title: Renal adaptation to dietary sodium restriction in moderate renal failure resulting from chronic glomerular disease.
abstract: The renal response to sodium restriction was evaluated, and the concurrent changes of the plasma levels of aldosterone (ALDO) and atrial natriuretic peptide (ANP), in healthy patients (NOR), in normotensive patients with non-nephrotic chronic glomerulonephritis and normal renal function (GN), and in patients with glomerulonephritis and moderate renal failure (GFR, 41 +/- 4 mL/min; CRF). The three groups were studied for 1 wk after changing from a normal-sodium diet (NSD, 235 mEq NaCl/day) to a low-sodium diet (LSD, 35 mEq NaCl/day). All patients reached a steady sodium balance within the 4th and 5th day of LSD with an analogous cumulative loss of sodium. After salt restriction, the fractional urinary sodium excretion diminished by the same extent in the three groups, whereas the fractional free-water generation, measured during water diuresis, did not vary in NOR and markedly decreased in GN and CRF. Plasma levels of ALDO were similar in all groups at NSD and similarly increased during LSD. In GN and CRF, as compared to NOR, ANP levels were higher at NSD and decreased by a minor extent during LSD. Notably, in GN and CRF, but not in NOR, the attainment of the new sodium balance after sodium restriction was preceded by a significant parallel reduction of blood pressure and GFR; the GFR decline was secondary to a major decrement of RPF so that filtration fraction (FF) increased. It was concluded that in NOR, distal tubular effects of ANP and ALDO account for the attainment of sodium balance during LSD. As a difference, both GN and CRF patients achieve the new sodium balance primarily through hemodynamic changes: the renal hypoperfusion secondary to a decrease in blood pressure that diminishes the filtered load of sodium, and the increase of FF that enhances the proximal tubular sodium reabsorption. This abnormal response seems related to both the minor suppression of ANP and the increased salt-sensitivity of blood pressure that are likely the result of the presence of volume expansion.
authors.affiliation: Division of Nephrology, School of Medicine, First University, Naples, Italy.
authors.forename: B
authors.initials: B
authors.lastname: Cianciaruso
authors.forename: V
authors.initials: V
authors.lastname: Bellizzi
authors.forename: R
authors.initials: R
authors.lastname: Minutolo
authors.forename: G
authors.initials: G
authors.lastname: Colucci
authors.forename: V
authors.initials: V
authors.lastname: Bisesti
authors.forename: D
authors.initials: D
authors.lastname: Russo
authors.forename: G
authors.initials: G
authors.lastname: Conte
authors.forename: L
authors.initials: L
authors.lastname: De Nicola
mesh_terms: D000222:Adaptation, Physiological; D000328:Adult; D000450:Aldosterone / Q000097:blood; D009320:Atrial Natriuretic Factor / Q000097:blood; D001794:Blood Pressure; D004039:Diet, Sodium-Restricted; D006801:Humans; D007668:Kidney / Q000503:physiopathology*; D007674:Kidney Diseases / Q000150:complications; D007676:Kidney Failure, Chronic / Q000209:etiology* / Q000503:physiopathology / Q000628:therapy*; D007678:Kidney Glomerulus; D008297:Male; D016896:Treatment Outcome
chemical_list: D000450:Aldosterone; D009320:Atrial Natriuretic Factor