Experimental studies suggest that salt intake plays a critical role in the progressive glomerular filtration rate (GFR) loss of established renal disease; however, this issue has never been addressed in humans. To this aim, we have retrospectively analyzed the clinical data of patients with chronic renal failure (CRF), in whom a low-protein diet was prescribed, over a period of about 3 years. On the basis of the daily urinary sodium output, the patients were divided into two groups: a group of patients constantly ingesting >200 mEq NaCl/day (high sodium intake, HSD, n = 30) and a group in which salt intake was <100 mEq/day (low sodium intake, LSD, n = 27). Patients taking diuretics or ACE inhibitors were excluded. At baseline, the LSD group, as compared to the HSD group, was characterized by significantly lower creatinine clearance (24 ± 2 vs. 28 ± 2 ml/min) and higher proteinuria (2.9 ± 0.3 vs. 1.5 ± 0.2 g/day). Despite the presence of these risk factors for progression, and a similar control of blood pressure (the average of the mean arterial pressure during follow-up was 111 ± 2 mm Hg in LSD and 107 ± 2 mm Hg in HSD), the LSD patients showed a better renal outcome: in this group, as compared to HSD, the GFR decline was lower (0.25 ± 0.07 vs. 0.51 ± 0.09 ml/min/month, p < 0.05), and proteinuria did not change while it markedly increased in HSD. During follow-up, LSD patients also ingested a significantly lower amount of protein. This study therefore suggests that efficacious salt restriction in CRF patients improves the outcome of renal disease independent from its antihypertensive effects.

This study represents the first evidence that in CKD patients a protein intake of 0.55 g/kg/day, compared with a 0.8 g/kg/day, guarantees a better metabolic control and a reduced need of drugs, without a substantial risk of malnutrition.

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In moderate CRF, the tonic release of NO is constant and, likely, not impaired, and ARG supplementation does not lead to an enhancement of NO activity, thus resulting in no renal effect.