title: Salt restriction reduces hyperfiltration, renal enlargement, and albuminuria in experimental diabetes.
abstract: The effects of dietary salt restriction on the renin-angiotensin system, glomerular filtration rate (GFR), renal size, and albuminuria were assessed in streptozotocin diabetic rats. Two series of experiments were performed: one short-term with severe salt restriction and the second long-term with moderate salt restriction. The first studied the effect of a very-low-salt diet for 4 weeks on GFR, renal size, and plasma angiotensin II concentration in diabetic and control rats. Diabetic and control male Sprague-Dawley rats received either a very-low-salt (0.005% NaCl) or a normal-salt (0.4% NaCl) diet. Diabetes was associated with a 49% increase in GFR, a 34% increase in kidney weight, and an 85% reduction in plasma angiotensin II when compared with control rats (P < 0.001). Sodium restriction in diabetic rats reduced GFR, restored plasma angiotensin II to control values, and retarded kidney growth when compared with diabetic rats receiving a normal sodium diet. GFR correlated negatively with plasma angiotensin II (r = -0.65, P < 0.001) and positively with kidney weight (r = 0.66, P < 0.001). In the second experiment, serial measurements of albuminuria and GFR were performed in control, diabetic, and salt-restricted (0.05% NaCl) control and diabetic rats over 24 weeks. Albuminuria showed a continuous rise in the diabetic rats when compared with control rats. Salt restriction attenuated the increase in albuminuria over the whole study period as well as reducing blood pressure and kidney weight in the diabetic rats. In conclusion, sodium restriction was associated with a lower GFR and kidney weight after 4 weeks and reduced levels of albuminuria, kidney weight, and blood pressure after 24 weeks in diabetic rats. Salt restriction may have an important role in the prevention and treatment of diabetic nephropathy.
authors.affiliation: Department of Medicine, Austin and Repatriation Medical Centre, Heidelberg, Australia. terri@austin.unimelb.edu.au
authors.forename: T J
authors.initials: TJ
authors.lastname: Allen
authors.forename: M J
authors.initials: MJ
authors.lastname: Waldron
authors.forename: D
authors.initials: D
authors.lastname: Casley
authors.forename: G
authors.initials: G
authors.lastname: Jerums
authors.forename: M E
authors.initials: ME
authors.lastname: Cooper
mesh_terms: D000419:Albuminuria / Q000517:prevention & control*; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000097:blood / Q000503:physiopathology* / Q000517:prevention & control; D004039:Diet, Sodium-Restricted; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000502:physiology / Q000503:physiopathology*; D008297:Male; D009929:Organ Size; D051381:Rats; D017207:Rats, Sprague-Dawley; D012016:Reference Values; D012044:Regression Analysis; D012083:Renin / Q000097:blood; D013997:Time Factors
chemical_list: D001786:Blood Glucose; D000804:Angiotensin II; D012083:Renin