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Portuguese Journal of Nephrology & Hypertension

Print version ISSN 0872-0169


LUCAS, Carlos. RAAS Intervention in Chronic Kidney Disease. Port J Nephrol Hypert [online]. 2013, vol.27, n.3, pp.163-171. ISSN 0872-0169.

Chronic kidney disease (CKD) has usually a progressive nature dependent of multiple factors including blood pressure values and degree of proteinuria. Control of blood pressure to levels below those desirable in the non-CKD population and reduction of proteinuria have been the cornerstone of renoprotection for many years. Blockade of the renin-angiotensin-aldosterone system (RAAS) is the most effective pharmacological strategy for that purpose and has been validated by numerous trials. However, the risk of adverse renal events and of progression for end-stage-kidney disease remains high, which led to the development of several treatment-intensification strategies of RAAS blockade. Among the strategies evaluated, dual-agent blockade has been the target of several long-term trials after promising results in short-term studies more focused on surrogate markers of CKD progression like proteinuria. Unfortunately, the results were disappointing and such dual-agent strategies not only failed to show a significant beneficial effect in slowing CKD progression, but were associated with a worse renal long-term outcome. Among such dual-agent strategies were combinations of an angiotensin-converting enzyme (ACE) inhibitor plus an angiotensin receptor blocker (ARA), ACE inhibitor or an ARB plus the direct renin inhibitor aliskiren. RAAS blockade with an ACE inhibitor and an ARB plus the mineralocorticoid receptor antagonist (MRA) spironolactone is also unproven. Single-agent RAAS blockade intensification with moderate dietary sodium restriction appears promising in retrospective data but currently lacks prospective confirmation. The addition of the vitamin D analogue paricalcitol to single-agent RAAS blockade appears to be beneficial but is still unproven in long-term hard outcome focused trials

Keywords : Progressive chronic kidney disease; proteinuria; renin-angiotensin-aldosterone system; sodium restriction.

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