Renal complications in diabetes impose substantial morbidity globally, yet early risk stratification remains challenging. The neutrophil-to-HDL cholesterol ratio (NHR) represents an integrated biomarker reflecting both immune activation and dyslipidemia, with neutrophilia promoting renal inflammation and low HDL-C impairing renoprotective mechanisms. We evaluated whether NHR is associated with diabetic nephropathy (DN) in a population-based cross-sectional study. We analyzed 2005 diabetic adults from six NHANES cycles (2007-2018). DN was defined as microalbuminuria (UACR ≥ 30 mg/g) or reduced eGFR (<60 mL/min/1.73m2) calculated via CKD-EPI 2021. NHR was computed as the ratio of neutrophil count to HDL-C concentration. Multivariable logistic regression with sequential covariate adjustment (demographics, socioeconomic factors, and comorbidities) was used to examine NHR-DN associations. Quartile-based dose-response analysis and restricted cubic spline modeling were additionally performed to characterize the association shape. DN prevalence reached 37.31% (n = 748). Individuals with nephropathy exhibited 15% higher median NHR (3.691 vs. 3.211, P < .001). Fully adjusted models revealed that per-unit NHR elevation increased DN odds by 22.48% (OR 1.2248, 95%CI 1.1533-1.3017, P < .001). Quartile analysis demonstrated dose-response relationships: top quartile participants showed 2.70-fold higher nephropathy risk versus bottom quartile (OR 2.6967, 95%CI 1.9965-3.6556, p-trend < 0.001). Higher NHR independently correlates with diabetic nephropathy presence in US adults. This readily calculated index combining inflammatory and metabolic dimensions may enhance clinical risk assessment. These observational findings suggest that NHR may serve as a complementary marker to support kidney disease risk stratification in diabetic patients, pending confirmation by prospective studies.

Recent evidence links organophosphate pesticide exposure to cardiometabolic and kidney disorders in adults, but its impact in children remains poorly understood. This study evaluated associations between urinary dialkyl phosphate (DAP) metabolite concentrations and early markers of kidney and cardiovascular stress in children. A nationwide population sample of 2928 children less than 18 years of age from the 2015-2020 National Health and Nutrition Examination Survey (NHANES) was evaluated. The six DAP metabolites examined were dimethylphosphate (DMP), diethylphosphate (DEP), dimethylthiophosphate (DMTP), diethylthiophosphate (DETP), dimethyldithiophosphate (DMDTP) and diethyldithiophosphate (DEDTP). Clinical outcomes measured included both systolic and diastolic blood pressure indices, hypertensive status, microalbuminuria (albumin-to-creatinine ratio greater than 30 mg/g), and kidney hyperfiltration (estimated glomerular filtration rate greater than 135 mL/min/1.73m[2]). Multivariate linear and logistic regression models were used with adjustments made for age, gender, body mass index z-score, and poverty income ratio to evaluate the relationships among each of these clinical outcomes and levels of the metabolites. Statistical significance was set at p < 0.0167 due to the number of comparisons made. In adjusted models, higher urinary DAP metabolite concentrations were not significantly associated with systolic or diastolic blood pressure indices or hypertensive status (p > 0.05). However, higher DEDTP was significantly associated with both microalbuminuria (OR 1.290, 95% CI [1.051-1.583], p = 0.016) and kidney hyperfiltration (OR 2.348, 95% CI [1.658-3.324], p < 0.001). Additionally, higher DMDTP was significantly associated with hyperfiltration (OR 1.466, 95% CI [1.116-1.926], p = 0.007). In conclusion, higher urinary concentrations of specific DAP metabolites were associated with microalbuminuria and kidney hyperfiltration in U.S. children. These findings highlight the potential kidney effects of early-life organophosphate pesticide exposure and warrant further investigation into underlying mechanisms.

Background: Albuminuria is a marker of cardiovascular and renal risk and may reflect dynamic haemodynamic changes in acute heart failure (AHF). However, the prognostic value of early urine albumin-to-creatinine ratio (UACR) monitoring during the vulnerable post-discharge phase remains unclear. Methods: We conducted a prospective single-centre study, including 88 patients with hospitalization for AHF. UACR was measured at discharge and at a two-week follow-up visit. Patients were stratified according to UACR trajectory: (1) persistent normoalbuminuria; (2) microalbuminuria with significant reduction (>50%) or normalization; and (3) persistent microalbuminuria without significant reduction or macroalbuminuria. Clinical outcomes included HF readmissions, all-cause mortality and a composite endpoint of HF readmission or all-cause mortality. Results: Albuminuria was prevalent in 64.8% of patients. Group 3 showed a higher burden of comorbidities, worse renal function and higher congestion markers. During a median follow-up of 553 days, group 3 had a higher incidence of HF events and the composite endpoint. In multivariable analysis, group 3 was independently associated with HF hospitalization (HR 3.09, 95% CI 1.19-8.04; p = 0.021) and the composite endpoint (HR 3.31, 95% CI 1.18-9.35; p = 0.024), whereas no independent association was observed for group 2. Renal function remained stable in groups 1 and 2, while group 3 showed worse renal outcomes. Conclusions: Albuminuria is frequently observed during AHF and is closely related to haemodynamic congestion. Persistent albuminuria identifies a high-risk phenotype, whereas early reduction was associated with more favourable unadjusted outcomes. Early post-discharge UACR trajectory may improve risk stratification during the vulnerable phase.

Diabetic kidney disease (DKD) is a major microvascular complication of type 2 diabetes mellitus (T2DM) and a leading cause of progressive renal failure worldwide. Although urinary albumin-to-creatinine ratio (UACR) and estimated glomerular filtration rate remain the cornerstone measures for DKD assessment, simple and readily available biomarkers may provide complementary clinical information. In this cross-sectional study, 300 patients with T2DM were categorized into three groups according to UACR. The study evaluated and compared the triglyceride-glucose (TyG) index, neutrophil-to-lymphocyte ratio (NLR), and high-sensitivity C-reactive protein (hs-CRP) across albuminuria categories. All three biomarkers differed significantly among the albuminuria categories, with the highest levels observed in patients with macroalbuminuria. Receiver operating characteristic analyses demonstrated good discriminatory performance for albuminuria, with both NLR and hs-CRP exhibiting significantly greater discriminatory ability than the TyG index in several comparisons. In adjusted multinomial logistic regression analysis, NLR was independently associated with both microalbuminuria and macroalbuminuria, whereas the TyG index and hs-CRP were independently associated only with macroalbuminuria. These findings support the complementary role of these readily available biomarkers in the assessment of albuminuria in T2DM and provide a basis for future longitudinal studies to clarify their clinical significance.

Essential hypertension is a leading cause of chronic kidney disease, but conventional renal markers detect injury only after substantial nephron loss. Urinary nephrin, a slit-diaphragm protein released during podocyte injury, has been proposed as an early biomarker of hypertensive nephropathy, yet stage-specific data are scarce, particularly from Central Asia. In this single-centre, prospective study, we enrolled 60 adults with essential hypertension stratified by stage (I, II, III; n = 20 per group) in Bukhara, Uzbekistan; patients with diabetes, heart failure, primary kidney disease, or prior SARS-CoV-2 infection were excluded. Urinary nephrin, serum cystatin-C, TGF-β1, aldosterone, and VEGF-A were measured by ELISA, and renal Doppler ultrasonography and an oral protein-loading test for renal functional reserve (RFR) were performed at baseline and after 6 months of an ACE inhibitor or angiotensin receptor blocker, with eplerenone where indicated. Urinary nephrin rose progressively across stages (91.9 ± 8.3, 124.9 ± 9.3, 164.5 ± 9.7 ng/mL) and was already elevated in stage I despite normal creatinine, cystatin-C, and eGFR. Nephrinuria correlated with systolic blood pressure (r = 0.58), aldosterone (r = 0.54), and microalbuminuria (r = 0.71), and inversely with eGFR (r = -0.74) and RFR (r = -0.76; all P < 0.01). After 6 months, urinary nephrin declined by 32%, 31%, and 23% across stages, with parallel reductions in TGF-β1, VEGF-A, and aldosterone and partial RFR recovery. Urinary nephrin is elevated while conventional markers remain normal and responds to nephroprotective therapy, supporting its potential as an early biomarker of hypertensive kidney injury.

This cross-sectional study aimed to analyze whether inter-ankle systolic blood pressure difference (sIAND) was associated with different stages of hypertensive renal damage. 1,658 and 831 nondiabetic hypertensive patients were included from two cohorts. The hypertensive renal damage was reflected by urinary albumin-to-creatinine ratio (UACR), Cystatin C, and estimated glomerular filtration rate. Logistic regression results showed that sIAND was only associated with subclinical hypertensive renal damage reflected by microalbuminuria (UACR > 30 mg/g) independently. Receiver operating characteristic curves indicated sIAND can identify microalbuminuria more effectively. sIAND can aid in identifying microalbuminuria to provide useful clues for risk stratification and clinical management.

Primary aldosteronism (PA) is the most common curable cause of secondary hypertension and an independent risk factor for chronic kidney disease (CKD). This review focuses on the pathophysiological mechanisms of aldosterone-induced renal injury, including mineralocorticoid receptor activation, nongenomic signaling via GPER, oxidative stress, and the upregulation of profibrotic and inflammatory mediators such as TGF-β1, NF-κB, and NLRP3. Chronic aldosterone excess leads to podocyte injury, microvascular dysfunction, and interstitial fibrosis, resulting in decreased glomerular filtration rate and CKD progression.Genetic mutations (KCNJ5, ATP1A1, CACNA1D) and tubular stress biomarkers (L-FABP, KIM-1, microalbuminuria) are discussed as key factors of early nephron injury. Comparative clinical data show that adrenalectomy provides superior nephroprotection compared to pharmacological blockade, while long-term therapy with mineralocorticoid receptor antagonists requires careful renal monitoring. Emerging therapeutic strategies, including nonsteroidal MR antagonists and aldosterone synthase inhibitors (baxdrostat), offer new prospects for targeted nephroprotection.By integrating molecular and clinical evidence, this review highlights the central role of aldosterone in renal pathology and emphasizes early detection and personalized treatment approaches to prevent CKD progression in patients with PA.

ObjectiveSuperselective adrenal arterial embolization with ethanol has demonstrated promising efficacy in patients with primary aldosteronism and lateralized aldosterone secretion. However, approximately 40% of patients have nonlateralized disease, defined as bilateral primary aldosteronism based on adrenal venous sampling.MethodsIn this prospective observational cohort study, 30 patients with primary aldosteronism underwent superselective adrenal arterial embolization, including 16 patients with unilateral primary aldosteronism and 14 patients with bilateral primary aldosteronism confirmed by adrenal venous sampling. Patients were stratified into the unilateral primary aldosteronism and bilateral primary aldosteronism groups. Blood pressure and biochemical parameters were assessed at 15-40 h and at 1, 3, and 6 months after the procedure.ResultsPlasma aldosterone concentration, plasma renin activity, and the aldosterone-to-renin ratio improved significantly in both groups within 15-40 h after superselective adrenal arterial embolization compared with baseline. At 6 months, the rates of complete or partial clinical and biochemical success were 85.7% and 92.9%, respectively, in the bilateral primary aldosteronism group compared with 81.3% and 87.5%, respectively, in the unilateral primary aldosteronism group. Significant reductions in serum sodium levels and microalbuminuria were observed in patients undergoing bilateral superselective adrenal arterial embolization. Body mass index also decreased significantly at 1, 3, and 6 months in both groups. No procedure-related complications were observed during a median follow-up of 6 months.ConclusionsBilateral superselective adrenal arterial embolization may represent a valuable adjunctive treatment strategy for patients with bilateral primary aldosteronism.