Atrial natriuretic factor in cirrhosis: relationship to renal function and hemodynamic changes

Plasma atrial natriuretic factor concentrations and different hemodynamic parameters, including the evaluation of femoral arteriovenous shunting by measuring the arteriovenous difference of oxygen content (Ca-vO2), were determined in eight healthy subjects and 24 patients with cirrhosis without renal failure (group I: seven patients without ascites, group II: nine patients with ascites and UNaV > 10 mEq/24 h and group III: eight patients with ascites and UNaV < or = 10 mEq/24 h). Atrial natriuretic factor was 34 +/- 4.7 pg/ml in the control group and 44.28 +/- 5.4, 67.89 +/- 8.8 and 84 +/- 10.8 pg/ml in groups I, II and III respectively (p < 0.001. group III vs. I and control and II vs. control). Atrial natriuretic factor directly correlated with cardiac index (p < 0.01), blood volume (p: 0.01), femoral blood flow (p < 0.01) and inversely with systemic and femoral vascular resistances (p < 0.02), Ca-vO2 (p < 0.01), serum albumin (r: -0.61; p < 0.01) and prothrombin index (r: -0.63; p < 0.02). These results indicate that plasma atrial natriuretic factor is increased in patients with cirrhosis, especially in those with advanced disease and marked renal sodium retention. This suggests that in cirrhosis, arteriolar vasodilation and peripheral arteriovenous shunting influence renal function while inducing a state of overflow at the central venous compartment leading to increased atrial natriuretic factor secretion. Increased production of this vasodilatory hormone may thus contribute to the hyperkinetic circulation of cirrhosis.