Aldosterone and progression of renal disease.
OBJECTIVE
The aim of this review is to look at the role of aldosterone in the progression of chronic kidney disease. The reduction of blood pressure and proteinuria in patients suffering from chronic kidney disease decreases the rate of disease progression. Suppression of angiotensin formation by angiotensin converting enzyme inhibitors and blockade of the angiotensin II receptor by angiotensin II type 1 antagonists are powerful therapeutic strategies that effectively lower blood pressure and slow the progression of renal disease. These therapies, however, provide only imperfect protection, since they cannot always prevent endstage renal failure.


RESULTS
Aldosterone plays a significant role in the pathogenesis of arterial hypertension and renal disease. Angiotensin converting enzyme inhibitors and angiotensin II type 1 antagonists are incomplete in suppressing aldosterone production and 'aldosterone breakthrough' can be observed under continued treatment. Aldosterone blockade reduces blood pressure in virtually all patients with hypertension. In proteinuric patients, the addition of an aldosterone antagonist to an angiotensin converting enzyme inhibitor or to angiotensin II type 1 antagonists reduces proteinuria.


CONCLUSIONS
The use of aldosterone antagonists in addition to either angiotensin converting enzyme inhibitors or angiotensin II type 1 antagonists in proteinuric patients reduces proteinuria, which may translate into preservation of the glomerular filtration rate in the longer term. Therefore, blockade of the aldosterone pathway may prove to be a beneficial therapy for chronic kidney disease.
Wenzel
Ulrich
U
Department of Medicine, Division of Nephrology, University Hospital of Hamburg, Hamburg, Germany. wenzel@uke.uni-hamburg.de
D000450:Aldosterone / Q000378:metabolism*; D000818:Animals; D018450:Disease Progression; D006801:Humans; D006973:Hypertension / Q000378:metabolism / Q000473:pathology; D007674:Kidney Diseases / Q000378:metabolism / Q000473:pathology*; D011507:Proteinuria / Q000378:metabolism / Q000473:pathology; D011956:Receptors, Cell Surface / Q000378:metabolism; D000093342:Prorenin Receptor
D011956:Receptors, Cell Surface; D000450:Aldosterone; D000093342:Prorenin Receptor