Key result
Glomerulonephritis is linked to a ~2-fold increase in cortical collecting duct Na+/K+-ATPase activity.
Enhancement of Na+/K+-ATPase activity in the cortical collecting duct is a shared characteristic of both chemically induced and autoimmune glomerulonephritis models.
Hypothesis-generating for Na+/K+-ATPase upregulation in glomerulonephritis; should not yet change clinical practice.
BACKGROUND: In rats with puromycin aminoglucoside-induced (PAN) nephrotic syndrome, micropuncture studies have localized the site of sodium retention to the collecting duct. We have confirmed this finding by demonstrating a two-fold increase in Na+/K+-ATPase activity specifically limited to the cortical 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+-ATPase activity in nephron segments from mice with spontaneous lupus-like nephritis. METHODS: Hydrolytic activity of Na+/K+-ATPase was measured in three isolated nephron segments: proximal convoluted tubule, thick ascending limb and cortical collecting duct. The Na+/K+-ATPase activities were measured in PAN rats, sham-injected controls, and in (MRL x BXSB) F1 male mice which develop a well established spontaneous lupus-like glomerulonephritis by 4 months of age and their controls. Control mice have the same genetic background, but 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) F1 male mice, Na+/K+-ATPase was similar to control mice in the proximal convoluted tubule and the thick ascending limb. In contrast, cortical collecting duct Na+/K+-ATPase activity was two times higher in (MRL x BXSB) F1 mice than controls. These results were identical to those observed in PAN rats compared to their sham-injected controls studied 7 days after an intraperitoneal injection of puromycin or isotonic saline, respectively. CONCLUSIONS: Enhancement of Na+/K+-ATPase activity localized to the cortical collecting duct is a general characteristic of glomerulonephritis independent of its mode of induction, i.e. chemical versus autoimmune. Therefore, the experimental model of PAN is suitable to study the underlying mechanisms leading to Na+/K+-ATPase dysfunction.
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Zolty et al. (1999) studied Glomerulonephritis. Glomerulonephritis (PAN-induced or spontaneous) vs. Controls (sham-injected rats or mice lacking Yaa mutant gene) was evaluated on Na+/K+-ATPase activity in isolated nephron segments. Glomerulonephritis, whether chemically induced or spontaneous autoimmune, was associated with a two-fold increase in Na+/K+-ATPase activity in the cortical collecting duct.
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