Key result
Eprosartan improves small vessel compliance vs placebo in CKD alongside a ~12 mmHg SBP drop.
Why the study?
Does eprosartan improve small vessel compliance in patients with stage 2 and 3 chronic kidney disease?
RCT (n=25)
randomized
Does eprosartan improve small vessel compliance in patients with stage 2 and 3 chronic kidney disease?
In a small pilot study of patients with stage 2-3 CKD, the addition of eprosartan to antihypertensive therapy improved small vessel compliance independent of blood pressure lowering.
Answers are grounded in this paper and cite their sources.
Eprosartan improves small vessel compliance in CKD beyond BP reduction; extends ARB vascular effects to stage 2-3 renal disease.
Systolic blood pressure (SBP) is a strong predictor of cardiovascular (CV) mortality in people with chronic kidney disease (CKD). Increased arterial stiffness, defined by a wide pulse pressure is present in the majority of people with CKD. There are no studies with angiotensin receptor blockers (ARB) examining vascular compliance in CKD. The current pilot study was undertaken to determine whether arterial stiffness in could be improved in CKD. 25 participants with stages 2 and 3 CKD (assessed by estimated GFR) and < 1 gram of proteinuria were randomized to either the ARB eprosartan 600 mg daily or placebo. Eprosartan was titrated to a maximum of 1200 mg daily and other antihypertensive medications added to achieve a goal SBP of < 130 mm Hg. Baseline characteristics included: a mean age of 65 ± 11 years, median GFR 65 ± 15 ml/min, 44% male, 60 % African American, median BP 144 ±12/80± 8 mm Hg median heart rate 76± 10.beats per minute. At the time of presentation all but 4% were taking more than one medication. At each visit over two months, serum creatinine, blood pressure (obtained 3 separate times and measured by the same physician) as well as arterial compliance were obtained. Arterial compliance was assessed using the HDI device. Data were analyzed using SPSS. Given the small sample size and data distribution nonparametric statistics were used. The primary endpoint was an increase in small vessel compliance which was noted (see Table). Data are expressed as median (10-90% CI). Change in heart rate could note explain differences in small vessel compliance (P=0.93). SBP was markedly reduced in both groups baseline 142 (121-160) mmHg to 130 (99-154) mmHg at two months. No differences in large vessel compliance or SBP between groups were observed. We conclude that use an ARB to achieve recommended SBP is associated with improved small vessel compliance in people with CKD. A large scale study needs to be performed to confirm these findings.
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R ELLIS (2004) conducted an RCT in Chronic kidney disease (n=25). Eprosartan vs. Placebo was evaluated on Increase in small vessel compliance. Eprosartan improved small vessel compliance in patients with CKD, alongside a median SBP reduction from 142 mmHg to 130 mmHg across both groups at two months.
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