Hypertension but not sodium intake determines progression of renal failure in experimentally uremic rats.

Background/aims: High sodium intake is implicated in contributing to progression of chronic renal failure. We studied the effect of high sodium consumption on progression of rat experimental renal failure while sodium-induced hypertension was pharmacologically controlled.

Methods: 64 Sprague-Dawley rats underwent 5/6 nephrectomy. Subsequently, they were divided in three groups which were fed either low, normal, or high sodium diet. Only the high sodium-consuming group developed hypertension. This group was further divided in two subgroups in which hypertension was either untreated or titrated to normotension by hydralazine alone or with propranolol.

Results: Sequential GFR values did not differ between the respective normotensive groups. Survival downslopes of all three normotensive groups (including the pharmacologically treated, high sodium-consuming subgroup) were also similar, extending over 10 weeks. By contrast, pharmacologically untreated animals exhibited severe hypertension and 100% mortality within 3 weeks. In all experimental groups, 24-hour urinary sodium excretion paralleled sodium intake. Proteinuria rose similarly and significantly in all animals on high sodium. A significant correlation between 24-hour sodium and proteinuria was evident throughout the experimental period.

Conclusions: (1) In 5/6 nephrectomized rats, renal function deterioration was not affected by dietary sodium, provided hypertension was pharmacologically controlled. (2) Enhanced proteinuria secondary to high sodium consumption had no adverse effect on progression of renal failure in this model.