Mechanisms of tubular volume retention in immune-mediated glomerulonephritis

摘要: Glomerulonephritis is characterized by hematuria, proteinuria, hypertension, and edema, but the mechanisms contributing to volume disorders are controversial. Here we used rat anti-Thy1 model of mesangioproliferative glomerulonephritis test hypothesis that disturbed salt water homeostasis based on tubular epithelial changes cause retention. In this there was an early onset pronounced proteinuria lipiduria associated with reduced fractional sodium excretion a lowering renin–angiotensin–aldosterone system. The glomerular filtration rate creatinine clearance were decreased day 6. There abundance major transport proteins proximal brush border membrane which paralleled cellular protein overload, enhanced cholesterol uptake cytoskeletal changes. Alterations in thick ascending limb moderate. Changes collecting ducts increased subunit cleavage channel, both events consistent reabsorption. We suggest irrespective changes, altered duct reabsorption may be crucial for retention acute glomerulonephritis. proteolytic ion transporter subunits might novel mechanism channel activation diseases. Whether these proteases filtered or locally secreted awaits determination.