Changes in the renin-aldosterone axis have long been recognized as occurring in patients with liver cirrhosis; different patterns are encountered during the different stages of the disease. Patients in whom ascites has not yet developed usually show depressed plasma renin activity or concentration. The low levels may be due to effective extracellular fluid volume expansion, although this view is not accepted by all authors. According to the overflow theory of ascites formation, sodium retention should occur before the appearance of ascites and, hence, volume expansion should ensue. Since plasma aldosterone concentration is usually normal or even depressed at this stage, increased sodium retention can only be explained by an enhanced renal tubular sensitivity to mineral-corticoid hormone. Mounting evidence suggests that such an abnormality is present in nonascitic patients and progresses as the disease worsens. This abnormality also explains why greater than 50% of patients with ascites and avid renal sodium retention have plasma renin activity and aldosterone within the normal range. In the late stages of the disease, the development of massive compartmentalization of fluid as ascites, along with changes in cardiovascular homeostasis (reduced peripheral resistances, opening of arterovenous shunts, and reduced efficiency of the sympathetic nervous system), lead to striking activation of the renin-angiotensin-aldosterone system. The system is responsible for sodium retention and for the maintenance of arterial pressure, and can be involved, at least in part, in reducing renal perfusion.