title: Renal functional deterioration is not affected by the magnitude of sodium consumption in a normotensive model of moderate renal failure.
abstract: OBJECTIVE
  High sodium consumption has been repeatedly reported to exert deleterious effects on severe chronic renal failure progression, mainly via glomerular mechanisms. However, the role of high sodium intake in renal function deterioration in a model of moderate chronic tubulointerstitial disease has not yet been addressed. We evaluated the effects of exaggerated dietary sodium and the resultant increase in proteinuria on renal function deterioration in experimental tubulointerstitial disease in rats.
  
  
  METHODS
  In 48 Sprague-Dawley rats, moderate renal failure (approximately 50% of normal glomerular filtration rate) was induced by administration of lithium chloride in drinking water. The animals were divided into three groups fed low (<0.2% Na(+)), normal (0.5% Na(+)), or high (8% Na(+)) sodium diets.
  
  
  RESULTS
  Animals in all groups remained normotensive with a similar course of GFR downslope and 100% survival, irrespective of sodium regimen. Rats consuming high sodium diets developed significantly greater proteinuria compared to their counterparts fed normal or low sodium chow.
  
  
  CONCLUSIONS
  (1) Deterioration of renal function in a lithium-induced model of normotensive moderate chronic renal failure was not affected by dietary sodium. (2) Unlike in some other human or experimental renal failure models, the magnitude of proteinuria had no adverse effect on the progression of renal deterioration.
authors.affiliation: Division of Nephrology, Assaf Harofeh Medical Center, Zerifin, Israel. Weissgarten@asaf.health.gov.il
authors.forename: Joshua
authors.initials: J
authors.lastname: Weissgarten
authors.forename: Sylvia
authors.initials: S
authors.lastname: Berman
authors.forename: Shai
authors.initials: S
authors.lastname: Efrati
authors.forename: Michael
authors.initials: M
authors.lastname: Rapoport
authors.forename: Mordechay
authors.initials: M
authors.lastname: Aladjem
authors.forename: David
authors.initials: D
authors.lastname: Modai
authors.forename: Ahuva
authors.initials: A
authors.lastname: Golik
authors.forename: Natan
authors.initials: N
authors.lastname: Cohen
authors.forename: Elena
authors.initials: E
authors.lastname: Galperin
authors.forename: Zhan
authors.initials: Z
authors.lastname: Averbukh
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004195:Disease Models, Animal; D018450:Disease Progression; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000473:pathology; D007676:Kidney Failure, Chronic / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D018021:Lithium Chloride; D008297:Male; D009395:Nephritis, Interstitial / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D011507:Proteinuria / Q000139:chemically induced; D051381:Rats; D017207:Rats, Sprague-Dawley; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage* / Q000494:pharmacology / Q000652:urine
chemical_list: D017673:Sodium Chloride, Dietary; D018021:Lithium Chloride