Renal Failure最新文献

Regional citrate anticoagulation (RCA) is recommended for critically ill patients at high bleeding risk undergoing continuous renal replacement therapy (CRRT). Nafamostat mesylate (NM), a short-half-life serine protease inhibitor, is a popular alternative in East Asia. Direct comparisons of their efficacy and safety are limited. This retrospective single-center study included 81 critically ill patients receiving CRRT with either NM (n = 31) or RCA (n = 50) from January 2022 to January 2023. The primary outcome was filter lifespan. Secondary outcomes included circuit patency, bleeding events, and metabolic complications. The median filter lifespan was significantly shorter in the NM group compared to the RCA group (23.4 vs. 29.6 h, p = 0.02). The NM group also had a higher rate of unplanned circuit discontinuation (52.3 vs. 39.1%, p = 0.03). Multivariable analysis confirmed RCA was independently associated with a lower risk of circuit failure (HR = 0.44, p = 0.03). Although not statistically significant, trends favored NM regarding metabolic safety, with lower incidences of severe metabolic alkalosis (16.1 vs. 36.0%, p = 0.09) and hypocalcemia (9.7 vs. 26.0%, p = 0.13). RCA demonstrated superior anticoagulation efficacy in prolonging filter survival, while NM may offer a more favorable metabolic safety profile. The choice of anticoagulant should be individualized based on efficacy priorities and metabolic risk.

Quantitative assessment of donor kidney quality remains challenging in transplantation medicine. This study investigated the correlation between Shore durometer-measured renal hardness and established quality indicators (hypothermic machine perfusion [HMP] parameters and pathological scores) in deceased donor kidneys. We prospectively analyzed 58 kidneys from 29 deceased donors. Renal hardness was measured at 10 standardized locations before and after perfusion using a Shore durometer (Type OOO). HMP parameters (flow rate and resistance index [RI]) were recorded during machine perfusion, and histological assessment was performed using Remuzzi scoring. Pearson correlation analysis examined relationships between hardness parameters (pre-perfusion, post-perfusion, and perfusion-induced difference) and quality indicators. Pre-perfusion hardness correlated significantly with HMP resistance (r = 0.745, p < 0.001) and vascular damage scores (r = 0.299, p = 0.023). The perfusion-induced hardness difference showed strong negative correlations with all pathological scores (Remuzzi: r=-0.602; glomerulosclerosis: r=-0.517; interstitial fibrosis: r=-0.454; tubular atrophy: r=-0.403; vascular damage: r=-0.385; all p < 0.05). Shore durometer-measured kidney hardness significantly correlates with both HMP parameters and histological scores, with perfusion-induced hardness change emerging as a particularly promising indicator of underlying pathology. These findings support incorporating quantitative hardness assessment into donor kidney evaluation protocols.

Background: BK polyomavirus-associated nephropathy (BKPyVAN) is a major cause of allograft injury and dysfunction in kidney transplant recipients. Current monitoring tools, including viremia and biopsy, have limitations in sensitivity, invasiveness, and timing.

Objective: To evaluate donor-derived cell-free DNA (dd-cfDNA) in urine and plasma as a dynamic, noninvasive biomarker for monitoring treatment response and predicting rejection risk in patients with biopsy-proven BKPyVAN.

Methods: In this prospective cohort study, 25 kidney transplant recipients with biopsy-proved BKPyVAN were enrolled and stratified into two cohorts: conventional immunosuppression reduction (CISR, n = 20) and early immunosuppression reduction (EISR, n = 5). A total of 224 urine and plasma samples were collected before biopsy and at 1, 2, 3, and 6 months post-biopsy. dd-cfDNA levels were quantified and correlated with histological features and clinical outcomes.

Results: Urinary dd-cfDNA levels significantly declined in the CISR cohort by month 2 (p < 0.01), preceding changes in creatinine and BKPyV reads. In the EISR cohort, urinary dd-cfDNA levels remained stable, suggesting early therapeutic response. Plasma dd-cfDNA effectively identified acute rejection, with elevations in two CISR patients. Histologic injury patterns, including edema and cast formation, correlated with urinary dd-cfDNA concentrations (r = 0.44-0.51, p < 0.05).

Conclusion: Combined urinary and plasma dd-cfDNA measurements are promising for noninvasive, dynamic surveillance of BKPyVAN and rejection risk in kidney transplant recipients. Larger, multicenter studies are warranted to define clinical thresholds and standardize integration into immunosuppression management.

Introduction: Erythropoiesis-stimulating agents (ESAs) are widely used to manage anemia in chronic hemodialysis patients. However, some individuals exhibit ESA resistance, and its underlying mechanisms remain unclear. Sirtuin-1 (SIRT1), a key regulator of hypoxia and iron metabolism, may influence ESA responsiveness. This study investigates the relationship between SIRT1 levels and ESA resistance.

Methods: This cross-sectional study analyzed 391 chronic hemodialysis patients, including ESA-treated and untreated individuals. ESA responsiveness was assessed using the Erythropoietin Resistance Index (ERI), calculated as weekly body-weight-adjusted ESA dose divided by hemoglobin concentration. Associations between SIRT1 levels, ERI quartiles, and ESA responsiveness were examined.

Results: A total of 385 patients were included in the analysis. Serum SIRT1 levels were significantly lower in ESA-treated patients than in untreated individuals. A negative correlation was found between SIRT1 levels and ERI (r = -0.179, p < 0.001). Multiple regression analysis confirmed that both ERI (β = -0.158, p = 0.002) and ferritin levels (β = -0.121, p = 0.015) were independent negative predictors of SIRT1 (R²= 0.081). Patients with high ERI (≥50th percentile) had significantly lower SIRT1 levels. Logistic regression indicated that only SIRT1 was significantly associated with high ERI (B = -0.035, p = 0.018).

Conclusion: This study examined the relationship between SIRT1 levels and ESA hyporesponsiveness in patients undergoing hemodialysis. The findings demonstrate that lower SIRT1 levels are associated with higher ERI values, suggesting a potential role for SIRT1 in modulating ESA resistance.

Lycium barbarum polysaccharides (LBP) have shown renal protection effects. However, research on other active components of L. barbarum extract (ELB) for the therapy of chronic kidney disease (CKD) is limited. This study aims to investigate the renoprotective effects and molecular mechanisms of ELB in CKD. ELB was extracted from L. barbarum fruits using 85% ethanol reflux, followed by vacuum concentration and sequential extraction to remove polysaccharides. Chemical components and target genes were identified using TCMSP and UniProt databases, followed by pharmacology network construction and GO/KEGG pathway analysis. A 5/6 nephrectomy model in Sprague-Dawley rats was used to study the renoprotective effects of ELB, with H&E staining and biochemical analyses. Western blot analysis assessed IL-6 and VEGF expression in renal tissues. Chemical analysis of ELB identified 188 components, with 45 meeting screening criteria, and 34 linked to 94 target genes. The intersection with CKD-related genes yielded 39 overlapping genes, with quercetin having the most targets. GO/KEGG pathway analyses highlighted significant biological processes and pathways. A PPI network identified IL-6, VEGFA, CASP3, EGFR, ESR1, and PPARG as hub genes. In a 5/6 nephrectomy rat model, ELB treatment significantly reduced renal damage, serum BUN and SCr levels, as well as IL-6 and VEGF expression in renal tissues, validating its renoprotective effects and supporting bioinformatics predictions. This work identified the intricate components and pharmacological actions of ELB, which is devoid of LBP. The findings preliminarily confirm the potential of ELB as a novel therapeutic agent for preventing and managing CKD.

Background: Vascular calcification (VC), especially coronary artery calcification (CAC), serves as a robust predictor of cardiovascular mortality in chronic kidney disease (CKD) patients. Recent studies have revealed that the presence of extra-coronary calcifications (ECCs) contributes to cardiovascular disease (CVD). Elevated myocardial injury markers predict mortality risk in CKD patients and are associated with CVD. Nevertheless, the relationship between VC, including CAC and ECCs, and myocardial injury markers remain unexplored in non-dialysis CKD patients.

Methods: In 278 non-dialysis CKD patients of stage G3 to G5, we assessed calcified scores in CAC (Agatston score) and ECCs including thoracic aortic calcification (TAC), abdominal aortic calcification (AAC), carotid artery calcification, and valvular calcification. We analyzed the relationships between VC and myocardial injury markers of cardiac troponin T (cTnT) and creatine kinase-MB (CK-MB).

Results: A total of 278 non-dialysis CKD patients (median age 52.4 ± 13.2; male 65.1%; diabetes 33.5%) were enrolled. A total of 71.8% (227) of patients had cTnT levels above the upper limit of normal (> 0.014 ng/mL). Moderate to severe (calcified score ≥100 vs. <100), CAC (OR 6.39; 95% CI 1.03-39.61) and TAC (OR 6.16; 95% CI 1.76-21.55) were significantly associated with higher cTnT concentrations after adjustment for confounders. Additionally, male sex and a lower eGFR were also associated with cTnT elevation. However, when we included CAC and TAC in one model, only moderate to severe TAC (OR 4.85; 95% CI 1.38-16.96) was a risk factor for cTnT elevation, but not CAC. Furthermore, patients with severer TAC presented lower diastolic blood pressure (DBP), wider pulse pressure (p < 0.001) and higher prevalence of left ventricular hypertrophy (LVH).

Conclusion: Moderate to severe thoracic aortic calcification (TAC score ≥ 100) is significantly associated with elevated cTnT concentrations in non-dialysis CKD patients of stage G3 to G5. The linkage may result from decreased coronary perfusion and relative myocardial ischemia.

Objective: The innate immune defense plays a pivotal role in protecting the urinary tract from uropathogenic invasion and maintaining immune homeostasis. Dysregulation of the innate immune system can result in recurrent urinary tract infections (RUTI) due to heightened susceptibility to uropathogens. Despite this, predicting the risk of recurrence and the degree of immune compromise in patients who have had one urinary tract infection remains challenging. Also identifying which patients are more susceptible to developing pyelonephritis rather than the more local disease of cystitis is imperfect, although delayed diagnosis of a UTI is a good indicator for developing pyelonephritis. This study aims to assess the potential of urinary Tamm-Horsfall protein (THP) and Pentraxin 3 (PTX3) as predictors of RUTI symptom severity and recurrence, while also evaluating the efficacy of the Chinese herbal formulation Tailin Formula (TLF) as a clinical therapeutic intervention for RUTI.

Methods: A single-center cohort study was conducted involving 142 participants, consisting of 31 healthy individuals (non-RUTI group, n = 31) and 111 patients with RUTI. The RUTI patients were divided into two groups: one group received continuous low-dose antibiotic therapy (CLAT group, n = 55), and the other group received herbal preparations (Tailin formula) (TLF group, n = 56). All patients received consistent lifestyle guidance. Descriptive analysis was performed on the RUTI cohort.

Results: Urinary THP levels were significantly lower in RUTI patients (TLF and CLAT groups) compared to the non-RUTI, whereas PTX3 levels showed a tendency toward elevation. After treatment, urinary THP levels were markedly higher in the TLF group (27.43 ± 7.07) compared to pretreatment levels (10.00 ± 2.79), while levels remained lower in the CLAT group (8.91 ± 2.23) than in the TLF group. Urinary PTX3 levels decreased post-treatment in both groups after treatment than before (CLAT: 0.30 ± 0.13 vs. 1.04 ± 0.38; TLF: 0.29 ± 0.12 vs. 1.15 ± 0.36). Additionally, THP was negatively correlated with renal tubular injury markers NAG/Cr and β2-MG in RUTI patients (r = -0.5041 and -0.6169, respectively), while PTX3 showed a positive correlation with NAG/Cr and β2-MG (r = 0.28 and 0.498, respectively). Notably, as RUTI symptoms improved and recurrence rates decreased, urinary THP levels increased, while PTX3 levels decreased.

Conclusion: This study suggests that urinary THP and PTX3 are likely involved in the pathogenesis of RUTI. These biomarkers may serve as valuable predictors for assessing symptom severity, recurrence risk, and therapeutic efficacy in patients with RUTI at risk of disease progression.

Background: Adjusting dietary potassium intake based on 24-hour urinary potassium excretion is the primary method of preventing hyperkalemia. Currently, there is no accurate and convenient method for calculating maximum 24-hour urinary potassium excretion in kidney failure without replacement therapy patients. We developed and validated two new models to assess the upper limit of dietary potassium consumption in this high-risk cohort, using the maximum 24-hour urinary potassium excretion as a proxy.

Methods: The data of 145 kidney failure without replacement therapy patients with hyperkalemia was gathered. The prediction models were developed using multilayer perceptron and stepwise multiple linear regression utilizing a stochastic sample of 102 (70%) patients. Within the rest 43 (30%), the performance of various models was independently verified.

Results: The two new models had low bias (-0.02 and -0.57 mmol/24h vs 66.74 and 79.91 mmol/24h, mean absolute error = 5.57 and 5.22 vs 68.95 and 81.37), high accuracy (percentage of calculated values within_±30% of measured values = 83.45% and 84.14% vs 0.00% and 0.00%), high correlation with measured values (Spearman correlation coefficient = 0.72 and 0.72 vs 0.46 and 0.45, intraclass correlation coefficient = 0.67 and 0.70 vs 0.03 and 0.03) and high agreement with 24-hour urine potassium measurements (95% limits of agreement of Bland-Altman plot = 13.70 and 13.20 mmol/24h vs 113.8 and 191.3 mmol/24h).

Conclusion: These new models show high clinical application value for the calculation of maximum 24-hour urinary potassium excretion in kidney failure without replacement therapy patients with hyperkalemia.