Urinary nephrin as an early biomarker of podocyte dysfunction in essential hypertension: a stage-stratified study from Bukhara, Uzbekistan

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• Picked for Biochemistry (medical) (paper of the day, 10 August 2026): Urinary nephrin rises early in hypertensive kidney injury

Abstract

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.

Abstract as published, via PubMed.