Circadian variation in renal sodium and potassium handling in cirrhosis. The role of aldosterone, cortisol, sympathoadrenergic tone, and intratubular factors.

Renal sodium and potassium handling, plasma aldosterone and cortisol concentrations, and urine free norepinephrine excretion were determined every 4 h for 24 h in 15 cirrhotics (7 without ascites, group 1; 8 with ascites, group 2) and 7 healthy controls during controlled salt intake and recumbency. Renal sodium excretion was significantly reduced in group 2, whereas it exceeded threefold the salt intake in group 1. Its circadian rhythm was disrupted in both groups of patients. Significant inverse correlations with plasma aldosterone were found erratically in controls, never in group 1, and at every 4-h interval in group 2. In the latter, the indexes of tubular activity and effectiveness of aldosterone were also significantly increased. Urine norepinephrine excretion was never related to sodium excretion in either controls or patients; in group 2 it was directly correlated with glomerular filtration rate in many instances. The cortisol-related circadian rhythm of kaliuresis was retained only in group 1. The 24-h renal potassium excretion of controls and patients was comparable, in spite of the striking hyperaldosteronism, and the more than doubled contribution of aldosterone to kaliuresis shown in group 2. The influence of aldosterone on potassium excretion was also witnessed by the direct correlation between these variables found in group 1 and, when kaliuresis was corrected by the distal sodium delivery, group 2. Renal sodium handling in cirrhosis is altered even before ascites formation and compensated patients can undergo "spontaneous natriuresis." Aldosterone is the main cause of sodium retention in nonazotemic ascitic patients, while sympathoadrenergic hyperactivity may contribute to preserve renal perfusion. The influence of aldosterone on kaliuresis is enhanced, but renal potassium wasting in patients with ascites and hyperaldosteronism is prevented by reduced distal tubular availability of sodium.