López ÁL, Flores AG

Language: Spanish
References: 17
Page: 131-138
PDF size: 126.38 Kb.

ABSTRACT

Background: Cardiovascular disease is leading cause of death in patients with CRF, caused by traditional and nontraditional cardiovascular risk factors, which are identifiable and quantifiable biomarkers; being the most relevant the lipid profile, microalbuminuria, serum albumin, homocysteine, IL-6 and fibrinogen. Drugs that block the RAAS have antiproteinuric effect. The pharmacological blockade of the RAAS by administration of ACE inhibitors, ARAs and spironolactone decreases albuminuria. It is unknown the role of these drugs on other biomarkers of cardiovascular risk related or independent to microalbuminuria.
Objective: To determine the effect of RAAS blockade on cardiovascular risk biomarkers in patients with CKD Stage 1-3 KDOQI.
Material and methods: It was co-administered enalapril, telmisartan and spironolactone, in adults with CKD 1-3. Biomarkers were determined at weeks 0, 8 and 16. The statistical analysis used arithmetic mean, standard deviation, Student's t and correlation, with statistical significance when p ≤ 0.05.
Results: After the blockade of the RAAS, it was reported a decrease on albuminuria, an increase on HDL cholesterol and a decrease on LDL cholesterol. Fibrinogen was significantly less.
Conclusions: Triple RAAS blockade modifies the cardiovascular risk biomarkers. The decrease of microalbuminuria (a marker of vascular disease) is possibly secondary to decreased systemic vascular microinflammation. The decrease of fibrinogen (a marker of inflammation) after blockade of the RAAS, supports the supposition that angiotensin and aldosterone regulate fibrinolysis and vascular remodeling, proposing to triple RAAS blockade as a microvascular antiinflammatory.

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