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: Patients with end-stage kidney disease undergoing chronic hemodialysis (HD) have an unparalleled risk of vascular calcification (VC) and high alkaline phosphatase (Alk-P) levels. However, whether VC contributed to the cardiovascular risk modified by serum Alk-P levels was not addressed in the population.

Methods: A retrospective cohort study was conducted on chronic HD patients, between October 1 and December 31, 2018, with aortic arch calcification (AoAC) scores and serum Alk-P levels. Patients were categorized into four groups: non-to-mild AoAC/low Alk-P, non-to-mild AoAC/high Alk-P, moderate-to-severe AoAC/low Alk-P, and moderate-to-severe AoAC/high Alk-P. The Cox proportional hazard model and Kaplan-Meier analysis were used to evaluate the risks of major adverse cardiovascular effects (MACEs) and cardiovascular and all-cause mortality after multivariate adjustment.

Results: Among 376 chronic HD patients recruited, 125 (33%) had non-to-mild AoAC/low Alk-P, 76 (20%) had non-to-mild AoAC/high Alk-P, 89 (24%) had moderate-to-severe AoAC/low Alk-P, and 86 (23%) had moderate-to-severe AoAC/high Alk-P. After 3 years of follow-up, patients with coexisting moderate-to-severe AoAC and high Alk-P had a higher risk of MACEs (aHR 1.76; 95% CI 1.06-2.92), and cardiovascular (aHR 2.49; 95% CI 1.21-5.11) and all-cause mortality (aHR 2.67; 95% CI 1.39-5.13) compared to those with non-to-mild AoAC/low Alk-P even after adjustments for significant clinical variables.

Conclusions: In chronic HD patients, moderate to severe AoAC co-existed with high Alk-P levels and enhanced the risk of MACEs and cardiovascular and all-cause mortality. Interventions to attenuate these risk factors simultaneously should be emphasized in this population.

Background: Diabetic kidney disease (DKD) is the leading cause of chronic kidney disease globally. Recent research has identified insulin-like growth factor-binding proteins 2 (IGFBP2) and 4 (IGFBP4) as potential biomarkers for DKD. Overactivation of the complement pathway in DKD remains poorly understood.

Methods: Blood samples were collected from patients for proteomic analysis, complemented by both in vitro and in vivo experiments to investigate the roles of IGFBP2, IGFBP4, and the complement pathway in DKD.

Results: Elevated levels of IGFBP2 and IGFBP4 were observed in DKD patients. The levels of IGFBP2 and IGFBP4 increased in DKD mice, accompanied by the activation of the complement pathway, and a deterioration in renal function. High glucose and serum from DKD mice stimulated an increase in the levels of IGFBP2 and IGFBP4 in HK-2 cells. The supernatant from HK-2 cells was used to culture THP-1 cells, resulted in an increase in the M1 type of THP-1 cells, a decrease in the M2 type, and activation of the complement pathway. The supernatant from THP-1 cells affected the growth of primary human renal podocytes. The exogenous addition of IGFBP2 and IGFBP4 proteins to primary human renal podocytes did not affect their growth. However, when human renal podocytes were cultured with the supernatant from THP-1 cells, the growth of the podocytes was affected.

Conclusions: IGFBP2 and IGFBP4 interact to stimulate the activation of the complement pathway in macrophages, which induces podocyte apoptosis and subsequently promotes the development of DKD.

Smoking is widely acknowledged for its harmful effects on multiple organs. However, its specific causal relationship with chronic kidney disease (CKD) remains uncertain. This study applied bivariate causal analysis and two-sample Mendelian randomization (MR) methods to examine the association between various smoking behaviors - initiation, cessation, age at initiation, cigarettes smoked per day, and lifetime smoking - and CKD, using genome-wide data. The inverse variance weighted (IVW) method was the primary analytical tool, supported by sensitivity analyses, pleiotropy assessments, and mediation analyses. External validation was conducted using independent datasets. The results revealed positive associations between CKD and smoking initiation (Pivw = 1.8 × 10^-2, OR = 1.192), earlier age at initiation (Pivw = 2.3 × 10^-3, OR = 1.481), cigarettes smoked per day (Pivw = 8.8 × 10^-3, OR = 1.216), and lifetime smoking (Pivw = 2.3 × 10^-7, OR = 2.445). In contrast, smoking cessation demonstrated a protective effect against CKD (Pivw = 4.0 × 10^-12, OR = 0.791). External validation results aligned with the primary findings, and the absence of significant heterogeneity confirmed the robustness of the MR analysis. Additionally, the effect of smoking on CKD was mediated by factors such as body mass index, cardiovascular disease, hypertension, and type 2 diabetes. These findings identify smoking as a contributing factor to CKD and suggest that reducing smoking prevalence could significantly lower the incidence of CKD in the population.

Objective: To explore the risk factors for uric acid-lowering therapy-resistant gout (UALT-RG) and its relationships with the estimated glomerular filtration rate (eGFR), body roundness index (BRI), and visceral adiposity index (VAI) via 2007-2018 National Health and Nutrition Examination Survey (NHANES) data.

Methods: We calculated the BRI using waist circumference and standing height; the VAI using triglycerides (TGs), high-density lipoprotein cholesterol (HDL-C), and body mass index (BMI); and the eGFR from serum creatinine levels. We also collected gout data. We explored the relationships of the eGFR, BRI, and VAI with UALT-RG risk via univariable and multivariable weighted logistic regression, trend analysis, and restricted cubic splines.

Results: Among the 1,811 patients with gout, ∼9.08% had UALT-RG; these patients were more likely to have obesity, comorbid diabetes (36% [27-47%] vs. 25% [22-28%]) or impaired kidney function (eGFR < 60 mL/min/1.73 m², 34.5% [27-43%] vs. 22.5% [20-26%]); be former smokers; and take colchicine (10% [5.6-19%] vs. 4.3% [2.8-6.7%]). Logistic regression and trend analysis suggested that an elevated BRI and decreased eGFR were independent risk factors and potential screening indicators for UALT-RG. Restricted cubic spline analysis revealed a negative linear trend between the eGFR and UALT-RG risk (p-overall < 0.0001) and a significant positive correlation between the BRI and UALT-RG risk (p-overall < 0.0001).

Conclusion: An increased BRI and decreased eGFR may be independent risk factors and assessment indicators for UALT-RG in U.S. adults. It is necessary to monitor serum urate levels more closely and conduct early multidisciplinary comanagement when gout is comorbid with visceral obesity and chronic kidney disease stages 3-5.

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.

Background: In patients undergoing hemodialysis (HD), cardiovascular (CV) disease, particularly sudden cardiac death (SCD), is a major cause of mortality. Independent predictors of SCD include a prolonged QT interval on electrocardiography (ECG) and elevated levels of natriuretic peptides (NPs). This study explores the association between the QTc interval and NPs in HD patients.

Methods: This cross-sectional study involved 207 HD patients, having a heart rate of 57 to 103 bpm, displaying sinus rhythm and no extrasystoles in ECG reports. Before the 2nd HD of the week, we conducted ECG and blood tests for atrial NP (ANP), brain NP (BNP), and N-terminal proBNP (NT-proBNP). The heart rate-corrected QT (QTc) was calculated using Bazett formula. Our analysis focused on the association between QTc and each NP, along with evaluating clinically relevant variables related to the QTc interval.

Results: Univariate analyses indicated robust correlations among the NPs, with each NP significantly associated with the QTc interval. Multiple regression analyses of the three NPs revealed that NT-proBNP demonstrated the strongest predictive ability for the QTc interval. Independent predictors of prolonged QTc included lower corrected calcium (cCa) levels (p = 0.001), lower potassium (K) levels (p < 0.001), and higher log NT-proBNP (p = 0.004).

Conclusion: In HD patients, NT-proBNP shows a stronger link with the QTc interval than BNP or ANP. Integrating clinical management considering both QTc and log NT-proBNP levels might help reduce CV events. Additionally, vigilance regarding low K or cCa levels is recommended from the perspective of the QTc interval.

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.