title: 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.
abstract: 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.
authors.affiliation: Department of Internal Medicine, University of Geneva, Switzerland.
authors.forename: E
authors.initials: E
authors.lastname: Zolty
authors.forename: N
authors.initials: N
authors.lastname: Ibnou-Zekri
authors.forename: S
authors.initials: S
authors.lastname: Izui
authors.forename: E
authors.initials: E
authors.lastname: Féraille
authors.forename: H
authors.initials: H
authors.lastname: Favre
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents; D005921:Glomerulonephritis / Q000378:metabolism* / Q000473:pathology; D007685:Kidney Tubules, Collecting / Q000201:enzymology*; D008181:Lupus Nephritis / Q000201:enzymology*; D008297:Male; D051379:Mice; D009399:Nephrons / Q000201:enzymology; D009404:Nephrotic Syndrome / Q000139:chemically induced / Q000201:enzymology*; D011691:Puromycin; D051381:Rats; D017208:Rats, Wistar; D012016:Reference Values; D012964:Sodium / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D014018:Tissue Distribution
chemical_list: D000900:Anti-Bacterial Agents; D011691:Puromycin; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase