The response of atrial natriuretic factor and sodium excretion to dietary sodium challenges in patients with chronic liver disease

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 less than 0.05) on a 100 mmol/day sodium diet.(ABSTRACT TRUNCATED AT 250 WORDS)

The role of atrial natriuretic peptide (ANP) in chronic liver disease

“…On a 100 mmol, as compared to 20 mmol, per day sodium diet, patients with cirrhosis and a history of volume retention showed a more marked increase of plasma ANP concentration than patients without ascites or controls (Warner et aL, 1990). Furthermore, diuretic therapy influences plasma concentrations in patients with ascites.…”

Refractory ascites: Modulation of atrial natriuretic factor unresponsiveness by mannitol

“…These may be compensated in part by vasodilatory substances, such as atrial natriuretic factor (ANF), that are also increased in cirrhosis (9). However, cirrhotic patients become refractory to the natriuretic effect of ANF in the advanced stages of ascites, when antinatriuretic mechanisms are most activated (10)(11)(12)(13).…”

The effect of single oral low-dose losartan on posture-related sodium handling in post-TIPS ascites-free cirrhosis

“…9 Therefore, in many ways, their sodium handling appears to be similar to that of pre-ascitic patients who are also ascites-free. In pre-ascitic patients with cirrhosis, sodium balance is achieved when they are either on a low-sodium diet of 22 mmol/day or 100 mmol/day, 11 but subtle sodium retention occurs when challenged with a high sodium diet of 200 mmol/day. 12 Similar to the post-TIPS ascites-free patients, pre-ascitic patients also have a low to normal neurohormonal profile, especially in the supine posture, 13 , confirming the presence of an adequately filled EABV in the supine posture.…”