The pathogenesis of renal sodium retention and ascites formation in Laennec's cirrhosis.

This chapter critically reviews our current understanding of the pathogenesis, clinical syndrome, and therapy of the disturbances of renal sodium handling, renal perfusion, and glomerular filtration rate that occur in patients with Laennec's cirrhosis. Avid renal sodium reabsorption, a characteristic feature of cirrhosis, occurs independent of moderate changes in renal function and precedes the onset of ascites. The initiation of sodium retention may be a direct consequence of the hepatic disease process and may also result from defective intravascular filling. In the presence of ascites the most important sodium retaining signal is a defective intravascular volume. The principal effectors of renal sodium retention and vasoconstriction are stimulation of the renin-angiotensin-aldosterone axis and augmentation of renal sympathetic nerve activity. Deficient production of natriuretic hormone(s) and endogenous renal vasodilators, such as prostaglandins and kinins, also contributes to the sodium retention and renal hypoperfusion seen in cirrhosis. The hepatorenal syndrome is an extreme imbalance in these renal vasoconstrictor and vasodilator forces. In the therapy of ascites in Laennec's cirrhosis, abstention from alcohol, sodium restriction, and cautious diuresis are the principal therapeutic measures. A grave prognosis accompanies the diagnosis of the hepatorenal syndrome although recoveries have been reported.