Urokinase Promotes Redundantly Intratubular C3a-Formation But Not ENaC-Driven Hypertension in DOCA/Salt Kidney Injury.

ABSTRACT:

Background

uPA (urokinase-type plasminogen activator) inhibitors mitigate salt retention, plasmin, and complement activation in acute proteinuric kidney diseases. We hypothesized that in chronic kidney injury with albuminuria, uPA contributes to hypertension and complement-dependent tissue inflammation and injury.

Methods

Wild-type and uPA KO (knockout) mice underwent either sham surgery or unilateral nephrectomy, followed by insertion of deoxycorticosterone acetate (DOCA)- or sham pellets and a high (4%) or control (0.5%) sodium chloride diet for 21 days. Glomerular filtration rate was estimated by transcutaneous fluorescein-isothiocyanate-sinistrin, and arterial blood pressure was recorded continuously by indwelling femoral catheters. Urine was analyzed for albumin, plasmi

SUBMITTER: Bach ML 

PROVIDER: S-EPMC12928799 | biostudies-literature | 2026 Mar

REPOSITORIES: biostudies-literature