Renal Failure最新文献

Background: Chronic kidney disease (CKD) is a prevalent chronic, non-communicable disease. The long-term health effects of dietary live microbes, primarily probiotics, on CKD patients remain insufficiently understood. This study aims to investigate the association between dietary intake of live microbes and long-term health outcomes among individuals with CKD.

Methods: Utilizing the National Health and Nutrition Examination Survey (NHANES) database, Cox regression analysis assessed the association between medium and high categories dietary live microbe intake and health outcomes (all-cause, cardiovascular disease [CVD], and cancer-related mortality) in CKD patients.

Results: A total of 3,646 CKD patients were enrolled. During the follow-up period, 1,593 all-cause mortality events were recorded, including 478 CVD deaths and 268 cancer deaths. In the fully adjusted model, compared to CKD patients in the lowest quartile (quartile 1) of live microbes intake, those in quartiles 3 and 4 exhibited a 20% and 26% reduced risk of all-cause mortality, with hazard ratios (HR) of 0.80 (95% confidence interval, CI: 0.69, 0.94) and 0.74 (95% CI: 0.62, 0.90), respectively. Additionally, compared to those with low live microbe intake (quartile 1), higher live microbe intake in quartile 4 was associated with a 37% reduction in the risk of CVD mortality for CKD patients, with an HR of 0.63 (95% CI: 0.45, 0.88). Consistent results were observed in subgroup and sensitivity analyses. A significant negative association was observed between live microbe intake and the risk of all-cause mortality as well as CVD mortality in the CKD population, with a p-value for trend < 0.05.

Conclusion: Our study indicated that high dietary live microbe intake could mitigate the risk of all-cause and CVD mortality in CKD patients. These findings support the inclusion of live microbes in dietary recommendations, highlighting their significant roles in CKD.

Background: Vascular calcification is highly prevalent and associated with mortality in hemodialysis patients. However, extreme splanchnic arterial calcification in calciphylaxis with poor prognosis raises questions regarding the reliability of previous vascular calcification scoring methods. Therefore, this study aimed to examine the distribution characteristics of abdominal aortic branch calcification and identify a more reliable predictor of mortality in hemodialysis patients.

Methods: The cohort study included 237 hemodialysis patients. The distribution characteristics of abdominal aortic branch calcification were determined by quantifying the calcification volumes. The primary and secondary outcomes were all-cause mortality and new-onset cardiovascular events, respectively. We compared the prognostic values of abdominal aortic branch calcification and constructed a predictive nomogram model.

Results: The prevalence of abdominal vascular calcification in hemodialysis patients was 95.36%, with the highest prevalence in the abdominal aorta (88.61%) and internal iliac artery (85.65%). During a median follow-up period of 3.92 years, 137 patients died. Internal iliac artery and mesenteric artery calcification showed the greatest predictive values for mortality. Internal iliac artery calcification and serum albumin level were independently associated with mortality in hemodialysis patients (p < .001). The nomogram model constructed with internal iliac artery calcification, serum albumin level, age, and comorbid cardiovascular disease was well discriminative, calibrated, and clinically applicable for predicting 3-year survival.

Conclusion: Abdominal aortic branch calcification, particularly internal iliac artery calcification, is a preferable prognostic predictor than abdominal aorta or coronary artery calcification in hemodialysis patients.

Background: Peritoneal dialysis-associated peritonitis (PDAP) frequently arises as a complication in patients undergoing peritoneal dialysis. However, the understanding of the role of Neisseria, a gram-negative coccus, in PDAP is limited.

Methods: This study retrospectively analyzed data for patients with Neisseria-associated PDAP who were treated at our center from January 2010 to June 2022. These patients were classified into the Neisseria group (Group N) and matched 1:2 by sex, age, dialysis duration, and residual kidney Kt/V with a coagulase-negative staphylococci group (Group CNS) and a Staphylococcus aureus group (Group S) as controls. Statistical analysis was conducted via SPSS 25.0 and was supplemented with a review of the relevant literature, to investigate clinical features, pathways of infection, and patient outcomes.

Results: This study included 10 cases of Neisseria-associated PDAP, comprising 6 male and 4 female patients. The patients had an average age of 58.10 ± 14.52 years, and the average duration of peritoneal dialysis was 72.00 ± 46.99 months. Among these patients, 3 had first-time infections, while 7 had a prior history of PDAP. After treatment, 9 patients achieved medical cure, and 1 patient was transferred to hemodialysis (HD). Baseline comparisons across the 3 groups indicated notable differences in body temperature upon admission, which were statistically significant (p < 0.05), with patients in Group S having higher body temperatures compared to Group N and Group CNS. Compared with Group N, Group S presented a markedly elevated high-sensitivity C-reactive protein (hs-CRP) level, decreased serum albumin levels, reduced serum potassium levels, whereas Group CNS presented a significantly lower neutrophil percentage (N%) than did Group N (p < 0.05). Although survival analysis did not reveal statistically significant differences due to the limited sample size, Kaplan-Meier curves indicated a trend toward lower cure rates and slightly worse long-term outcomes in Group S than in Group N and Group CNS, with the latter 2 groups showing similar results.

Conclusion: Neisseria-associated PDAP generally has favorable outcomes, similar to those of CNS-related PDAP and better than those of S-related PDAP. Hypoalbuminemia, hypokalemia and elevated hs-CRP are key risk factors affecting outcomes, emphasizing the need to address them during treatment.

Objectives: This study evaluates the relationship between renal amyloid deposition burden in kidney biopsy and a renal staging system based on proteinuria and estimated glomerular filtration rate (eGFR) in AL amyloidosis.

Methods: A total of 248 patients diagnosed via renal biopsy were included. The extent of amyloid deposition in glomeruli, blood vessels, and tubulointerstitium were evaluated semiquantitatively. The total amyloid load (TA) was defined by the sum of glomerular, vascular and interstitial deposits.

Results: Patients were categorized into three renal stages: I, II, and III. Findings showed that scores of pathological parameters increased progressive with advancing renal stage. The median TA values were 6 (IQR 3-8) in Stage I, 7 (IQR 5-8) in Stage II, and 8 (IQR 7-11) in Stage III (p < 0.001). Baseline eGFR was inversely correlated with TA (r = -0.363, p < 0.001), while proteinuria showed no significant association. Cox regression analysis identified eGFR <50 mL/min/1.73 m² as an independent risk factor for renal survival (HR, 6.519; 95% CI, 3.110-13.665; p < 0.001), whereas proteinuria did not show such an effect.

Conclusions: These findings suggest that in the renal staging system, eGFR - but not proteinuria - is significantly associated with amyloid deposition and independently affects renal survival.

Background/aim: Concerning the related factors for kidney disease and high chronic kidney disease (CKD) progression risk, there is still a lack of study in the adult-onset type 1 diabetes mellitus (T1DM) patients from China.

Methods: Four hundred and eighty-one adult-onset T1DM patients from the Guangdong T1DM translational medicine study were included. Logistic regression analysis (Forward: LR) was utilized to identify glycemic- and nonglycemic-related factors associated with moderate albuminuria, severe albuminuria, mildly reduced estimated glomerular filtration rate (eGFR), decreased eGFR, and high CKD progression risk, and to calculate the odds ratio (OR) and 95% confidence interval (CI).

Results: High CKD progression risk was positively associated with males (OR = 3.13, 95% CI:1.20 - 8.14, p = 0.019), duration of T1DM (OR =1.13, 95% CI:1.05 - 1.21, p < 0.001), triglyceride (OR =1.52, 95% CI:1.11 - 2.08, p = 0.008), and systolic blood pressure (SBP) (OR =1.04, 95% CI:1.02 - 1.07, p = 0.001), and negatively correlated with BMI (OR = 0.80, 95% CI:0.68 - 0.95, p = 0.011). Meanwhile, moderate albuminuria, severe albuminuria, mildly reduced eGFR and decreased eGFR had different each of glycemic- and nonglycemic-related factors.

Conclusions: Hyperglycemia, hypertension, hyperuricemia, and BMI may be associated with different stages of kidney disease in adult-onset T1DM patients. Early-stage adult-onset T1DM patients with male, low BMI, prolonged diabetes duration, and comorbid hypertension and dyslipidemia should undergo a thorough evaluation of albuminuria and renal function to detect those at high CKD progression risk, who should be timely transferred to the nephrology specialty to receive professional treatment for kidney disease.

Introduction: Predicting the outcome of a kidney transplant involving a living donor advances donor decision-making donors for clinicians and patients. However, the discriminative or calibration capacity of the currently employed models are limited. We set out to apply artificial intelligence (AI) algorithms to create a highly predictive risk stratification indicator, applicable to the UK's transplant selection process.

Methodology: Pre-transplant characteristics from 12,661 live-donor kidney transplants (performed between 2007 and 2022) from the United Kingdom Transplant Registry database were analyzed. The transplants were randomly divided into training (70%) and validation (30%) sets. Death-censored graft survival was the primary performance indicator. We experimented with four machine learning (ML) models assessed for calibration and discrimination [integrated Brier score (IBS) and Harrell's concordance index]. We assessed the potential clinical utility using decision curve analysis.

Results: XGBoost demonstrated the best discriminative performance for survival (area under the curve = 0.73, 0.74, and 0.75 at 3, 7, and 10 years post-transplant, respectively). The concordance index was 0.72. The calibration process was adequate, as evidenced by the IBS score of 0.09.

Conclusion: By evaluating possible donor-recipient pairs based on graft survival, the AI-based UK Live-Donor Kidney Transplant Outcome Prediction has the potential to enhance choices for the best live-donor selection. This methodology may improve the outcomes of kidney paired exchange schemes. In general terms we show how the new AI and ML tools can have a role in developing effective and equitable healthcare.

Long-term exposure to ambient air pollution is a recognized environmental risk factor for chronic kidney disease (CKD), but its dynamic effects on kidney function remain incompletely understood. This nationwide longitudinal study included 5,306 participants from the China Health and Retirement Longitudinal Study (CHARLS) to examine associations between five major air pollutants (PM₁, PM_2.5, PM₁₀, NO₂, and O₃) and kidney function decline, measured by the annual slope of estimated glomerular filtration rate (eGFR). Air pollutant exposures were assessed both as continuous variables and dichotomized by median levels. Higher exposure to PM₁, PM_2.5, PM₁₀, and NO₂ was consistently associated with faster eGFR decline. In fully adjusted models, each 1 μg/m³ increase in PM_2.5 corresponded to a steeper decline in eGFR (β = -0.02; 95% CI: -0.03 to -0.02), while participants in high PM_2.5 areas had an annual decline of -0.51 mL/min/1.73 m² (95% CI: -0.72 to -0.31). O₃ showed a significant association only in binary models. Weighted quantile sum regression identified PM_2.5 and PM₁ as dominant contributors. A favorable lifestyle markedly mitigated pollution-related decline; under high PM₁ exposure, eGFR declined by -0.69 (95% CI: -1.06 to -0.33) in those with favorable lifestyles versus -2.20 (95% CI: -2.65 to -1.75) in those with unfavorable lifestyles. These findings were robust across multiple sensitivity analyses. These findings emphasize the adverse impact of long-term air pollution exposure on kidney function and suggest that healthy lifestyle behaviors may offer significant protective benefits.

The urotensin II (UII) system comprises UII, UII-related peptide (URP), and their shared receptor UT. Bioactive UII can be generated from its precursor, prepro-UII, through proteolytic cleavage by the serine protease furin. The kidney serves as a significant source of UII, with elevated levels reported in infants with chronic kidney disease. Here, we investigated the contribution of the UII system to the loss of kidney function during ischemia-reperfusion (IR)-induced acute kidney injury (AKI) in neonatal pigs. Intra-arterial renal infusion of porcine UII reduced renal blood flow and increased vascular resistance, effects reversed by the UT antagonist urantide. Although IR did not alter whole-kidney UT expression, it increased furin, UII, URP, and vascular UT levels. Urantide attenuated IR-induced kidney hypoperfusion, elevations in AKI biomarkers and circulating cytokines, and histological kidney injury. In primary neonatal pig proximal tubule epithelial cells (PTECs), chemical IR (cIR), modeled by 1 h of ischemia (ATP-, glucose-, and serum-depleted medium) followed by reperfusion (restoration of complete medium), elevated furin and UII production. The furin inhibitor SSM 3 trifluoroacetate (SSM 3) suppressed cIR-induced UII synthesis. Moreover, both urantide and SSM 3 mitigated cIR-induced PTEC injury. These findings suggest that in neonatal pigs: (1) renal IR upregulates furin, UII, and URP in kidney tissue and UT in the microvasculature, (2) furin promotes UII biosynthesis in renal epithelial cells, and (3) UT inhibition protects against ischemic AKI.

Background: Inflammation is a key contributor to contrast-induced acute kidney injury (CI-AKI), yet its predictive role remains unclear. The systemic immune-inflammation index (SII) is a novel inflammatory biomarker, but its association with CI-AKI risk in coronary artery disease (CAD) patients undergoing coronary angiography is not well established. This study aimed to evaluate the relationship between preoperative SII and CI-AKI in a large multicenter cohort.

Methods: This retrospective cohort study analyzed CAD patients from five tertiary hospitals in China (2007-2020). Patients were stratified into SII tertiles, and multivariable logistic regression, restricted cubic splines (RCS), and two-piecewise logistic regression models were employed to assess the association between SII and CI-AKI risk.

Results: Among 30,822 patients, 3,246 (10.5%) developed CI-AKI. Higher preoperative SII levels were associated with increased CI-AKI risk ([SII-M vs. SII-L]: OR = 1.22, 95% CI [1.09-1.36], p = 0.001; [SII-H vs. SII-L]: OR = 1.70, 95% CI [1.53-1.90], p < 0.001). RCS analysis demonstrated a nonlinear relationship (p for nonlinearity = 0.008). The inflection point was at 19.12 × 10¹¹/L. Below this inflection point, each 100-unit increase in SII correlated with a 5% higher CI-AKI risk (OR = 1.05, 95% CI [1.04-1.06], p < 0.001), while no significant association was observed above this level.

Conclusion: Preoperative SII may be an independent predictor of CI-AKI risk in CAD patients undergoing undergoing coronary angiography, demonstrating a nonlinear dose-response relationship with a significant threshold effect. These findings suggest that SII may serve as a useful biomarker for early CI-AKI risk stratification in clinical practice.