[To salt or not to salt in kidney diseases? Not more than quantum satis!]

The salt intake in former Czechoslovakia is twice as high as recommended 5 g/24 hours, which corresponds to 85 mmol//24 hours of sodium in the urine. In the population, the systemic blood pressure level correlates with a urinary excretion of sodium/24 hours. On the other hand, limited salt intake decreases blood pressure in salt-sensitive hypertensive patients. Albuminuria also positively correlates with a salt intake in the population. In patients with renal disease, a diet with low salt content suppresses proteinuria, and, in contrast, proteinuria is elevated with increased salt intake. The positive influence of the decreased salt intake on the progression of renal insufficiency was confirmed in many experimental studies. However, in humans, this finding was not unequivocally established in control randomized studies. The high salt intake worsens metabolic acidosis in patients with renal insufficiency. Salt is detrimental to the kidneys either by increased systemic and intraglomerular blood pressures or by pressure independent mechanisms of the tissue injury, which are mediated by a higher sodium concentration. The present knowledge concerning the relationship between sodium intake and extracellular fluid volume probably will be modified in light of new discoveries about the osmotically inactive sodium. The public enlightenment and medical application of these new findings related to harmful effects on an inappropriate salt intake in treatment of the kidney disease and in other fields of medicine is strongly desirable.