Glomerulonephritis and sodium retention: enhancement of Na+/K+-ATPase activity in the collecting duct is shared by rats with puromycin induced nephrotic syndrome and mice with spontaneous lupus-like glomerulonephritis

Background. In rats with puromycin aminoglucoside-induced (PAN) nephrotic s yndrome, micropuncture studies have localized the site of sodium retention to the collecting duct. We have confirmed this finding by demonstrating a t wo-fold increase in Na+/K+-ATPase activity specifcally limited to the corti cal collecting duct in PAN rats. To further define whether this phenomenon was dependent on the chemical induction of the nephrotic syndrome or was a general phenomenon observed in glomerulonephritis. we measured Na+/K+-ATPas e activity in nephron segments from mice with spontaneous lupus-like nephri tis. Methods. Hydrolytic activity of Na+/K+-ATPase was measured in three isolate d nephron segments: proximal convoluted tubule, thick ascending limb and co rtical collecting duct. The Na+/K+-ATPase activities were measured in PAN r ats, sham-injected controls, and in (MRL x BXSB) F1 male mice which develop a well established spontaneous lupus-like glomerulonephritis by 4 months o f age and their controls. Control mice have the same genetic background, bu t lack the Yaa mutant gene responsible for autoimmune acceleration and are free of glomerular lesions at 4 months of age. Results. In (MRL x BXSB) Fl male mice, Na+/K+-ATPase was similar to control mice in the proximal convoluted tubule and the thick ascending limb. Tn co ntrast, cortical collecting duct Na+/K+-ATPase activity was two times highe r in (MRL x BXSB) Fl mice than controls. These results were identical to th ose observed in PAN rats compared to their sham-injected controls studied 7 days after an intraperitoneal injection of puromycin or isotonic saline, r espectively. Conclusions. Enhancement of Na+/K+-ATPase activity localized to the cortica l collecting duct is a general characteristic of glomerulonephritis indepen dent of its mode of induction, i.e. chemical versus autoimmune. Therefore, the experimental model of PAN is suitable to study the underlying mechanism s leading to Na+/K+-ATPase dysfunction.