Indirect evidence to suggest that prolactin induces salt retention in cirrhosis.

Prolactin is known to have renal sodium retention properties in animals. In man, only two studies have suggested a similar effect in healthy volunteers or in patients with microprolactinoma. Since hyperprolactinemia is frequently observed in liver disease, this prospective study of 19 patients evaluated the influence of prolactin on urinary electrolytes excretion in cirrhosis. Basal hyperprolactinemia was found in 14 out of 19 cases. The effect of serum prolactin elevation on renal sodium and potassium excretion was studied in all patients after thyrotropin-releasing hormone stimulation (200 micrograms), with seven consecutive hourly urinary samples. Patients were separated into two groups according to amount of prolactin discharge after thyrotropin-releasing hormone injection. Group I included patients with "low prolactin release", defined as the difference between basal and peak prolactin values (delta prolactin) < 1000 mu u/ml (n = 8), and no change in natriuresis could be observed. In contrast, in group II with a "high PRL release" (delta prolactin > 1000 mu u/ml, n = 11), significant reductions in urinary sodium (p < 0.01) and potassium (p < 0.02) excretion were observed, which lasted until the third hour after thyrotropin-releasing hormone injection. A significant correlation was found between peak prolactin values and the decrements of natriuresis (r = 0.70, p < 0.02). The pattern of urinary electrolyte changes and the stability of the ratio UK/UK+Na suggest a possible sodium-retaining effect of prolactin localized proximally to the distal tubule.