We have reviewed the role of salt intake in kidney diseases, particularly in relation to renal hemodynamics, renal excretion of proteins, renal morphological changes and progression of chronic renal failure. High salt intake may have detrimental effects on glomerular hemodynamics, inducing hyperfiltration and increasing the filtration fraction and glomerular pressure. This may be particularly important in elderly, obese, diabetic or black patients, who have a high prevalence of salt-sensitivity. Changes in salt intake may influence urinary excretion of proteins in patients with essential hypertension, or diabetic and non diabetic nephropathies. Moreover, high sodium intake may blunt the antiproteinuric effect of various drugs, including angiotensin-converting-enzyme inhibitors and calcium antagonists. Experimental studies show a direct tissue effect of salt on the kidney, independent of its ability to increase blood pressure, inducing hypertrophy, fibrosis and a decrease in glomerular basement membrane anionic sites. However, no firm conclusion can be drawn about the relationship between salt consumption and progression of chronic renal failure, because most information comes from conflicting, small, retrospective, observational studies. In conclusion, it would appear that restriction of sodium intake is an important preventive and therapeutic measure in patients with chronic renal diseases of various origin, or at risk of renal damage, such as hypertensive or diabetic patients.