This study aimed to investigate regional epidemiological trends of chronic kidney disease (CKD) to elucidate their etiologies and inform the development of preventive and diagnostic strategies. We retrospectively analyzed 2100 hospitalized patients undergoing native renal biopsy from January 1, 2012, to December 31, 2021. The clinical presentation, the prevalence of nephropathy revealed by biopsy, the age-distribution differences of main pathological types, and changes in the prevalence of different diseases between period 1 (2012-2016) and period 2 (2017-2021) were further analyzed. Hematuria or proteinuria not within the range of the nephrotic syndrome (NS) (36.7%), NS (32.6%), chronic renal insufficiency (22.3%) and acute kidney injury (3.1%) were the 4 major clinical indications for renal biopsy. Although the proportion of primary glomerulonephritis (primary GN, from 85.0% to 75.9%) has shown a downward trend, it remained the predominant diagnosis, with secondary glomerulonephritis (secondary GN, from 11.2% to 16.5%) ranking second. Combined nephropathy showed a significant increase (from 0.3% to 2.6%) especially the diabetic nephropathy (DN) combined with other kidney diseases (from 0.2% to 1.8%). Among primary GN, IgA nephropathy (IgAN) was the most common type, followed by membranous nephropathy (MN). Although the proportion of IgAN did not change for the general population, among individuals aged 30-65, there was an upward trend. However, for secondary GN, DN increased significantly while lupus nephritis (LN) showed a downward trend. Additionally, there were significant differences in the age-distribution between DN and IgAN, DN and minimal change disease (MCD), IgAN and MN, and MN and MCD. The epidemiological trend of renal diseases has changed significantly over time. Although the proportion of primary GN has shown a downward trend, it remained the predominant component, with secondary GN ranking second, and combined nephropathy showing a significant increase. Among primary GN, IgAN was the most common type in the study, followed by MN. However, for secondary GN, from period 1 to period 2, DN gradually surpassed LN to become the most common disease type.

BACKGROUND AND AIMS:Sleep disturbances are linked to individual cardiometabolic diseases, but their association with the emerging cardiovascular-kidney-metabolic (CKM) syndrome, a constellation of interrelated conditions, remains less clear. To evaluate the association of sleep factors (sleep duration, diagnosed sleep disorder, self-reported trouble sleeping) with the risk of CKM syndrome. METHODS AND RESULTS:We included 11,949 adults from the National Health and Nutrition Examination Survey (NHANES). A composite sleep score (0-3, from healthy to poor) was derived from sleep duration, diagnosed sleep disorder, and self-reported trouble sleeping. CKM syndrome was defined and staged (Stage 0-4) based on the coexistence and severity of cardiometabolic and kidney diseases. Systemic inflammation was assessed using the systemic immune-inflammation index (SII) and systemic inflammation response index (SIRI). A poor sleep pattern was significantly associated with higher odds of CKM syndrome (fully adjusted odds ratio [OR] = 1.64, 95% confidence interval (CI): 1.37-1.95) and with more advanced CKM stages in an ordinal model, indicating a dose-response relationship. In exploratory mediation analysis, SII and SIRI appeared to partially mediate the association between self-reported trouble sleeping and CKM syndrome in initial models. However, this mediating effect was substantially attenuated and became nonsignificant for SII after comprehensive adjustment for adiposity (body mass index (BMI) and waist circumference) and lifestyle factors. CONCLUSIONS:Poor sleep patterns are robustly associated with an increased risk and severity of CKM syndrome. While systemic inflammation was correlated with both sleep disturbances and CKM, its role as an independent mediator was largely explained by shared variance with obesity and metabolic factors. These findings underscore sleep health as a potential target for multimodal risk reduction within the CKM framework, though causality needs confirmation in longitudinal studies.

The objective of this completed, randomized, open-label trial across 11 hemodialysis centers in Shanghai, China, was to evaluate whether hemoadsorption combined with hemodialysis (HAHD) reduces mortality compared to hemodialysis (HD) alone in end-stage kidney disease patients (maintenance HD ≥ 3 months, Kt/V ≥ 1.2). We randomized 1362 patients 1:1 to receive HAHD (n = 683) or HD alone (n = 679; mainly low-flux HD plus intermittent HDF). All 1362 randomized patients were analyzed. The primary outcome was all-cause mortality, while secondary outcomes included cardiovascular mortality and major cardiovascular events. Over a median follow-up of 39.5 months, all-cause mortality occurred in 117 (17.1%) of HAHD patients compared to 144 (21.2%) of HD patients (hazard ratio [HR]: 0.778, 95% confidence interval [CI]: 0.609-0.994; P = 0.045). HAHD also significantly reduced cardiovascular mortality (HR: 0.659, 95% CI: 0.481-0.901; P = 0.009) and major cardiovascular events (HR: 0.772, 95% CI: 0.621-0.959; P = 0.019). Important adverse events, primarily infections and abnormal blood pressure, were comparable between the two groups. Adding hemoadsorption significantly reduced all-cause mortality, cardiovascular mortality, and major cardiovascular events compared to HD alone (mainly low-flux HD plus intermittent HDF). Trial Registration: ClinicalTrials.gov NCT03227770.

Patients receiving maintenance hemodialysis (MHD) experience a high mortality burden, with cardiovascular disease remaining a major cause of death. This study aimed to evaluate the association between adjunctive hemoperfusion combined with conventional hemodialysis (HD + HP) and long-term survival outcomes in patients receiving MHD. This single-center retrospective cohort study was conducted at Shanghai Changhai Hospital. Patients with end-stage renal disease who received MHD between January 2015 and December 2023 were retrospectively identified from the center’s hemodialysis records. Among the 640 eligible patients, 419 (65.5

Diabetic kidney disease (DKD) is a common complication, affecting approximately 40% of patients with diabetes and imposing substantial health and economic burdens worldwide. As DKD prevalence rises, existing treatments remain limited in efficacy, necessitating innovative therapeutic strategies. Soluble guanylate cyclase (sGC) modulators, including activators and stimulators, have emerged as promising treatments by enhancing cyclic guanosine monophosphate production, thereby exerting vasodilatory, anti-inflammatory, and anti-fibrotic effects. Preclinical studies have demonstrated their efficacy in improving renal function and reducing proteinuria in DKD models. Notably, clinical trials involving sGC activators, such as avenicguat, suggest potential benefits in managing DKD, particularly in combination with renin-angiotensin-aldosterone system inhibitors. While initial findings indicate renal protection and good tolerability, further large-scale studies are needed to confirm long-term efficacy and safety. The development of sGC modulators offers hope for improving DKD outcomes and reducing its global healthcare burden.

Objective Maintenance hemodialysis (MHD) patients face a high risk of mortality. This study aimed to identify factors associated with mortality and assess the survival benefit of hemodialysis combined with hemoperfusion (HD + HP) using HA130/KHA80 cartridges in MHD patients. Methods A single-center retrospective cohort study was conducted at Shanghai Changhai Hospital, enrolling 640 MHD patients treated from January 2015 to December 2023. Clinical data were extracted from electronic medical records and hemodialysis management systems. Patients were stratified into HD alone (n = 419) and HD + HP (n = 221) groups. Univariate and multivariate logistic regression were used to identify factors associated with all-cause mortality. Time-dependent Cox regression (with HP as a time-varying covariate) was applied to evaluate the association between HP exposure and mortality. Propensity score matching (1:1, caliper width = 0.02) was performed based on sex, age, primary renal disease, vascular access, and comorbidities, yielding 173 balanced patients per group. Simon–Makuch curves and Mantel–Byar tests were used for survival analysis. Results Diabetic kidney disease (DKD) was the most common primary renal disease (30.9%). The overall all-cause mortality rate was 54.4%, and cardiovascular disease was the leading cause of death (32.8%). Exploratory logistic regression identified older age, higher red blood cell distribution width (RDW), DKD, and elevated creatine kinase-MB (CK-MB) as factors associated with increased all-cause mortality, while higher chloride (Cl), total protein (TP), prealbumin (PAB), hemoglobin (HB), and HD + HP therapy were associated with lower mortality (all P < 0.05). As the primary analytical approach for time-to-event outcomes, time-dependent Cox regression showed that HP exposure was associated with a 25% reduction in all-cause mortality after adjustment for confounders (HR = 0.75; 95% CI: 0.58–0.98; P = 0.03). After propensity score matching, HD + HP significantly reduced both all-cause mortality (31.2% vs 64.2%) and cardiovascular mortality compared with HD alone (Mantel–Byar test: P = 0.032 and P = 0.003, respectively). Conclusion Cardiovascular disease is the leading cause of death in MHD patients. HD + HP therapy is associated with a reduced risk of all-cause and cardiovascular mortality in MHD patients, supporting its potential as a strategy to improve survival in this high-risk population.

Macrophage-driven inflammation is central to the pathogenesis of sepsis-induced acute kidney injury (SI-AKI), yet the role of RNA-binding proteins (RBPs) in post-transcriptionally regulating this process remains elusive. Here, we identify the RBP zinc finger X-linked duplicated B (ZXDB) as an upstream contributor to SI-AKI by promoting a pathogenic, pro-inflammatory macrophage activation state. We found that ZXDB expression is consistently elevated in M1-like macrophages within the kidney during SI-AKI, where it stimulates pro-inflammatory cytokine secretion and glycolytic reprogramming. Mechanistically, we discovered that ZXDB directly interacts with EIF4A3, a core exon junction complex (EJC) DEAD-box RNA helicase, via its aa151-300 region, thereby enhancing ACACA 5 ' UTR-dependent translation of ACACA, a metabolic enzyme that mediates downstream pathogenic effects associated with ZXDB activation. Critically, macrophage-specific deletion of Zxdb attenuated disease severity in a mouse model of SI-AKI, preserving renal function and attenuating inflammation. Taken together, our study uncovers a novel ZXDB-EIF4A3-ACACA axis that orchestrates macrophage-mediated kidney injury through translational control of metabolism, thereby suggesting ZXDB as a potential therapeutic candidate for SI-AKI.

BACKGROUND:Several cytokine levels in dialysate, particularly interleukin-6 (IL-6), have been investigated as potential biomarkers for peritoneal solute transport rate (PSTR). However, studies examining the relationship between systemic cytokine levels and PSTR have yielded contradictory results. In this study, we aimed to assess 12 kinds of cytokines in serum and explore their potential relationship with peritoneal transport function. METHODS:Patients undergoing peritoneal dialysis (PD) from September 2022 to September 2024 were retrospectively analyzed at our PD center. The patients were categorized into fast and non-fast PSTR groups based on the 4-h dialysate creatinine /plasma creatinine ratio (D/P Cr). The systemic levels of 12 cytokines (IL-1β, IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12p70, IL-17 A, TNF-α, IFN-α, and IFN-γ) in both groups were measured using flow cytometry and compared. The relationship between serum cytokine levels and baseline peritoneal transport status was analyzed by univariate and multivariate logistic regression analyses. RESULTS:A total of 284 patients were enrolled in this study. According to the D/P Cr, 171 patients (60.2 %) were classified as non-fast PSTR group, while 113 patients (39.8 %) were classified as fast PSTR group. Among the 12 cytokines analyzed, serum IL-8 exhibited a significant difference between the two groups (P = 0.01). IL-8/IL-10 and IL-12p70/IL-10 ratios were also significantly higher in fast PSTR group. In the subgroup of incident PD patients, multivariate analysis revealed that total cholesterol (OR 0.559, 95 % CI 0.323-0.966, P = 0.037) and serum IL-8 (OR 1.040, 95 % CI 1.006-1.075, P = 0.021) were significantly and independently associated with baseline fast PSTR. CONCLUSION:The systemic IL-8 level is positively correlated with PSTR in patients undergoing PD, which may serve as an indicator of baseline peritoneal transport function.

OBJECTIVES:Bisphosphonate-related osteonecrosis of the jaw (BRONJ) is a severe complication of bisphosphonate therapy, with unclear mechanisms. This study investigates the regulatory impact of zoledronic acid (ZOL) on osteoclasts and microRNA (miRNA) expression. MATERIALS AND METHODS:Raw264.7 cells and bone marrow-derived macrophages (BMMs) were used to assess ZOL's effects on proliferation and apoptosis. miRNA array analysis was performed during osteoclastogenesis with ZOL treatment. The role of miR-483-5p was examined using miR-mimics and miR-inhibitors. A rat BRONJ model was established for in vivo validation. RESULTS:A concentration of 2 μM ZOL, which did not affect cell proliferation or apoptosis, was used in subsequent experiments. ZOL altered the expression of 64 miRNAs (39 upregulated, 25 downregulated). miR-483-5p mimics alleviated ZOL-induced inhibition of osteoclastogenesis, actin ring formation, bone resorption, and differentiation marker expression, whereas inhibitors enhanced these effects. In vivo, Ago-miR-483-5p promoted wound healing in the BRONJ model, while Antago-miR-483-5p impaired it. CONCLUSIONS:ZOL modulates osteoclast function in BRONJ through miR-483-5p inhibition. miR-483-5p may serve as a novel therapeutic target for BRONJ treatment, providing new insights into managing this complication.

Introduction Haemodialysis (HD) is an essential treatment for end-stage renal disease patients to improve their quality of life. However, conventional HD may not effectively remove medium and large molecules and protein-bound toxins, leading to the occurrence of various complications. Haemoadsorption (HA), on the other hand, can address this limitation. Therefore, a multicentre, open-label, randomised, parallel controlled study will be conducted to compare HA combined with HD (HAHD) with HD alone in maintenance haemodialysis (MHD) patients. The primary endpoint is the change in serum β2-MG, PTH and CRP values.Methods and analysis We plan to enrol 410 MHD patients from 10 participating medical centres in Shanghai. Patients will experience a 4-week washout period and a 52-week observation period. After the washout period, the eligible patients will be randomised in a 1:1 ratio to the two groups: the control group, 3 times/week conventional HD treatment; and the experiment group, 3 times/week conventional HD treatment+1 time/week HA treatment. The baseline and follow-up data at 0, 4, 12, 24, 36 and 52 weeks were collected from both groups, including the following: medical history, routine physical examination, dialysis regimen, laboratory tests, dialysis adequacy as defined by standard Kt/V, chest X-ray, ECG, cardiac ultrasound and three scales. Comorbidities, combined medications and adverse events will also be captured. The primary outcomes will include change in serum β2-MG, PTH and CRP values. Secondary outcomes will include change values for serum protein-bound toxins, improvement in patient quality of life, sleep disturbance and pruritus.Ethics and dissemination The protocol has been approved by the Ethics Committees of 10 participating medical centres. Shanghai Changhai Hospital Ethics Committee will oversee the study. The results will be presented at national and international academic meetings, and publications will be submitted to peer-reviewed journals.Trial registration number NCT05639010.

JOURNAL/mgres/04.03/01612956-202606000-00004/figure1/v/2025-08-18T154854Z/r/image-tiff Hydrogen sulfide (H2S) holds significant potential for clinical applications in the alleviation of fibrosis. This study aimed to verify the role of H2S in combating peritoneal fibrosis and elucidate its molecular mechanisms. A peritoneal fibrosis model was established through the intraperitoneal injection of 0.1% chlorhexidine gluconate. Subsequently, the mice were administered an intraperitoneal injection of the H2S donor GYY4137. The experimental data indicate that H2S mitigates the progression of peritoneal fibrosis, potentially by inhibiting the expression of high mobility group box-1 and consequently blocking the activation of the (TGF-β)/Smad3 signaling pathway. This study provides a scientific basis for the future clinical application of H2S in the treatment of peritoneal fibrosis.

Introduction Different roxadustat starting doses are used for anemia in chronic kidney disease (CKD) treatment. We tested the non-inferiority of weight-based lower starting dose to standard starting dose roxadustat for anemia in stage 3–5 CKD without dialysis. Methods Patients were randomized (1:1) and stratified by CKD stage to receive weight-based standard (<60 kg: 70 mg three times per week [TIW]; ≥60 kg: 100 mg TIW) or one-step-lower (<60 kg: 50 mg TIW; ≥60 kg: 70 mg TIW) roxadustat starting dose for 16 weeks. The primary endpoint was mean hemoglobin change from baseline over weeks 12–16. Secondary endpoints included the proportion achieving hemoglobin 100–120 g/L, hemoglobin variability, and rescue therapy. Results Overall, 254 patients were randomized. The mean (standard deviation) baseline hemoglobin was 89.88 (6.90) g/L. Most patients had stage 4 (39.0%) or 5 (40.2%) CKD. Mean hemoglobin increased from baseline at weeks 12–16 (lower: 21.57 g/L; standard: 26.35 g/L), but non-inferiority was not met. A comparable proportion achieved hemoglobin 100–120 g/L (lower: 46.0%; standard: 47.2%). The hemoglobin increase was comparable in CKD stage 3–4, but less with the lower dose in CKD stage 5 (17.28 vs. 26.71 g/L). The lower dose exhibited a lower hemoglobin rate of change (lower: 2.917; standard: 3.376) and less drug exposure. Drug-related adverse event rates were comparable. Conclusion The proportion of patients who achieved the hemoglobin target was comparable between the doses. The lower starting dose had less hemoglobin fluctuation and is recommended for stage 3–4 CKD.

Telitacicept, a B lymphocyte stimulator/A proliferation-inducing ligand dual-target fusion protein, mainly used for IgA nephropathy and systemic lupus erythematosus. We present two cases where adult patients with IgA vasculitis (IgAV) nephritis were successfully treated with Telitacicept, experienced no adverse reactions during the follow-up. Therefore, Telitacicept represents a promising additional treatment option for patients suffering from IgA vasculitis (IgAV).

Background:This study investigated predictive factors and personality determinants of kinesiophobia (fear of movement) in dialysis patients. Methods: Using the Chinese versions of the Ten-Item Personality Inventory (TIPI-C) and Tampa Scale for Kinesiophobia Heart (TSK-SV heart), we assessed 329 patients from December 2022 to February 2023. The influencing factors of fear of movement were identified by univariate analysis and multiple linear regression. Results:The mean score of fear of movement for dialysis patients was 45.128 (45.128 ± 7.023). Multiple linear regression revealed that advanced age,local medical insurance, and lower education significantly predicted higher kinesiophobia scores, while exercise habits, being married, alcohol and tobacco use served as protective factors. Personality analysis demonstrated that lower extraversion, emotional stability, and conscientiousness were associated with greater kinesiophobia. Conclusions:Personality determinants were significantly associated with fear of movement. These findings emphasize the clinical utility of personality assessment in identifying high-risk patients and personalizing rehabilitation strategies for this vulnerable population.

Introduction: Different starting doses of roxadustat are used for treating anemia in chronic kidney disease (CKD). We tested the noninferiority of weight-based lower starting dose compared with standard starting dose roxadustat for anemia in stage 3 to 5 CKD without dialysis. Methods: Patients were randomized (1:1) and stratified by CKD stage to receive weight-based standard (< 60 kg: 70 mg 3 times per week [TIW]; >= 60 kg: 100 mg TIW) or 1-step-lower (< 60 kg: 50 mg TIW; >= 60 kg: 70 mg TIW) roxadustat starting dose for 16 weeks. The primary endpoint was mean hemoglobin change from baseline over weeks 12 to 16. The secondary endpoints included the proportion achieving hemoglobin 100 to 120 g/l, hemoglobin variability, and rescue therapy. Results: Overall, 254 patients were randomized. The mean (SD) baseline hemoglobin was 89.88 (6.90) g/l. Most patients had stage 4 (39.0%) or stage 5 (40.2%) CKD. Mean hemoglobin increased from baseline at weeks 12 to 16 (lower: 21.57 g/l; standard: 26.35 g/l), but noninferiority was not met. A comparable proportion achieved hemoglobin of 100 to 120 g/l (lower: 46.0%; standard: 47.2%). The hemoglobin increase was comparable in CKD stage 3 to 4, but less with the lower dose in CKD stage 5 (17.28 vs. 26.71 g/l). The lower dose exhibited a lower hemoglobin rate of change (lower: 2.917; standard: 3.376) and less drug exposure. Drug-related adverse event rates were comparable. Conclusion: The proportion of patients who achieved the hemoglobin target was comparable between the doses. The lower starting dose had less hemoglobin fluctuation and is recommended for stage 3 to 4 CKD.

BACKGROUND:Chronic inflammation is well recognized as a key factor related to renal function deterioration in patients with diabetic kidney disease (DKD). Neutrophil extracellular traps (NETs) play an important role in amplifying inflammation. With respect to NET-related genes, the aim of this study was to explore the mechanism of DKD progression and therefore identify potential intervention targets. METHODS:Hub NET-related DEGs were screened via differential expression analysis and three machine learning methods, namely, LASSO, SVM-RFE and random forest. Consensus clustering was performed to analyze NET-related subtypes in DKD patients. KEGG enrichment analysis, GSEA, GSVA, ssGSEA and ESTIMATE were conducted to explore the molecular features of DKD patient subtypes. Leveraging single-nucleus RNA-seq datasets, the "scissor" and "bisqueRNA" algorithms were applied to identify the composition of renal cell types in DKD patient subtypes. Soft clustering analysis was performed to obtain gene groups with similar expression patterns during the development and progression of DKD. The correlations between hub NET-related DEGs and clinical parameters were mined from the Nephroseq V5 database. The core gene among the hub NET-related DEGs was selected by calculating semantic similarity. "Cellchat" algorithm, immunostaining, ELISA and flow cytometry were performed to explore the expression and function of the core gene. The Drug-Gene Interaction Database (DGIdb) was searched to identify candidate drugs. RESULTS:Six hub NET-related DEGs, namely, ACTN1, ITGB2, IL33, HRG, NFIL3 and CLEC4E, were identified. On the basis of these 6 genes, DKD patients were classified into 2 clusters. Cluster 1 patients, with higher NET scores, were evidently more immune-activating than those of cluster 2. Markedly increased numbers of immune cells, fibroblasts and proinflammatory proximal tubular cells were observed in cluster 1 but not in cluster 2. Cluster 1 also represented a more clinically advanced disease state. Among the 6 hub NET-related DEGs, the mRNA expression of ACTN1, ITGB2, IL33 and HRG was correlated with the eGFR. By semantic similarity analysis, IL33 was considered a central gene among the 6 genes. Cell-cell communication analysis further indicated that intercellular interactions via IL-33 were enhanced in DKD. Serum IL-33 concentration was negatively correlated with eGFR. IHC staining revealed that IL-33 expression was upregulated in the tubular epithelium in DKD patients. Supernatants from inflammatory tubular epithelial cells can increase MPO in neutrophils, whereas addition of anti-IL-33 antibody attenuated this phenotype. CONCLUSIONS:We identified 2 distinct NET-related subtypes in DKD patients, in which one subgroup was apparently more inflammatory and associated with a more severe clinical state. A significantly increased level of IL-33 in this inflammatory patient subgroup may play a role in aggravating inflammation via the IL-33-ST2 axis.

LN is a serious complication of systemic lupus erythematosus (SLE), affecting up to 60% of patients with SLE and may lead to end-stage renal disease (ESRD). Macrophages play multifaceted roles in the pathogenesis of LN, including clearance of immune complexes, antigen presentation, regulation of inflammation, and tissue repair. Macrophages are abundant in the glomeruli and tubulointerstitium of LN patients and are positively correlated with serum creatinine levels and the severity of renal pathology. It has been shown that the infiltration of macrophages is closely associated with several clinical indicators, such as serum creatinine and complement C3 levels, anti-dsDNA antibody titers, Austin score, interstitial fibrosis and renal tubular atrophy. Moreover, cytokines expressed by macrophages were upregulated at LN onset and downregulated after remission, suggesting that macrophages may serve as markers of LN pathogenesis and remission. Therapies targeting macrophages have been shown to alleviate LN. There are two main types of macrophages in the kidney: kidney-resident macrophages (KRMs) and monocyte-derived macrophages (MDMs). KRMs and MDMs play different pathological roles in LN, with KRMs promoting leukocyte recruitment at sites of inflammation by expressing monocyte chemokines, while MDMs may exacerbate autoimmune responses by presenting immune complex antigens. Macrophages exhibit high plasticity and can differentiate into various phenotypes in response to distinct environmental stimuli. M1 (proinflammatory) macrophages are linked to the progression of active SLE, whereas the M2 (anti-inflammatory) phenotype is observed during the remission phase of LN. The polarization of macrophages in LN can be manipulated through multiple pathways, such as the modulation of signaling cascades including TLR 2/1, S1P, ERS, metabolic reprogramming, and HMGB1. This paper provides a comprehensive overview of the role of macrophages in the progression of lupus nephritis (LN), and elucidates how these cells and their secretory products function as indicators and therapeutic targets for the disease in the context of diagnosis and treatment of LN.

Renal injury, a prevalent clinical outcome with multifactorial etiology, imposes a substantial burden on society. Currently, there remains a lack of effective management and treatments. Extensive research has emphasized the diverse biological effects of natural polysaccharides, which exhibit promising potential for mitigating renal damage. This review commences with the pathogenesis of four common renal diseases and the shared mechanisms underlying renal injury. The renoprotective roles of polysaccharides in vivo and in vitro are summarized in the following five aspects: anti-oxidative stress effects, anti-apoptotic effects, anti-inflammatory effects, anti-fibrotic effects, and gut modulatory effects. Furthermore, we explore the structure-activity relationship and bioavailability of polysaccharides in relation to renal injury, as well as investigate their utility as biomaterials for alleviating renal injury. The clinical experiments of polysaccharides applied to patients with chronic kidney disease are also reviewed. Broadly, this review provides a comprehensive perspective on the research direction of natural polysaccharides in the context of renal injury, with the primary aim to serve as a reference for the clinical development of polysaccharides as pharmaceuticals and prebiotics for the treatment of kidney diseases.

Object: The association between magnesium depletion score (MDS) and kidney stone disease (KSD) remains unknown. This study was designed to investigate the association of MDS with KSD in adults. Methods: A total of 19,654 participants were enrolled from the National Health and Nutrition Examination Surveys (NHANES). The MDS was calculated by assessing four aspects, including alcohol assumption, renal function, and use of diuretics and proton pump inhibitor. Multivariable logistic regressions were performed to explore the associations between MDS and the prevalence of KSD. Linear correlations were conducted explore the relationship of testosterone with MDS. Results: In the multivariable logistic regressions with full adjustment for confounding variables, the odds ratio of MDS associating with KSD was 1.28 (95% CI: 1.04-1.58, P = 0.022) in total population, and 1.70 (95% CI: 1.16-2.50, P=0.007) in female participants. Besides, compared to the lowest MDS, the highest MDS was associated with a lower testosterone (beta = -16.39, P=0.009) after full adjustment in non-menopause women. Conclusion: This study highlighted a positive correlation of high MDS with KSD in female population, which may be associated low level of serum testosterone.