MON-692 Effect of High Salt Diet on Kidney Weight in Neonatal Streptozotocin Induced Noninsulin Dependent Diabetic Rats

Diabetic kidney hypertrophy may contribute to the development of diabetic kidney disease. Hyperglycemia is recognized as a cause for the kidney endangerment. Salt may accelerate progression of kidney disease in diabetes. To further study the effect of high salt intake on kidney disease we used neonatal streptozotocin induced Noninsulin Dependent Diabetic (NIDD) rats fed ad libitum with regular Purina chow and 2% salt Purina chow. Rats in 5 groups were sacrificed at 6 weeks. Each group had 5–7 rats of diabetics on 2% salt and on regular chow and controls on 2% salt and on regular chow. Blood glucose in diabetics on salt ranged between 185±19–576±20 and in diabetics on regular chow 184±20–458±78 mg/dl. Controls on 2% salt 105±8.6–133±10.3 and controls on regular chow 110±8.9 - 130±3.11. Kidney weights in diabetics on salt was 1.85±0.09–2.0±0.06 gr, diabetics on regular chow 1.6±0.04 - 1.56±0.06 controls on salt 1.19±0.03–1.32±0.05 and controls on regular chow 1.23±0.03. Blood glucose in diabetics on salt and on regular chow was higher than in controls p˂0.05 but did not differ between the diabetic groups. Kidney weight was increased in both diabetic groups compared with controls p˂0.05 and was increased in diabetics on salt compared with diabetics on regular chow p˂0.05 at all glucose levels. Controls on salt and on regular chow had similar kidney weights. Also kidney weight relative to body weight was higher in diabetics than in controls p˂0.05 and was higher in diabetics on salt compared to diabetics on regular chow p˂0.05, but there was no difference between controls on salt and controls on regular diet. Kidney % of water was similar in all four groups but protein to kidney DNA ratio was higher in the diabetic groups p˂0.05 confirming the kidney hypertrophy. Insulin sensitivity measured in controls was not different between groups when glucose transport, glucose oxidation and lipogenesis were measured in fat cells showing no effect of salt on insulin sensitivity. We suggest that high salt intake is an additional risk factor for increased kidney weight in NIDDM that is additive to that of the prevailing glycemia.