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Abstract

Despite intensive investigation, the pathogenesis of sodium retention in patients with chronic liver disease is not fully known. We have studied 19 chronic liver disease patients, 13 without (group 1) and six with (group 2) histories of clinical sodium retention (ascites or edema) by varying dietary sodium intake. The patients were placed on a 20 mmol/day constant diet for 1 wk, followed by a constant 100 mmol/day sodium diet for 1 wk under strict metabolic conditions. After 5 days of equilibration on each diet, blood and urine samples were collected for plasma atrial natriuretic factor levels and urinary sodium excretion. Group 1 patients (n = 6) achieved near sodium balance in 5 days on both a 20-mmol (urinary sodium output = 17 ± 3 mmol/day) and a 100-mmol sodium diet (urinary sodium output = 80 ± 5 mmol/day). Atrial natriuretic factor levels in these patients tended to be elevated, but the increase was not significantly greater than that in normal control subjects (10 ± 4 pg/ml to 19 ± 4 pg/ml) on the same diets. In contrast, group 2 patients (n = 5) were in significant positive sodium balance on both the 20 mmol/day sodium diet (mean urinary sodium output = 9.5 ± 3.3 mol/day) and the 100 mmol/day sodium diet (urinary sodium output = 37 ± 13 mmol/day). This occurred despite significantly elevated baseline atrial natriuretic factor levels and a significant increase in plasma atrial natriuretic factor levels after sodium challenge (62 ± 9 pg/ml, p < 0.05) on a 100 mmol/day sodium diet. These results indicate that renal resistance to the natriuretic actions of atrial natriuretic factor occurs in this group of patients with a history of sodium retention. In preascitic, uncomplicated chronic liver disease patients corrected sinusoidal pressure was positively correlated with atrial natriuretic factor levels (n = 13, r = 0.75; p < 0.01). These results suggest that, in these patients, intrasinusoidal portal hypertension may have a role in the development of sodium retention and that sodium homeostasis is maintained on various sodium diets at the expense of a gradual elevation in atrial natriuretic factor levels. (HEPATOLOGY 1990;12:460–466).