Blockade of the renin-angiotensin-aldosterone system has proven effective in retarding progression of renal disease in the remnant kidney model, as well as other experimental diseases, and, most importantly, in a range of progressive human renal diseases. Attention has focused on the role of angiotensin II (Ang II) in propagating progression both by its hemodynamic and nonhemodynamic actions. Recent evidence, predominately in the remnant kidney model, indicates that the drugs used to block this hormone system, angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers, also lower aldosterone levels. Thus, aldosterone, as well as angiotensin II, appears to be instrumental in sustaining the hypertension and fibroproliferative destruction of the residual kidney.
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