title: Sodium retention in preascitic stage of cirrhosis.
abstract: Renal Na+ handling abnormalities have been shown in preascitic cirrhosis. To investigate the underlying pathophysiology, the effects of different sodium intakes on Na(+) balance and renal hemodynamics were assessed at 100 mEq Na+/day (low-sodium diet [LSD]) and after 6 days of 250 mEq Na+/day (high-sodium diet [HSD]). Eight asymptomatic patients with cirrhosis (Pugh-Child A class) (PAC) and 10 healthy controls (CON) were studied. At HSD, although CON readjusted Na+ excretion within the fourth day, PAC did not reach the new balance and developed a final greater Na+ retention (+437 mEq in PAC v +228 mEq in CON, P<.001). In PAC, fractional Na+ excretion (FENa) was significantly lower than in CON at LSD (P<.05), and, after HSD, increased in both groups (P<.05). In PAC, renal vascular resistances (RVR) at LSD resulted lower than in CON (P<.05) and failed to decrease after HSD. As a consequence, after HSD, glomerular filtration rate and renal plasma flow failed to increase in PAC. PRA and plasma aldosterone were significantly lower in PAC, than in CON at LSD (P<.05), and decreased in both groups after HSD (P<.05). Proximal Na+ reabsorption (RProx) [as indicated by fractional free water clearance measured in a state of maximal water diuresis] at LSD was lower in PAC than in CON (P<.05) and decreased in both groups after HSD (P<.05). In summary, early stages of cirrhosis are characterized by: (1) a reduction of RVR, probably associated with splanchnic vasodilation; (2) a Na+ retention already at LSD, as indicated by the lower FENa observed in PAC, that produces extracellular volume (ECV) expansion, with a consequent RProx and renin-angiotensin-aldosterone axis (RAS) suppression; (3) a greater Na+ retention after HSD, associated with an abnormal adaptation of renal hemodynamic, a greater ECV expansion and a consequent Rprox and RAS suppression. These data show the presence of early renal hemodynamic dysfunction in PAC. Our findings also show in this phase of the disease a preserved adaptation of RProx and RAS, thus suggesting that the observed tubular Na+ reabsorption derangement is probably related to abnormal ANP behavior.
authors.affiliation: Department of Nephrology, Federico II University of Naples, Italy. paola.margri@libero.it
authors.forename: P
authors.initials: P
authors.lastname: Magri
authors.forename: M
authors.initials: M
authors.lastname: Auletta
authors.forename: M
authors.initials: M
authors.lastname: Andreucci
authors.forename: G
authors.initials: G
authors.lastname: Somma
authors.forename: D
authors.initials: D
authors.lastname: Musone
authors.forename: M
authors.initials: M
authors.lastname: Fiorillo
authors.forename: S
authors.initials: S
authors.lastname: Torraca
authors.forename: S
authors.initials: S
authors.lastname: Antoniello
authors.forename: B
authors.initials: B
authors.lastname: Cianciaruso
mesh_terms: D000450:Aldosterone / Q000378:metabolism; D000704:Analysis of Variance; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007444:Inulin / Q000378:metabolism; D007668:Kidney / Q000378:metabolism*; D008103:Liver Cirrhosis / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D012083:Renin / Q000378:metabolism; D012982:Sodium, Dietary / Q000008:administration & dosage / Q000378:metabolism*; D010130:p-Aminohippuric Acid / Q000378:metabolism
chemical_list: D012982:Sodium, Dietary; D000450:Aldosterone; D007444:Inulin; D012083:Renin; D010130:p-Aminohippuric Acid