Key result
Aldosterone and angiotensin II appear to be instrumental in sustaining hypertension and fibroproliferative destruction of the residual kidney in progressive renal disease.
Population
Experimental models (remnant kidney model) and human progressive renal diseases
Design
Review
Authors
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Supports aldosterone antagonism in progressive CKD; leaves open whether mineralocorticoid receptor blockade improves outcomes beyond ACE inhibitors.
Aldosterone contributes to hypertension and fibroproliferative destruction in renal disease, and its reduction by ACE inhibitors and ARBs is a key mechanism of their renoprotective effects.
Hostetter et al. (2001) conducted a review in Renal disease. Renin-angiotensin-aldosterone system blockade was evaluated. Aldosterone and angiotensin II appear to be instrumental in sustaining hypertension and fibroproliferative destruction of the residual kidney in progressive renal disease.
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