| [ Summary ] |
Patients with end-stage renal disease often have elevated plasma aldosterone concentrations, which appear to correlate with the degree of renal dysfunction. The factors contributing to hyperaldosteronemia may be renin stimulus, hyperkalemia, erythropoietin treatment, and / or other factors including adipocyte-derived aldosterone releasing factor(s). Aldosterone is traditionally viewed as a hormone regulating electrolytes, volume, and blood pressure homeostasis by acting on the distal nephrons in the kidneys. Recently, a growing body of evidence has suggested that aldosterone also plays a pathogenetic role in cardiovascular and renal injury. Aldosterone has been shown to act on nonepithelial cells in the heart, vasculature, and kidneys to cause tissue remodeling, fibrosis, and endothelial dysfunction. Accumulating lines of evidence indicate that cardiovascular disease is the main cause of death in patients on long-term dialysis. Clinical studies have reported a correlation between left ventricular hypertrophy and plasma aldosterone concentrations in nondiabetic patients with end-stage renal failure treated with hemodialysis. If there exists a cause-effect relationship between hyperaldosteronism in chronic renal failure and cardiac hypertrophy, it is expected that aldosterone blockers may reduce left ventricular hypertrophy, leading to improved life expectancy in patients on hemodialysis. |