Key result
Urinary nephrin tracks hypertension severity and falls ~28% with RAS blockade.
Why the study?
Hypertensive kidney injury is often detected late by conventional markers, and urinary nephrin excretion reflecting podocyte injury may help identify renal involvement in essential hypertension.
Does antihypertensive treatment based on renin-angiotensin system blockade reduce urinary nephrin excretion and improve renal functional and haemodynamic markers in adults across stages I-III of essential hypertension?
Observational (n=60)
Open-label
No
Does antihypertensive treatment based on renin-angiotensin system blockade reduce urinary nephrin excretion and improve renal functional and haemodynamic markers in adults across stages I-III of essential hypertension?
Urinary nephrin excretion increases progressively across clinical stages I-III of essential hypertension—even when stage I eGFR is normal—and declines during 6 months of RAS blockade alongside profibrotic markers, supporting its potential as a candidate biomarker of podocyte injury.
Answers are grounded in this paper and cite their sources.
Urinary nephrin may mark early podocyte injury before eGFR decline; leaves open its value for monitoring or guiding RAS blockade.
Hypertensive kidney injury is often detected late by conventional markers. Urinary nephrin excretion (nephrinuria) reflects podocyte injury and may help identify renal involvement in essential hypertension. In this prospective, single-centre study, 60 adults with essential hypertension (20 per 2018 ESC/ESH stage, I–III; 20 men, 40 women) were assessed at baseline and after 6 months of antihypertensive treatment based on renin–angiotensin system (RAS) blockade (enalapril, n = 17; azilsartan, n = 43; add-on eplerenone, n = 21). Urinary nephrin, serum TGF-β1, VEGF-A and aldosterone, cystatin C–based eGFR, renal functional reserve (RFR; protein-loading test), 24-h albuminuria, echocardiography and renal Doppler were measured. Stages were compared by Welch’s ANOVA with Games–Howell post-hoc tests and Holm correction. Nephrinuria rose across stages (91.9 ± 8.3, 124.9 ± 9.3 and 164.5 ± 9.7 pg/mL, mean ± SEM; adjusted P < 0.001; all pairwise P ≤ 0.031), while eGFR at stage I remained within the normal range. RFR was lower at stage III than at stage I (12.5 ± 1.6% vs 22.5 ± 3.1%; P = 0.020), and segmental-artery flow velocity declined with stage, whereas VEGF-A showed only a trend. After 6 months, blood pressure fell and nephrinuria was lower at all stages (−32%, −31% and −23% at stages I, II and III), together with reductions in TGF-β1, VEGF-A and aldosterone. Nephrinuria is a candidate biomarker of podocyte injury in hypertension; controlled studies with assay-specific reference ranges are needed to establish its diagnostic value.
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Zokirov et al. (2026) conducted an observational in Essential hypertension (stages I-III) (n=60). Essential hypertension stage III (vs Stage I) and 6-month RAS blockade (enalapril or azilsartan ± eplerenone) vs. Stage I essential hypertension / Baseline prior to RAS blockade was evaluated on Baseline urinary nephrin excretion (nephrinuria, pg/mL) across hypertension stages III vs I (p=<0.001). Urinary nephrin rose across hypertension stages I–III and decreased by 23%–32% after 6 months of RAS blockade.
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