Abstract
Two recognized risk factors implicated in the pathogenesis of progressive renal disease are overactivation of the renin angiotensin system and male gender. The peptide hormone, angiotensin II, produced by the renin angiotensin system cascade, plays a crucial role in maintaining blood pressure and electrolyte homeostasis. Medications that block the action of angiotensin II by either inhibiting its synthesis or by blocking its ability to bind its receptor are in wide clinical use because of their ability to significantly retard the progression of kidney disease. Analysis of data from national end-stage renal disease registries, clinical trials, and experimental animal models suggest that the progression of chronic kidney disease from several etiologies is more rapid in men than in women. In this review, we examine the data supporting the hypothesis that modulation of the activity of the renin angiotensin system by sex steroids markedly contributes to the gender differences observed in the pathophysiology of progressive kidney disease.
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