Renal Failure最新文献

Chronic kidney disease (CKD) constitutes a significant global public health challenge, with emerging evidence suggesting that riboflavin may confer renoprotective effects. However, the association between dietary riboflavin intake and CKD risk remains inadequately elucidated. To investigate this, we analyzed National Health and Nutrition Examination Survey (NHANES) 2005-2018 datasets using weighted multivariate logistic regression, interaction testing, stratified subgroup analyses, and curve fitting. Additionally, network pharmacology and molecular docking simulations were employed to identify and validate potential therapeutic targets. Our results showed that patients with CKD exhibited significantly lower riboflavin intake than their non-CKD counterparts (1.98 vs. 2.21 mg/d, p < 0.001). After full adjustment, each 1 mg/d increment in riboflavin intake was associated with an 18.8% reduced risk of CKD (adjusted OR = 0.812, 95% CI: 0.686-0.962). Individuals in the highest intake quartile had a 42.7% lower risk compared to the lowest quartile (adjusted OR = 0.573, 95% CI: 0.400-0.822). A non-linear dose-response relationship was observed, characterized by an inflection point at 1.66 mg/d, indicating a more pronounced protective effect at lower intake levels. Mechanistic investigations suggested that riboflavin's benefits may be mediated through interactions with key targets like caspase-3 (CASP3), Erb-B2 receptor tyrosine kinase 2 (ERBB2), and matrix metallopeptidase 9 (MMP9), implicating apoptotic and metabolic pathways. In conclusion, dietary riboflavin intake is inversely associated with CKD risk, particularly at lower concentrations, and strategic augmentation of intake represents a promising dietary intervention for CKD prevention and management.

Background: Drug-coated balloons (DCBs) improve the patency of hemodialysis access, yet restenosis rates remain substantial. This may be partly attributable to suboptimal balloon sizing. The relationship between the balloon diameter ratio (BDR; the ratio of DCB diameter to final predilation balloon diameter) and restenosis risk has not been clearly elucidated.

Methods: This retrospective study analyzed 123 patients who underwent DCB angioplasty for dysfunctional arteriovenous fistulas (AVF) or arteriovenous grafts (AVG). The primary endpoint was clinically driven target lesion restenosis within six months. Multivariable Cox regression and restricted cubic spline (RCS) analyses were used to evaluate the association between BDR and restenosis.

Results: The six-month restenosis rate was 25.2%. BDR was an independent predictor of restenosis (p = 0.048). Compared to a BDR of 1.0 (a perfect 1:1 match), a BDR < 1 was associated with a significantly higher risk (HR 3.07, 95% CI 1.01-9.34). RCS analysis demonstrated a significant U-shaped nonlinear relationship (P for nonlinearity = 0.041), with the risk nadir observed at a BDR of approximately 0.98. A BDR within the 0.9-1.1 range constituted a "safe window" associated with the lowest risk of restenosis.

Conclusions: BDR is a key, modifiable technical factor influencing patency after hemodialysis access intervention. Maintaining a BDR within the 0.9-1.1 range correlates with the lowest 6-month restenosis risk, yielding a clear and practical technical target for optimizing DCB angioplasty procedures.

KDIGO stage-3 acute kidney injury (AKI), a life-threatening complication in critically ill patients with traumatic cervicothoracic spinal cord injury (TCTSCI), was associated with a 49.3% 60-day mortality and a median survival of 20 days in a combined MIMIC-IV/eICU analysis, underscoring its severe clinical consequences and the need for early identification and prediction. To address this need, MedFusion-GP-AKI was developed as a multimodal deep learning framework trained on the MIMIC-IV/eICU cohort and externally validated in 188 patients from four tertiary Chinese centers. Missing data were imputed with a GAN-based method, and key predictors were derived from the original dataset using NOTEARS, variational bottleneck, and adversarial analysis, yielding eleven variables led by lactate, mean arterial pressure, temperature, potassium, and TCTSCI level, with the dataset subsequently balanced using an SMOTified-GAN. Fifteen baseline models were benchmarked under uniform protocols, and the best-performing architectures were integrated into an ensemble that achieved AUCs of 0.938, 0.909, 0.969, 0.945, and 0.921 with APs of 0.841, 0.884, 0.992, 0.927, and 0.878 across pre- and post-SMOTE training, validation, and external cohorts, demonstrating reliable discrimination and calibration, stable clinical net benefit across thresholds, and balanced overall classification performance with strong generalizability across independent institutions. SHAP analysis confirmed that model attributions aligned with known clinical and physiological patterns, and a web-based calculator was developed for practical use. Overall, this study connects artificial intelligence, nephrology, and critical care by using multimodal deep learning and causal inference to predict severe AKI occurrence from early clinical data in critically ill TCTSCI patients.

Central venous catheters (CVCs) are used in hemodialysis patients when arteriovenous fistulas (AVFs) or grafts (AVGs) are not feasible. Catheter-locking anticoagulants (CLAs), such as low-concentration trisodium citrate (TSC) and unfractionated heparin (UFH), are used to prevent catheter dysfunction (CD), but comparative data on their safety and efficacy - especially at low concentration remain limited. This study evaluates the efficacy of low-concentration TSC versus low-concentration UFH as CLAs in hemodialysis CVCs. Patients undergoing hemodialysis were randomly allocated to receiving either 5% TSC or UFH 1000 U/mL as CLAs. The primary outcome was the CD rate. Secondary outcomes encompass catheter-related bloodstream infection (CRBSI), exit site infection (ESI), bleeding events, and mortality at 180 days. A total of 204 hemodialysis patients were randomized to receive either 5% trisodium citrate or 1,000 U/mL unfractionated heparin as catheter-locking anticoagulants. The CD rates at 180 days were 1.11 and 1.73 per 1,000 catheters-days for TSC and UFH, respectively, yielding an incidence rate ratio of 1.55 (95% CI: 0.72-3.45), p = 0.23. CRBSI and ESI were comparable in both groups. Bleeding and mortality were also not significantly different between the groups. In the sensitivity analysis of tunnel cuffed catheters (TCC), the rate of CD remained not significantly different between the groups; however, the rate of ESI was higher in the UFH group. Both 5% TSC and 1,000 U/mL UFH demonstrated comparable overall efficacy and safety as CLAs. A possible reduction in infectious complications with 5% TSC was observed only in the tunneled cuffed catheter subgroup.

Acute kidney injury (AKI) is a potentially fatal complication in patients with decompensated cirrhosis having therapeutic paracentesis, and early diagnosis is still difficult because of the low sensitivity of serum creatinine. We preemptively tested serum interleukin-18 (IL-18), kidney injury molecule-1 (KIM-1), and fibroblast growth factor-23 (FGF-23) in early prediction of post-paracentesis AKI in 80 hospitalized patients with tense ascites and normal baseline kidney function. Samples of blood were collected 2 h pre-paracentesis and 24 h post-paracentesis. Based on the Kidney Disease: Improving Global Outcomes definition, AKI, which happened within 72 h, was present in 40% of patients. Biomarkers levels at baseline were comparable. In 24 h of paracentesis, IL-18, KIM-1, and FGF-23 were high in patients who later developed AKI (all p value below .001) and had high-absolute changes than the non-AKI group. The largest discriminative performance was observed of FGF-23 (area under the curve 0.959), then IL-18 (0.931), and KIM-1 (0.903). In multivariate logistic regression controlling MELD-Na score, serum albumin, baseline eGFR and ascitic fluid volume, the post-paracentesis FGF-23 was still independently connected with AKI. Biomarkers of tubular injury, especially FGF-23, which increased shortly after the procedure were strongly correlated with future AKI and could increase risk stratification pending external validation.

Objective: The serum albumin-to-creatinine ratio (sACR) is a potential biomarker for multiple diseases, yet its prognostic role in chronic kidney disease (CKD) patients undergoing surgery remains unexplored. This study aimed to investigate the association between sACR levels and postoperative in-hospital mortality in this population. Methods: This retrospective cohort study analyzed 2,611 CKD patients from the INSPIRE database (2011-2020). Patients were stratified into tertiles based on admission sACR levels. Multivariable Cox regression models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between sACR and mortality. Restricted cubic spline (RCS) analysis was performed to assess potential nonlinear relationships. Sensitivity analyses were conducted to verify result robustness. Results: The cohort had a mean age of 61.1 ± 14.8 years and a median sACR of 1.2 (interquartile range: 0.7-2.6). Multivariable analysis revealed that each unit increase in sACR was associated with a 29% reduction in mortality (adjusted HR 0.71, 95% CI 0.61-0.83, p < 0.001). Compared with the lowest tertile (T1), the highest tertile (T3) demonstrated a 48% lower mortality risk (HR 0.52, 95% CI 0.33-0.82, p = 0.005). RCS analysis identified a nonlinear, L-shaped association between sACR and mortality (P for nonlinearity < 0.001), with a threshold effect observed at approximately 2.7. Sensitivity analyses confirmed the robustness of these findings. Conclusion: Lower sACR levels are independently associated with higher in-hospital mortality in surgical CKD patients, exhibiting an L-shaped relationship with a critical threshold at 2.7. sACR represents a practical, cost-effective early-warning biomarker for perioperative risk stratification in this high-risk population.

Radial-artery to cephalic-vein end-to-side arteriovenous fistulae (RCAVF) are the first-line vascular access for hemodialysis, yet early stenosis or thrombosis reduces its long-term patency. Indoxyl sulfate (IS), a protein-bound uremic toxin with diverse vascular effects, may impede fistula maturation. We conducted a single-center prospective cohort study enrolling 113 stage 5 chronic kidney disease patients who underwent RCAVF creation between February 2023 and August 2024. Patients were stratified by IS tertiles to assess fistula outcomes. Multivariable Cox regression, Kaplan-Meier analyses, and nomogram construction were used to identify risk factors and patency. Additionally, multiplex tyramide signal amplification immunofluorescence was applied to 40 samples of cephalic vein to quantify aryl hydrocarbon receptor (AHR) and tissue factor (TF) expression. After a median follow-up of 12 months, serum IS was higher in the dysfunction group (p = 0.005). Elevated IS (p = 0.013) and diabetes mellitus (p = 0.006) were independent risk factors for RCAVF dysfunction. Restricted cubic spline analysis showed a linear relationship between IS and risk. Kaplan-Meier curves revealed decreasing primary patency with increasing IS tertiles (p < 0.05), consistent in diabetic patients. The 1-year patency nomogram had good predictive performance (AUC = 0.87). Histopathology showed upregulated AHR and TF expression in veins from dysfunctional fistulas, with correlated fluorescence intensities (r = 0.60, p < 0.05), though neither correlated directly with serum IS (p > 0.05). In conclusion, elevated serum IS independently predicts RCAVF dysfunction, and the aberrant IS-AHR-TF signaling axis may contribute to its pathogenesis.

In-hospital outcomes among adults with chronic kidney disease (CKD) in low-resource settings are poorly characterized. We evaluated predictors of in-hospital mortality among adults admitted with CKD to Sierra Leone's national tertiary hospital, which houses the country's only public dialysis unit. We retrospectively reviewed case notes for all adults with CKD admitted to Connaught Hospital, Freetown, from January 1, 2022, through December 31, 2024. CKD stage was assigned according to KDIGO estimated glomerular filtration rate (eGFR) categories. The primary outcome was in-hospital death. Multivariable logistic regression was used to examine prespecified predictors of mortality. Among 385 admissions (median age, 48 years [interquartile range, 38 to 57]; 57.1% men), 64.2% presented with KDIGO G5 CKD and 41.0% received dialysis. In-hospital death occurred in 95 patients (24.7%). Each 10 mL/min/1.73 m² lower eGFR was associated with higher odds of death (adjusted odds ratio [aOR], 1.94; 95% confidence interval [CI], 1.42 to 2.66), as were heavier proteinuria (aOR, 2.23; 95% CI, 1.39 to 3.58 per one-category increase on dipstick) and diabetes (aOR, 1.97; 95% CI, 1.10 to 3.52). Receipt of dialysis was associated with lower adjusted odds of death (aOR, 0.55; 95% CI, 0.31 to 0.95). Age, sex, and hypertension were not statistically significant. Hospitalized adults with CKD in Sierra Leone typically present with advanced disease and heavy proteinuria, and approximately one in four died during hospitalization. Lower eGFR, greater proteinuria, and diabetes identify patients at highest risk, and access to dialysis was associated with lower short-term survival in this low-resource setting.

Background: Despite improved survival following kidney transplantation, cardiovascular disease (CVD) remains a leading cause of mortality in kidney transplant recipients (KTRs). This risk is driven by complex traditional and nontraditional mechanisms contributing to uremic cardiomyopathy. Cardiorespiratory fitness (CRF) is consistently reduced in KTRs and strongly associated with cardiovascular outcomes. However, while cardiac structure and function may partially improve post-transplant, recovery of CRF often remains incomplete compared to healthy individuals, suggesting that structural reverse remodeling does not necessarily equate to restored cardiovascular reserve.

Methods: This review synthesises current evidence on post-transplant changes in left ventricular structure and function and trajectories of CRF recovery. We highlight persistent discrepancies between echocardiography-based and cardiac magnetic resonance (CMR)-based findings, together with the limited use of cardiopulmonary exercise testing (CPET) in longitudinal studies.

Key findings: We discuss the concept of a 'transplant cardio-recovery gap', reflecting the dissociation between structural normalisation and functional capacity restoration.

Future directions: We outline future directions for research including phenotype-specific monitoring using CMR-derived strain, native T1 mapping, and CPET parameters, integrated through AI-enabled predictive analytics, to enable digital twin models capable of forecasting individualised recovery trajectories. We discuss CMR-CRF coupling models, and adaptive rehabilitation trials stratified by functional cardiovascular reserve rather than structural metrics alone.

Conclusion: While kidney transplantation offers partial cardiovascular recovery, restoration of cardiopulmonary resilience remains an unmet therapeutic target. Precision, AI-guided CRF evaluation and rehabilitation may redefine cardiovascular risk management in KTRs and inform the next generation of transplant optimisation strategies.

Chronic kidney disease (CKD) is characterized by renal fibrosis as its core pathological feature, and lipid metabolism disorders are a key driver of disease progression. However, the specific pathological significance of elevated lactate levels in patients with CKD remains unclear. This study aimed to verify the hypothesis that lactate exacerbates renal fibrosis by inhibiting the PPARα/FAO pathway. A total of 15 healthy controls and 75 CKD patients were enrolled. Serum lactate levels were measured, and their correlations with Scr, BUN, eGFR, and lipid metabolism parameters (triglycerides [TG], total cholesterol [TCH]) were analyzed. Meanwhile, unilateral ureteral obstruction (UUO) mouse models and transforming growth factor-β1 (TGF-β1)-induced human proximal tubular epithelial cells (HK-2 cells) were used to validate the regulatory role of lactate in renal fibrosis. Results showed that serum lactate levels in CKD patients significantly increased with disease stage progression, and were positively correlated with Scr, BUN, TG, and TCH (p < 0.05), while negatively correlated with eGFR (p < 0.0001). RNA sequencing and Western blot confirmed that UUO mouse kidney tissues exhibited lactate accumulation, downregulation of the PPARα/FAO pathway, lipid accumulation, and aggravated renal fibrosis. Exogenous lactate supplementation exacerbated TGF-β1-induced fibrosis and lipid disorders in HK-2 cells, whereas inhibition of lactate production by oxamic acid sodium significantly reversed these pathological effects. In conclusion, lactate disrupts renal lipid homeostasis and exacerbates renal fibrosis by inhibiting the PPARα/FAO pathway. This study provides an important theoretical basis for elucidating the pathological mechanism of CKD and developing novel therapeutic targets.