergoing maintenance hemodialysis, offering a new tool for managing hyperphosphatemia.

Background Body mass index (BMI) is associated with diabetic nephropathy (DN). However, the mediator factors in the BMI-DN effects remain unclear.Methods Univariate and multivariate Mendelian randomization (MR) analysis were performed to estimate the association between six lifestyles (moderate to vigorous physical activity levels, years of schooling, BMI, nap during day, number of treatments/medications taken and coffee intake) and DN. MR Egger, Weighted median, Simple mode, and Weighted mode was supplemental methods to Inverse variance weighted. Sensitivity analysis included heterogeneity test, horizontal pleiotropy test, and Leave-One-Out. Additionally, mediation MR was conducted to evaluate the mediating role of lifestyles between BMI and DN. Finally, functional enrichment analysis based on the mediation MR results was performed.Results univariate and multivariate Mendelian randomization (MR) analysis were performed to estimate the association between six lifestyles (moderate to vigorous physical activity levels, years of schooling, BMI, nap during day, number of treatments/medications taken and coffee intake) and DN. MR Egger, Weighted median, Simple mode, and Weighted mode was supplemental methods to Inverse variance weighted. Sensitivity analysis included heterogeneity test, horizontal pleiotropy test, and Leave-One-Out. Additionally, mediation MR was conducted to evaluate the mediating role of lifestyles between BMI and DN. Finally, functional enrichment analysis based on the mediation MR results was performed.Conclusion our results supported mediation role of vigorous physical activity level and number of treatments/medications in BMI-DN effects.

Objective: To develop and externally validate a nomogram to predict elevated serum uric acid (SUA) levels in older adults. Study Design: This is a longitudinal Chinese cohort study. Methods: A cohort of 2788 older adults was established at Huadong Hospital, followed-up for at least one year, and screened for risk factors for elevated SUA levels. A logistic regression model was built to predict elevated SUA, and its performance was validated. Results: The risk prediction model showed good discrimination ability in both the development cohort (area under the curve (AUC) = 0.82; 95% confidence interval (CI) =0.79 similar to 0.86) and the external validation cohort (AUC=0.76; 95% CI=0.70 similar to 0.82). The model was adequately calibrated, and the predictions correlated with the observed outcome (chi(2) = 6.36, P = 0.607). Men were more prone to elevated SUA levels than women were, and a baseline SUA level >= 360 mu mol/L was a common risk factor for both males and females. Proteinuria status was an additional risk factor for males, whereas a baseline estimated glomerular filtration rate (eGFR)<60 mL/min.1.73 m(2) and diabetes status were additional risk factors for females. Conclusion: The externally validated nomogram, which is predictive of elevated SUA in older adults, might aid in the detection of individual diseases, the development of preventive interventions and clinical decision-making.

Aim Renal artery stenosis (RAS) is an important cause of chronic kidney disease (CKD). The main purpose of this study was to explore the clinical characteristics and predictors of low-grade RAS in female patients with CKD. Methods One hundred and five female CKD patients from Huadong Hospital affiliated with Fudan University who underwent 3 T non-contrast renal artery magnetic resonance angiography (MRA) were analyzed. Basic statistics methods were used in the study, such as independent-sample t test,non-parametric test, binary logistic regression analysis and ROC analysis. Results In this cross-sectional study, there were 50 patients with RAS and 55 without RAS (47.6% versus 52.4%). Binary logistic regression analysis demonstrated that low-level ALB and lymphocyte count, high-level SP, BUN and NLR were independent risk factors for low-grade RAS in female patients with CKD. ROC analysis indicated that eGFR, FeNa and UBCR, ALB, lymphocyte count and NLR had the best predictive value for low-grade RAS, especially eGFR with a sensitivity of 65.50% and specificity of 72.00% and FeNa with a sensitivity of 71.10% and specificity of 72.20% and BUCR with a sensitivity of 71.10% and specificity of 68.10%. Conclusion In female patients with CKD, FeNa, eGFR, ALB, UBCR, lymphocyte count and NLR may be good predictors of low-grade RAS, especially eGFR, FeNa and BUCR.

Background Epidemiological evidence relating sleep disorders to end-stage renal disease (ESRD) has been obscure. The present study is sought to examine the association between sleep traits and ESRD. Methods For this analysis, we selected genetic instruments for sleep traits from published genome-wide association studies (GWAS). As instrumental variables, independent genetic variations linked with seven sleep-related features (sleep duration, getting up in the morning, daytime napping, chronotype of morning/evening person, sleeplessness/insomnia, non-snoring, and daytime dozing) were chosen. A two-sample Mendelian randomization (TSMR) study was conducted to assess the causal relationship between sleep traits and ESRD (N = 33,061). The reverse MR analysis subsequently determined the causal relationship between ESRD and sleep traits. The causal effects were estimated using inverse variance weighted, MR-Egger, weighted median. To conduct sensitivity studies, Cochran’s Q test, MR-Egger intercept test, MR-PRESSO, leave-one-out analysis, and funnel plot were used. To study the potential mediators, multivariable mendelian randomization analyses were undertaken further. Results Genetically predicted sleeplessness/ insomnia (OR = 6.11, 95%CI 1.00-37.3, P = 0.049, FDR = 0.105), getting up in the morning easily(OR = 0.23, 95%CI 0.063–0.85; P = 0.0278, FDR = 0.105), non-snoring (OR = 4.76E-02, 95%CI 2.29E-03-0.985, P = 0.0488, FDR = 0.105) was suggestively associated with the risk of ESRD. However, we found no evidence favoring a causal association between other sleep traits and ESRD through the IVW method. Conclusion The present TSMR found no strong evidence of a bidirectional causal association between genetically predicted sleep traits and ESRD.

Mixed lineage leukemia 1 (MLL1), a histone H3 lysine 4 (H3K4) methyltransferase, exerts its enzymatic activity by interacting with menin and other proteins. It is unclear whether inhibition of the MLL1-menin interaction influences epithelial-mesenchymal transition (EMT), renal fibroblast activation, and renal fibrosis. In this study, we investigated the effect of disrupting MLL1-menin interaction on those events and mechanisms involved in a murine model of renal fibrosis induced by unilateral ureteral obstruction (UUO), in cultured mouse proximal tubular cells and renal interstitial fibroblasts. Injury to the kidney increased the expression of MLL1 and menin and H3K4 monomethylation (H3K4me1); MLL1 and menin were expressed in renal epithelial cells and renal interstitial fibroblasts. Inhibition of the MLL1-menin interaction by MI-503 administration or siRNA-mediated silencing of MLL1 attenuated UUO-induced renal fibrosis, and reduced expression of α-smooth muscle actin (α-SMA) and fibronectin. These treatments also inhibited UUO-induced expression of transcription factors Snail and Twist and transforming growth factor β1 (TGF-β1) while expression of E-cadherin was preserved. Moreover, treatment with MI-503 and transfection with either MLL siRNA or menin siRNA inhibited TGF-β1-induced upregulation of α-SMA, fibronectin and Snail, phosphorylation of Smad3 and AKT, and downregulation of E-cadherin in cultured renal epithelial cells. Finally, MI-503 was effective in abrogating serum or TGFβ1-induced transformation of renal interstitial fibroblasts to myofibroblasts in vitro. Taken together, these results suggest that targeting disruption of the MLL1-menin interaction attenuates renal fibrosis through inhibition of partial EMT and renal fibroblast activation.

Abstract Background: The aim of our study was to explore short- and long-term mortality and risk factors affecting Chinese elderly patients with different glomerular filtration rate after hip fracture. Methods: This study included 513 patients aged≥65 years old and first been diagnosed with hip fracture in the Department Orthopedics of Huadong hospital between January 1st, 2010 and December 31st, 2011. Patients’ medical records were collected from the electronic medical record system. Survival status after hip fracture were assessed through telephone interviews and causes of death were verified. The patients were divided into three groups according to the renal function. Kaplan-Meier survival analysis was used to compare survival time between different groups. Univariate and multivariate Cox proportional hazards model was constructed to analyze differences between patients and factors associated with mortality. Results: According to the inclusion and exclusion criteria and excluded patients who were lost to follow-up, a total of 325 patients were available in this study. Of which 73.5% were female and 85.2% received surgical operation. One-year cumulative mortality were 9.30%, 19.81% and 22.53% for group 1, 2 and 3. Five-year cumulative mortality were21.87%, 55.86% and 78.87%, while the ten-year cumulative mortality were40.61%, 74.32% and 94.37% respectively. Our analysis found that age (1.076 (1.031-1.122)), cognitive function (2.279(1.101-4.718)) were associated with higher risk of one-year mortality. Age (1.062(1.035-1.090)), eGFR<60 mL/min/1.73m 2 (2.425(1.054-5.578)) were associated with higher risk of five-year mortality. Age(1.073(1.049-1.097)), eGFR<60 mL/min/1.73m 2 (2.120(1.110-4.048)) and mildly decreased cognitive function(1.949(1.163-3.265)) were associated with higher risk of ten-year mortality. Conclusion: Renal function seem to have little effect on short term mortality of Chinese elderly patients after hip fracture, but was an important risk factor affecting the medium to long-term mortality. For patients with decreased eGFR, fully evaluating the status of patients and choosing appropriate surgical method as soon as possible after fracture can greatly reduce the risk of death and ensure better survival in the elderly.

免疫检查点抑制剂( immune checkpoint inhibitors, ICIs)有多种类型,主要包括程序性死亡蛋白-1 ( pro-grammed death-1, PD-1 )/程序性死亡分子配体-1 ( pro-grammed death ligand-1, PD-L1)抑制剂、细胞毒性T淋巴细胞相关蛋白4 ( cytotoxic T-lymphocyte-associated protein 4, CTLA-4)抑制剂以及近期发现的淋巴细胞活化基因3 (lymphocyte activation gene 3, LAG-3)抑制剂等[1].研究显示,恶性肿瘤的发生风险随年龄增长而增加,老年人的恶性肿瘤发病率和相关死亡率分别为年轻人的8. 47倍和13. 96倍[2].ICIs的临床应用使多种恶性肿瘤的预后得到了显著改善,然而ICIs在提升机体抗肿瘤能力的同时也会引起一系列免疫相关的不良反应( immune-related adverse events, irAEs) ,如肾脏、皮肤、胃肠道和肝功能受损[3]或心肌炎等[4].ICIs所致的肾脏病变临床表现多样,以急性肾损伤( acute kidney injury, AKI)最为多见,急性间质性肾炎( acute interstitial nephritis, AIN)是其主要病理类型[5].本文针对ICIs所致肾损害的发生机制、危险因素、诊断策略、治疗与管理等研究进展作一综述.