Background/Aims: 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<sup>+</sup>), normal (0.5% Na<sup>+</sup>), or high (8% Na<sup>+</sup>) 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.