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Metabolic acidosis is common after kidney transplantation and has been linked to adverse renal outcomes. However, its relationship with histological injury in kidney allografts remains poorly characterized. We aimed to explore the association between metabolic acidosis and histopathological features in kidney allograft biopsies. This single-center, cross-sectional observational study included 63 adult kidney transplant recipients who underwent clinically indicated allograft biopsies. Metabolic acidosis was defined as a serum bicarbonate level < 22 mmol/L at the time of biopsy. Histological lesions were assessed according to the Banff classification. Lesion severity was evaluated using descriptive statistics, nonparametric comparisons, ordinal logistic regression, and multivariable logistic regression models adjusted for renal function, proteinuria, and time from transplantation. Sensitivity analyses additionally adjusted for hemoglobin and donor-related variables. Patients with metabolic acidosis exhibited numerically higher severity scores for both acute inflammatory lesions and chronic histological changes, including total inflammation and interstitial fibrosis/tubular atrophy (IFTA). Across ordinal analyses and multivariable regression models, consistent directional trends toward a greater histological injury burden were observed among acidotic patients; however, none of these associations reached statistical significance, and confidence intervals were wide. Sensitivity analyses yielded directionally consistent effect estimates. In this biopsy-based analysis, metabolic acidosis showed consistent directional trends toward a higher burden of inflammatory and chronic histological lesions, although these findings did not reach statistical significance.

(1) Background: Cardiovascular disease represents the leading cause of morbidity and mortality in patients with autosomal dominant polycystic kidney disease (ADPKD), often developing early in the disease course, even in the presence of preserved renal function. We aimed to evaluate circulating heart-type fatty acid-binding protein (H-FABP) as a marker of subclinical cardiac involvement and cardiorenal interaction in ADPKD. (2) Methods: In this single-center observational study, 80 adult patients with ADPKD receiving tolvaptan therapy were evaluated using echocardiography, renal function parameters, and circulating H-FABP levels. Associations between H-FABP and echocardiographic indices of cardiac structure and function, as well as renal parameters, were assessed using linear regression models. In addition, a composite severity score integrating CKD stage and H-FABP levels was constructed to assess the combined cardiorenal burden. (3) Results: Higher H-FABP concentrations were significantly associated with echocardiographic markers suggestive of subclinical cardiac involvement, particularly parameters related to impaired myocardial relaxation, including lower E/A ratio and reduced tissue Doppler e' velocities. These associations remained significant after adjustment for renal function and relevant clinical covariates. In parallel, H-FABP levels were also associated with markers of renal disease severity, including lower baseline eGFR and greater total kidney volume. The composite severity score showed a graded association with echocardiographic parameters, with a progressive trend toward less favorable diastolic indices as risk categories increased. These findings suggest a potential complementary role for H-FABP in the integrated evaluation of cardiorenal involvement in ADPKD. Given the cross-sectional design and single-centre setting, these results should be considered hypothesis-generating and require prospective validation in larger, independent cohorts.

Introduction: Metabolic acidosis is common after kidney transplantation and is associated with adverse outcomes. However, its vascular and functional correlates in kidney transplant recipients remain insufficiently characterized. Methods: We conducted a cross-sectional study of adult kidney transplant recipients attending routine outpatient visits at a tertiary transplant center. Metabolic acidosis was defined as serum bicarbonate < 22 mmol/L. Arterial stiffness was assessed by carotid–femoral pulse wave velocity (PWV), and physical frailty was evaluated using the Fried frailty phenotype. Multivariable regression models were used to identify determinants of metabolic acidosis and to examine its association with arterial stiffness and frailty severity. Results: Among 239 patients (median age 46 years), 154 (64%) had metabolic acidosis. Lower estimated glomerular filtration rate and higher systemic inflammation were independently associated with metabolic acidosis. Metabolic acidosis was independently associated with higher arterial stiffness, with a 1.41 m/s higher PWV after adjustment for age, sex, blood pressure, kidney function, and diabetes mellitus (p < 0.001). Although metabolic acidosis was associated with greater frailty severity in minimally adjusted models, this association was attenuated and no longer statistically significant after further adjustment for kidney function, diabetes, and inflammation. In stable kidney transplant recipients, metabolic acidosis is independently associated with increased arterial stiffness but not with frailty after accounting for key clinical confounders. Conclusions: These findings highlight metabolic acidosis as a marker of vascular vulnerability and a potential therapeutic target after kidney transplantation.

Background/Objectives: Chronic kidney disease (CKD) progression is strongly influenced by systemic inflammation. The neutrophil-to-lymphocyte ratio (NLR), derived from routine blood counts, reflects the balance between innate and adaptive immunity and has been proposed as a marker of adverse renal outcomes. We hypothesized that elevated baseline NLR is associated with reduced kidney function and increased risk of progression to end-stage kidney disease (ESKD) in adults with non-dialysis CKD. Methods: Following PRISMA guidelines, we systematically searched MEDLINE, Embase, and Scopus for studies enrolling adults with CKD stages 1–4 that reported renal outcomes according to baseline NLR. The primary outcome was progression to ESKD or renal replacement therapy (RRT) initiation. Results: Six eligible studies were identified, of which four provided sufficient data for meta-analysis. Across cohorts, elevated baseline NLR was consistently associated with adverse renal outcomes. In pooled analyses, high NLR nearly doubled the risk of ESKD or RRT (RR 1.96, 95% CI 1.30–2.97). Leave-one-out sensitivity analysis strengthened the association while reducing heterogeneity. For kidney function, higher NLR was associated with lower baseline eGFR (SMD −1.59, 95% CI −2.38 to −0.80). Conclusions: Elevated NLR is a robust prognostic marker of renal function decline and progression to ESKD or RRT in non-dialysis CKD. As a simple and inexpensive biomarker, NLR offers additional predictive value beyond eGFR and albuminuria. Incorporating NLR into risk models may refine stratification, guide follow-up, and enable earlier therapeutic optimization. Prospective large studies are warranted to establish thresholds and validate its role in clinical practice.