Resistance to Natriuresis in Patients with Peritonitis Carcinomatosa

The natriuretic effect of atrial natriuretic peptide (ANP) is blunted in certain clinical disorders such as congestive heart failure and liver cirrhosis, despite the elevated plasma ANP levels. These sodium-retaining states are characterized by increased activity of the renal sympathetic nerves. Recent studies have shown higher levels of circulating and urinary catecholamines in cancer patients. We hypothesized that the increased adrenergic activity may be responsible for ascites formation in patients with peritonitis carcinomatosa (PC). The objective of this study was to determine the renal responses to endogenous ANP in patients with PC. Patients, hospitalized at our institute for PC, were examined using renal clearance studies for 2 h. Non-cancer patients were also examined as control subjects. Statistical analysis was performed using Wilcoxon's rank sum test. The results showed that absolute and fractional sodium excretions were markedly lower in patients with PC (54 ± 16 µEq/min, means ± SE, p < 0.0005; 0.55 ± 0.15%, p < 0.005) than in control patients (166 ± 14 µEql/min; 1.14 ± 0.09%, respectively). Plasma ANP concentration was increased in patients with PC (34.7 ± 8.4 pg/ml, p < 0.001) in comparison with control patients (13.3 ± 2.0 pg/ml). Plasma and urinary levels of norepinephrine were significantly higher in cancer patients (0.36 ± 0.10 ng/ml, p < 0.05; 125 ± 20 ng/dl GF, p < 0.05) than in the controls (0.17 ± 0.02 ng/ml; 73 ± 13 ng/dl GF). These results suggest that increased renal sympathetic nerve activity may contribute to the attenuation of the natriuretic effect of ANP in patients with PC.

Key words

Atrial Natriuretic Peptide - Renal Nerves - Catecholamines - Ascites - Peritonitis Carcinomatosa - Sodium Excretion - Urinary cGMP Excretion