Hyponatremia and arginine vasopressin secretion in patients with refractory hepatic ascites undergoing peritoneovenous shunting

Abstract

Seven patients with persistent hyponatremia but normal or elevated serum arginine vasopressin levels and refractory ascites undergoing peritoneovenous shunting were studied in a Metabolic Unit on a 20 mEq sodium 1200 ml fluid-restricted diet to elucidate the mechanism of this response. The intravascular volume expansion after shunt implantation resulted in improvements in cardiac output, renal plasma flow and creatinine clearance (70.7 ± 9.5 to 140.1 ± 18.5 ml/min, p < 0.005). There was an immediate diuresis (632 ± 135 to 2450 ± 323 ml/day, p < 0.005) and natriuresis (3 ± 1 to 25.9 ± 10.6 mEq/24 h, p < 0.05), and urine osmolality decreased significantly (622 ± 91 to 251 ± 76 mosmol/L, p < 0.05) with a significant rise in serum sodium concentration by 72 h (131 ± 2 to 135 ± 1.6 mEq/L, p < 0.05) and serum osmolality. Serum arginine vasopressin levels remained elevated at 3.85 ± 0.94 μU/ml, however, although a transient depression cannot be excluded. Subsequently, a small but significant decrease in serum arginine vasopressin levels to 3.04 ± 0.65 μU/ml (p < 0.05) was associated with a further rise in serum sodium levels above baseline values (138 ±1.4 mEq/L, p < 0.01) and in serum osmolality. In conclusion, these results indicate that in this group of cirrhotic patients with refractory ascites, intrarenal factors, such as decreased delivery of filtrate to the distal nephron as well as elevated inappropriate levels of arginine vasopressin, are important in the pathogenesis of hyponatremia.