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Journal of Renin-Angiotensin-Aldosterone System
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Review: ACE inhibition or angiotensin receptor blockade: which should we use in diabetic patients?

Luis M Ruilope

Hypertension Unit, Hospital 12 de Octubre, Madrid, Spain, Luis_M_Ruilope @teleline.es

Julian Segura

Hypertension Unit, Hospital 12 de Octubre, Madrid, Spain

Ernesto L Schiffrin

Multidisciplinary Research Group on Hypertension, Clinical Research Institute, University of Montréal, Montréal, Quebec, Canada

Blockade of the effects of angiotensin II (Ang II) by using an angiotensin-converting enzyme (ACE) inhibitor has been proven to be of value in Type 1 diabetic nephropathy and in non-diabetic renal disease. Evidence in favour of Ang II blockade in Type 2 diabetic patients with renal damage is still lacking for ACE inhibitors (ACE-Is), while recent data indicate that angiotensin receptor blockers (ARBs) could be the drugs of choice in this situation. On the other hand, renal damage from the onset of disease is accompanied by a very significant increment in global cardiovascular risk. This fact, as well as that of simultaneous renal and cardiovascular protection, have to be considered for drug selection. In this sense, ACE-Is have been shown to be the drugs of choice when secondary cardiovascular prevention is required, while the evidence in primary prevention in hypertensive patients has been shown with losartan in the Losartan Intervention For Endpoint reduction in hypertension (LIFE) study. All these facts led to the conclusion that both ACE-Is and ARBs can be considered when both renal and cardiovascular protection are aimed for in Type 2 diabetic patients.

Key Words: ACE inhibition • angiotensin receptor antagonists • losartan • irbesartan • proteinuria • microalbuminuria • renal function • cardiovascular disease

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Journal of Renin-Angiotensin-Aldosterone System, Vol. 4, No. 2, 74-79 (2003)
DOI: 10.3317/jraas.2003.016


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G. Montalescot and J.-P. Collet
Preserving cardiac function in the hypertensive patient: why renal parameters hold the key
Eur. Heart J., December 2, 2005; 26(24): 2616 - 2622.
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