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.

This prospective, randomized, double-blind, placebo-controlled trial investigated the efficacy and safety of thiamin and folic acid for cognitive impairment in maintenance hemodialysis (MHD) patients. A total of 215 MHD patients aged 18-75 with cognitive impairment were randomized to receive either oral thiamin (90 mg/day) plus folic acid (30 mg/day) or a placebo for 96 weeks. The primary endpoint was the change in the Alzheimer's Disease Assessment Scale-Cognitive section (ADAS-Cog) score. After 96 weeks, the treatment group showed a significant improvement in ADAS-Cog scores (from 21.25 ± 9.2 to 15.07 ± 8.38, p < 0.001), whereas the placebo group showed a non‑significant improvement (from 24.53 ± 11.01 to 26.53 ± 14.43, p = 0.077). The treatment group also demonstrated significantly increased blood levels of thiamin (from 5.59 ± 0.95 to 18.21 ± 3.91 ng/mL) and folate (from 12.37 ± 4.62 to 63.33 ± 16.02 ng/mL), and a reduction in homocysteine levels (from 4709.06 ± 353.15 to 2962.68 ± 158.87 ng/mL, p < 0.001), with no significant changes in the placebo group. While mortality was similar between the two groups (12.1% vs. 12.0%, p = 0.978), the incidence of adverse events was significantly lower in the treatment group (31.8% vs. 62.0%, p = 0.0017), particularly cardiovascular and cerebrovascular events (13.1% vs. 25.9%, p = 0.001). The study concludes that combined thiamin and folic acid supplementation improves cognitive function in MHD patients with a favorable safety profile.

Emerging insights into lactate‑mediated protein lactylation illuminate novel regulatory axes in the pathogenesis of diabetic nephropathy (DN). While histone lactylation has established epigenetic associations with metabolic memory, expanding proteomic evidence reveals dynamic lactylation landscapes across extracellular matrix components, inflammatory mediators and redox regulators in renal compartments. The present review systematically catalogues DN‑relevant histones and non‑histone substrates undergoing functional lactylation, while mechanistically dissecting how hyperglycemia‑fueled lactate flux drives DN through lactate‑mediated protein modification landscapes. The present review further delineates the progress of research on the potential regulatory mechanisms involved in DN and delve into the possible functions and related mechanisms. This mechanistic reappraisal establishes lactylation topology mapping as a prerequisite for developing precision modulation approaches in DN management.

Objective·To investigate the mechanism by which wingless-type MMTV integration site family member 5A (WNT5A) promotes the transition from ischemia-reperfusion injury (IRI)-induced acute kidney injury (AKI) to chronic kidney disease (CKD).Methods·An IRI-induced AKI-to-CKD transition model was established in wild-type (WT) mice. Renal histopathological injury was assessed by hematoxylin-eosin (H-E) staining on the 3rd and the 14th day after IRI. Fibrosis was evaluated by Masson staining and immunohistochemistry for collagen type Ⅰ α1 chain (COL1A1). Wnt5a expression was quantified by RNA sequencing (RNA-seq), real-time quantitative PCR (qPCR), and Western blotting. Wnt5a heterozygous knockout (Wnt5a+/-) mice were used to establish the IRI-induced AKI-to-CKD transition model. Renal function was evaluated by serum creatinine (Scr) and blood urea nitrogen (BUN), and renal injury and fibrosis were assessed as described above. In vitro, a transforming growth factor-β (TGF-β)-induced fibrotic model was established in HK-2 cells (a human renal cortex proximal tubular epithelial cell line) with WNT5A overexpression. Differentially expressed genes identified by RNA-seq were subjected to Gene Ontology (GO) biological process enrichment analysis to identify key targets. Regulation of forkhead box protein P1 (FOXP1) by WNT5A was validated by qPCR and Western blotting. FOXP1 was overexpressed, or silenced in the context of WNT5A overexpression in HK-2 cells. Expression levels of notch receptor 2 (NOTCH2) pathway components, including NOTCH2, hairy/enhancer-of-split related with YRPW motif 1 (HEY1), and hairy and enhancer of split 1 (HES1), as well as fibrosis markers, including COL1A1 and vimentin (VIM), were analyzed by qPCR and Western blotting.Results·Wnt5a expression was increased in the renal tissue on the 3rd day after IRI, accompanied by marked tubular dilation and inflammatory cell infiltration. On the 14th day, Wnt5a expression was further increased, along with significant upregulation of fibrotic markers. Compared with WT mice, Wnt5a+/- mice exhibited reduced Scr and BUN levels on the 14th day after IRI, indicating improved renal function. FOXP1 expression was decreased, and tubular injury and renal fibrosis were attenuated in Wnt5a+/- mice. Mechanistically, WNT5A overexpression markedly upregulated FOXP1 in TGF-β-treated HK-2 cells. RNA-seq and GO analysis indicated significant enrichment of fibrosis-related processes and activation of the NOTCH signaling pathway. FOXP1 overexpression increased the mRNA and protein levels of NOTCH2 and its downstream targets HEY1 and HES1, along with elevated COL1A1 and VIM expression. In contrast, silencing FOXP1 in WNT5A-overexpressing cells reversed the upregulation of NOTCH2 pathway components and fibrosis markers.Conclusion·WNT5A upregulates the transcription factor FOXP1, which activates the NOTCH2 signaling pathway, thereby accelerating the IRI-induced AKI-to-CKD transition, and promoting renal fibrosis progression.

Chronic diabetic wounds pose a significant clinical challenge due to their complex pathophysiology and limited treatment options. In this study, we developed a dual-pronged glycopeptide hydrogel (OPAD-M) based on oxidized glucomannan (OGM) and poly (γ-glutamic acid) grafted with hydrazide and dopamine groups (PAD), incorporating bioactive Mg2+ ions. The OPAD-M hydrogel exhibits excellent porosity, self-healing, and adhesive properties owing to the dynamic covalent Schiff base bonds and metal-coordination interactions within its crosslinked network. In vitro, the screened OPAD-M hydrogel inhibited pro-inflammatory factors expression, promoted cell migration and angiogenesis via PI3K/AKT pathways. Furthermore, the new mechanism revealed that the OPAD-M hydrogel accelerated angiogenesis by upregulating the expression of glycolysis-related genes, resulting in collagen deposition and rapid wound closure in diabetic wound mice. Collectively, these findings underscore the potential of the OPAD-M hydrogel as a promising strategy for metabolic modulation and effective diabetic wound healing in diverse clinical applications.

Introduction:This study evaluated the clinicopathological profiles and prognostic trajectories of nondiabetic renal disease (NDRD) subtypes coexisting with type 2 diabetes mellitus (T2D). Methods:The study cohort comprised of 123 patients with predominant NDRD subtypes: IgA nephropathy (T2D-IgAN, n = 52), membranous nephropathy (T2D-MN, n = 48), and podocytopathies (T2D-Podo, n = 23). Multivariate Cox regression was used to identify prognostic factors for renal outcomes over a median follow-up period of 80 months (interquartile range 62-102). Results:T2D-MN patients exhibited distinct characteristics compared to T2D-IgAN and T2D-Podo, including advanced age, higher incidence of nephrotic-range proteinuria and elevated total cholesterol. This group also demonstrated a greater susceptibility to atherosclerotic plaque formation. Pathological analysis revealed more severe glomerular sclerosis, interstitial inflammation, and C3 deposition in T2D-IgAN. Multivariate Cox regression identified three independent predictors of renal endpoints: glomerular C3 deposition (HR 3.021, 95% CI: 1.084-8.419), preserved estimated glomerular filtration rate (>60 mL/min/1.73 m2; HR 0.296, 95% CI: 0.110-0.796), and prolonged T2D duration (>10 years; HR 4.168, 95% CI: 1.389-12.503). Conclusion:These findings suggest that integrating clinical and pathological parameters enhances the prognostic accuracy of NDRD in patients with diabetes, enabling timely therapeutic interventions to mitigate complications in high-risk cases.

Patients with chronic kidney disease (CKD) are at an increased risk of lipid perturbation. A diminished capacity of kidney beta-oxidation results in fatty acid accumulation, which drives CKD progression. Based on the publications in the Web of Science Core Collection (WoSCC) from 1999 to 2023, this study conducted a bibliometric analysis of this field, aiming to understand its development trend and frontier and provide basic information and potential points for in-depth exploration. All articles on lipid metabolism in CKD published between January 1, 1999, and October 10, 2023, were collected and identified in WoSCC. Bibliometric analysis was performed using Excel 2019, CiteSpace, VOSviewer, and the Bibliometricsx R package (R-Studio). A total of 1,201 articles in WoSCC met our criteria. Analysis results show that the number of publications and citations in this field has been increasing annually. The University of California, Irvine of the United States is the institution with the highest number of citations, and total link strength. Nosratola D. Vaziri is one of the most important scholars in this field, and Kidney International is the most authoritative journal. Keywords and references analysis indicate that dysregulation of lipid perturbation contributes to the progression of CKD. Inflammation and ferroptosis play a key role in regulating lipid metabolism. Furthermore, lipidomics is the principal tool for dissecting dysregulated lipid metabolism. This study revealed trends in research and public interest in lipid metabolism in CKD. Our findings suggest that the field is growing rapidly, and future research hot spots might focus on deeper exploration of the molecular mechanism, application of metabolomics, and clinical therapy, which may pave the way for further research.

Background Fluid retention and the obesity paradox often mask true muscle wasting in patients with proteinuric chronic kidney disease (CKD), and conventional quantity-based metrics such as body mass index or cross-sectional tissue area fail to capture this. We asked whether tissue radiodensity, a quality-based measure, is more sensitive to proteinuric injury than volumetric indices, and examined the role of “0 HU drift”—the convergence of tissue attenuation toward water density—as an early signal of metabolic remodeling. Methods We retrospectively analyzed 1,416 CKD patients grouped by urinary albumin-to-creatinine ratio (KDIGO stages A1–A3). A custom 2D U-Net segmented muscle and adipose compartments on non-contrast CT at the T12 level. Monotonic trends across stages were tested with the Jonckheere–Terpstra test. We built a three-step hierarchical linear regression model to link visceral fat mean attenuation (VF-HU) to proteinuria severity, adjusting stepwise for demographics, BMI, comorbidities, eGFR, and serum albumin. Binary logistic regression tested VF-HU as a predictor of sarcopenia tendency. Results Quality metrics clearly outperformed quantity metrics in tracking proteinuria severity. Subcutaneous fat area did not change across KDIGO stages (P = 0.541), yet its mean attenuation rose significantly toward 0 HU (Z = 4.738, P < 0.001), a pattern consistent with progressive fluid infiltration. VF-HU climbed (visceral fat “whitening”) and skeletal muscle density fell (myosteatosis) as proteinuria worsened. After adjusting for serum albumin, eGFR, and comorbidities, VF-HU remained linked to proteinuria severity (standardized β = 0.16, P = 0.015), which argues against a pure edema artifact and points to genuine adipose remodeling. In the logistic model, each 1-HU rise in VF-HU raised the odds of sarcopenia tendency by 11.6% (OR 1.116, 95% CI 1.097–1.135, P = 0.002); eGFR did not reach significance (P = 0.418). Conclusions At the T12 level, radiodensity metrics discriminated proteinuria stages better than volumetric indices. VF-HU was independently tied to both disease severity and low muscle quality, making it a candidate marker for metabolic risk stratification. Because routine chest CT already captures T12, AI-based opportunistic screening of tissue quality is feasible in clinical practice. Longitudinal work is now needed to test whether qualitative changes truly precede volumetric loss and to confirm their prognostic value.

Purpose We examined whether chest CT-derived visceral adipose tissue attenuation (VAT_Hu), an imaging marker of adipose tissue quality, was associated with anemia and hypoalbuminemia in adults with non-dialysis chronic kidney disease (CKD) stages 1–4. Methods In this retrospective cross-sectional study, 2,817 adults with CKD stages 1–4 who underwent chest CT and had available clinical and laboratory data were included. VAT_Hu was analyzed per standard deviation (SD) increase and by quartiles. The primary outcomes were anemia and hypoalbuminemia. Multivariable logistic and linear regression models adjusted for age, sex, body mass index, systolic blood pressure, smoking, alcohol use, diabetes, hypertension, estimated glomerular filtration rate, albuminuria, and albuminuria source. Results VAT_Hu was available in 2,803 participants. Mean age was 64.4 ± 10.8 years, 63.4% were men, 30.5% had anemia, and 10.7% had hypoalbuminemia. Each 1-SD increase in VAT_Hu was associated with higher odds of anemia (OR 1.47, 95% CI 1.33–1.62) and hypoalbuminemia (OR 1.60, 95% CI 1.39–1.84). Compared with the lowest quartile, the highest quartile was associated with higher odds of anemia (OR 2.26, 95% CI 1.71–2.98) and hypoalbuminemia (OR 2.80, 95% CI 1.80–4.36). Higher VAT_Hu was also associated with lower hemoglobin and serum albumin independent of visceral adipose tissue area. Conclusion Higher chest CT-derived VAT attenuation was independently associated with anemia and hypoalbuminemia in non-dialysis CKD stages 1–4, suggesting that CT-derived adipose tissue quality may provide information beyond adipose quantity alone.

Background & Aims The purpose of this study was to assess the association between N-terminal prohormone of type B natriuretic peptide (NT-proBNP) and long-term mortality in hospitalized oldest-old adults and to explore the mediating role of malnutrition and muscle loss. Methods This prospective cohort study was conducted among 360 hospitalized patients ≥ 80 years of age (median age 87 [IQR 84–90] years, 24.4% women) in the Department of Geriatrics. The Geriatric Nutritional Risk Index (GNRI) and Mini Nutritional Assessment Short Form (MNA-SF) were used for nutritional assessment, while calf circumference was used as a measure of muscle mass. A Cox proportional hazard model was used to assess the relationship between NT-proBNP levels and mortality. Mediation analysis was used to explore the mediating effects of malnutrition and muscle loss. Results The median follow-up was 4.1 years with 159 (44.1%) deaths. Mortality risk increased by 32% per 2-fold increase in NT-proBNP levels (full adjusted hazard ratio: 1.32 [95% CI, 1.20–1.46]). A mediation analysis showed that a lower GNRI score and decreased calf circumference mediated the effects of high NT-proBNP and mortality risk, with an estimated relative effect size of 28.9%, while MNA-SF and calf circumference mediated the effect, with an estimated relative effect size of 25.3%. Conclusions NT-proBNP levels were associated with long-term mortality in hospitalized older patients. Moreover, the detrimental effects of NT-proBNP on survival were partly mediated by malnutrition and muscle loss.

Preventing the progression from acute kidney injury (AKI) to chronic kidney disease (CKD) remains a considerable clinical challenge. In this study, we elucidate the role of WNT5A in accelerating the AKI-to-CKD transition and its underlying mechanisms. Renal biopsies from patients with AKI showed marked upregulation of WNT5A and its receptor, CD146, in proximal tubules, with higher expression in patients with CKD progression. In murine AKI models, Wnt5a knockdown attenuated CKD progression. Conversely, proximal tubular overexpression of Wnt5a exacerbated renal fibrosis in ischemia-reperfusion injury (IRI) mice, which was alleviated by Box5, a specific WNT5A antagonist. In vitro, WNT5A overexpression in transforming growth factor β (TGF-β)-stimulated HK-2 cells promoted CD146 upregulation, activated JNK phosphorylation, and enhanced SNAI1 expression. The genetic silencing of WNT5A/CD146 and JNK inhibition suppresses SNAI1 expression and attenuates fibrotic responses. Mechanistically, JNK-mediated c-JUN phosphorylation promoted its interaction with KLF5 at the SNAI1 promoter, driving renal fibrosis. Elevated serum levels of soluble CD146 correlated with renal function in patients with AKI and were higher in patients exhibiting CKD progression. Inhibition of WNT5A could serve as a therapeutic target for delaying renal fibrosis in AKI progression.

BACKGROUND:Ectopic calcification, especially in soft tissues such as subcutaneous adipose tissue, is a rare and serious complication in chronic kidney disease (CKD) patients. It is commonly associated with cardiovascular morbidity and mortality. This case report highlights the occurrence of multiple ectopic calcifications in a patient with end-stage renal disease (ESRD) on peritoneal dialysis, emphasizing the role of inflammatory cytokines in the pathogenesis of this condition. Early and appropriate intervention can facilitate partial reversibility, highlighting the importance of regular follow-ups and the optimization of prescriptions, particularly in ensuring intensified high-quality, goal-oriented dialysis. CASE PRESENTATION:A 68-year-old female patient with diabetic nephropathy had been on maintenance peritoneal dialysis for four years. She presented with multiple subcutaneous nodules, particularly in the abdomen and lower limbs, for over a month. Ultrasound and non-contrast CT imaging revealed hyperechoic lesions and calcifications in the subcutaneous tissue, along with vascular and kidney calcifications. Laboratory results indicated inadequate dialysis, hypocalcemia, hyperphosphatemia, and significantly elevated serum parathyroid hormone (PTH) and inflammatory cytokines, including IL-6. The biopsy of the subcutaneous nodule from the lower abdomen revealed calcification and inflammation, accompanied by pronounced IL-6 expression. Treatment included intensified automated peritoneal dialysis (APD) combined with icodextrin peritoneal dialysis solution for long-term retention in the abdomen, cinacalcet, phosphate binders, calcitriol, and nutritional support. After one month, the patient's condition showed significant improvement, with reduced calcification confirmed by follow-up ultrasound. CONCLUSIONS:This case underscores the rarity of subcutaneous adipose tissue calcification in ESRD patients and highlights the crucial role of inflammatory factors, particularly IL-6, in the development of ectopic calcifications. Early, targeted interventions, especially high-quality, goal-directed dialysis, can significantly improve outcomes, illustrating the importance of regular monitoring and tailored treatment in preventing and managing calcification in CKD patients. CLINICAL TRIAL NUMBER:Not applicable.

Lipid metabolism reprogramming is critical for the initiation and progression of hepatocellular carcinoma (HCC). However, how the dysregulation of lipid metabolism contributes to HCC development remains largely unknown. Here, we report that the m6A reader YTHDC1-mediated epigenetic regulation of the long noncoding RNA NEAT1 activates stearoyl-CoA desaturase (SCD)-associated lipid metabolic processes during HCC progression. Mechanistically, histone lactylation in HCC induces increased expression of YTHDC1, increasing the stability of m6A-modified NEAT1. The histone acetyltransferase p300 is then recruited by NEAT1 and activates SCD by increasing the level of histone acetylation at the SCD promoter, thus facilitating HCC progression via hepatocellular lipid metabolism remodeling. Taken together, these discoveries suggest a close link between the epigenetic machinery and lipid metabolic abnormalities, which promotes cancer progression.

End-stage renal disease (ESRD) is often complicated by left ventricular dysfunction, which is associated with a poor prognosis. This study aims to investigate the association between baseline left ventricular ejection fraction (LVEF) plus left ventricular end-diastolic diameter (LVEDD) with outcomes in peritoneal dialysis (PD) patients. In this multicenter retrospective study, 1,511 incident Chinese patients on PD between 1 January 2005 and 31 December 2021 were enrolled. Restricted cubic splines (RCS) were used to explore the non-linear associations between LVEF+LVEDD and the risk of mortality. Parametric models for interval-censored survival-time data (stintreg) were used to examine the association between LVEF+LVEDD quartiles and the outcomes. During 6,451.11 person-years of follow-up [median 4.81 (IQR 3.61-6.81) years], 247 (17.8%) patients died, including 88 cardiovascular deaths. RCS showed a U-shaped association between LVEF+LVEDD and the risks of all-cause and CV mortality. According to the quartiles, the optimal range of LVEF+LVEDD associated with the lowest risk of all-cause and CV mortality was 103-107, which was set as the reference range. Both higher (≥115) and lower (<103) levels of LVEF+LVEDD were associated with increased risks of all-cause mortality (hazard ratio [HR] 2.20, 95% confidence interval [CI] 1.58-3.07; HR 1.68, 95% CI 1.19-2.36) and cardiovascular mortality (HR 2.51, 95% CI 1.33-4.75; HR 1.86, 95% CI 0.96-3.61). Low and high levels of baseline LVEF+LVEDD were associated with increased risks of all-cause and cardiovascular mortality in PD patients.

An imbalance in the serum sodium to chloride ratio (Na/Cl) was linked to higher mortality among heart failure patients. Nonetheless, the prognostic significance of Na/Cl in individuals undergoing peritoneal dialysis (PD) remains unexplored. This study seeks to explore the association between initial Na/Cl levels and mortality in PD patients. The study, conducted across multiple centers, included 3341 patients undergoing PD from January 1, 2005, to December 31, 2021. Patients were stratified into quartiles according to baseline Na/Cl and followed up for a median of 5.77 years. To explore the association between Na/Cl levels and mortality, we employed Cox proportional hazards models, competing risks models, and restricted cubic spline analysis. Of 3341 patients, 722 patients died, including 259 cardiovascular deaths. Following adjustments for comorbidities and multiple covariates, individuals in the highest Na/Cl quartile (>1.42) exhibited lower all-cause mortality (hazard ratio [HR] 0.63, 95% confidence interval [CI] 0.47-0.86) and cardiovascular mortality (HR 0.38, 95% CI 0.22-0.67) compared with those in the lowest quartile (<1.33). A similar pattern was also found when Na/Cl was dealt with continuous variables. Initial levels of Na/Cl at the start of PD were negatively correlated with all-cause mortality and cardiovascular mortality in PD patients.

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.

BACKGROUND:A combination of multiple nutritional indexes may more comprehensively and favorably reflect dialysis patient's prognosis. In the present study, we aimed to evaluated the association between total cholesterol/(body mass index × serum albumin) (TC/BA) and mortality in patients with continuous ambulatory peritoneal dialysis (CAPD). METHODS:We conducted a multicenter retrospective cohort study that included 2907 incident Chinese CAPD patients from seven peritoneal dialysis centers in China between January 1, 2005, and May 31, 2023. The primary outcome was all-cause mortality. We used restricted-cubic-spline plots to explore the shape of the association between TC/BA and outcome. Cause-specific hazard models examined the association between TC/BA and mortality. RESULTS:Of 2907 patients, 754 (25.9%) patients died, including 351 (46.6%) deaths due to cardiovascular disease. A positive linear relationship was observed between TC/BA and all-cause mortality (nonlinear, p = 0.374). In the multivariate cause-specific hazard model, a per-1.0 increase of TC/BA had a 1.29-fold (95% confidence interval [CI] 1.19-1.39) risk of all-cause mortality in the total population. Similar trends were observed in subgroup analyses (all P for interactions > 0.05). Notably, the hazard ratio (HR) of TC/BA (per-1.0 increase) was 1.32 (95% CI 1.23-1.41), 1.29 (95% CI 1.19-1.41), and 1.25 (95% CI 1.22-1.27) times higher than the HR of body mass index (per-1.0 decrease), total cholesterol (per-10 increase), and serum albumin (per-1.0 decrease), respectively. CONCLUSIONS:TC/BA was positively linearly related to mortality and may outperform each index in assessing CAPD patient prognosis. The combined nutritional index may more comprehensively and favorably evaluate CAPD patients' prognosis.

Diabetic kidney disease (DKD), affecting 20-40% of individuals with diabetes, is the leading cause of end-stage renal disease and represents a considerable global public health challenge owing to its high morbidity and mortality rates. Although traditional DKD management has focused on renin-angiotensin system blockade, the residual risk of renal failure persists despite optimised therapy. New therapeutic drugs, including glucagon-like peptide-1 receptor agonists, have triggered a paradigm shift in DKD treatment. Sodium-glucose cotransporter-2 inhibitors, nonsteroidal mineralocorticoid receptor antagonists, and selective endothelin receptor antagonists have shown notable efficacy in improving renal outcomes in patients with type 2 diabetes mellitus. Furthermore, traditional Chinese medicine (TCM), with its holistic approach and evidence-based refinements, has shown considerable promise in DKD treatment, particularly as its theoretical framework continues to evolve. This study highlighted the transformative potential of multitargeted strategies in mitigating DKD progression, improving cardiovascular outcomes, and alleviating healthcare burdens. Future research should prioritise standardised trials, long-term safety assessments of TCM and personalised therapeutic regimens to optimise clinical management and patient quality of life.