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The renin-angiotensin-aldosterone system in human hepatic cirrhosis
Abstract:
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.
Insights
In liver cirrhosis, the renin-aldosterone system changes with disease stage. Early stages show low renin and aldosterone, with increased kidney sodium retention due to enhanced sensitivity to aldosterone.
Area of Science:
- Endocrinology
- Nephrology
- Hepatology
Background:
- The renin-aldosterone axis is altered in liver cirrhosis, with distinct patterns across disease stages.
- Ascites formation in cirrhosis is linked to sodium retention and fluid shifts.
Purpose of the Study:
- To elucidate the role and changes in the renin-aldosterone system throughout the stages of liver cirrhosis.
- To understand the mechanisms of sodium retention in nonascitic and ascitic cirrhotic patients.
Main Methods:
- Analysis of plasma renin activity and aldosterone concentration in different stages of liver cirrhosis.
- Evaluation of renal tubular sensitivity to mineralocorticoids.
- Correlation of hormonal changes with fluid balance and cardiovascular homeostasis.
Main Results:
- Nonascitic patients often exhibit depressed plasma renin activity/concentration, potentially due to extracellular fluid expansion.
- Increased renal sodium retention in early cirrhosis is attributed to enhanced renal tubular sensitivity to aldosterone, not elevated levels.
- Late-stage cirrhosis shows marked activation of the renin-angiotensin-aldosterone system, contributing to sodium retention and arterial pressure maintenance.
Conclusions:
- Renin-aldosterone axis dysfunction is a progressive feature of liver cirrhosis, impacting fluid balance and cardiovascular stability.
- Enhanced renal tubular sensitivity to aldosterone is a key mechanism for sodium retention in early cirrhosis.
- The activated renin-angiotensin-aldosterone system in advanced cirrhosis plays a critical role in managing arterial pressure and fluid distribution.