Nephrinuria as a marker of podocyte dysfunction in hypertensive nephropathy: relationship with renal functional reserve and changes during renin–angiotensin system 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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