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Effects of irbesartan on serum uric acid levels in patients with hypertension and diabetes

Authors Nakamura M, Sasai N, Hisatome I, Ichida K

Received 28 January 2014

Accepted for publication 14 March 2014

Published 3 May 2014 Volume 2014:6 Pages 79—86

DOI https://doi.org/10.2147/CPAA.S61462

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 4

Makiko Nakamura,1 Nobuo Sasai,2 Ichiro Hisatome,3 Kimiyoshi Ichida1

1Department of Pathophysiology, Tokyo University of Pharmacy and Life Sciences, Tokyo, Japan; 2Sasai Clinic, Kanagawa, Japan; 3Division of Regenerative Medicine and Therapeutics, Institute of Regenerative Medicine and Biofunction, Graduate School of Medical Sciences, Tottori University, Tottori, Japan

Background: Hyperuricemia has been proposed to be a risk factor for cardiovascular disease and chronic kidney disease. Since diabetes is often complicated by hypertension and hyperuricemia, efficient therapeutic strategy against these two complications is very important in diabetic treatment. It has been reported that the antihypertensive drug, irbesartan, inhibits the renal uric acid reabsorptive transporters, URAT1 and GLUT9; this result suggests that irbesartan decreases serum uric acid level (SUA).
Subjects and methods: A retrospective study of 107 patients with hypertension and diabetes was performed to analyze the effects of irbesartan on blood pressure, estimated glomerular filtration rate (eGFR), and SUA. The follow-up period was 6–12 months. Seventy percent of the patients were diagnosed with diabetic nephropathy stage II–IV. We excluded patients treated with drugs that influenced SUA. The multiple logistic regression analysis was introduced to identify the relative factors for SUA decline. The time-dependent SUA changes were examined in a mixed-linear model.
Results: Irbesartan reduced blood pressure significantly after 1, 6, and 12 months’ treatment. No subject showed significant change in eGFR from baseline level throughout the period. The multiple logistic regression analysis revealed that SUA baseline significantly influenced SUA decline after 6–12 months. In patients whose SUA baseline was ≥5.9 mg/dL, the SUA was significantly decreased from 6.6±0.16 mg/dL to 6.2±0.16 mg/dL (P=0.010), after 12 months’ irbesartan treatment. In the SUA baseline <5.9 mg/dL group, the SUA did not show significant change over the monitoring period.
Conclusion: Our results demonstrate that irbesartan reduces the risk of hyperuricemia. No decline in renal function was observed after the initiation of irbesartan treatment. The present report determines the criteria of SUA baseline for introducing an antihyperuricemic effect using irbesartan. Its antihypertensive effect coupled with SUA decline would be effective for the treatment of hypertension complicated by hyperuricemia.

Keywords: angiotensin-receptor blocker, diabetes, hypertension, hyperuricemia, serum uric acid

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