Short-Term Administration of an Angiotensin II
Receptor Blocker in Patients with Long-Term
Hemodialysis Patients Improves Insulin Resistance
Bancha Satirapoj MD*, Kulachon Leelasiri MD*,
Ouppatham Supasyndh MD*, Panbubpa Choovichian MD*
Affiliation :
* Division of Nephrology, Department of Medicine, Phramongkutklao Hospital and College of Medicine, Bangkok, Thailand
Background : Insulin resistance is commonly observed in uremic patients. Angiotensin II receptor blockers (ARB) are
reported to act as insulin sensitizers in the animal model of hypertension and hypertensive patients. The authors investigated
the effects of valsartan on insulin resistance and glucose metabolism in patients with long-term hemodialysis in the prospective,
randomized controlled study.
Material and Method: Thirty-three hemodialysis patients were randomized into two treatment groups, valsartan 80 to
320 mg/day (n = 18) or non-renin-angiotensin-aldosterone-system blocking antihypertensive agents (control, n = 15),
treated for 12 weeks. Insulin resistance determined by homeostasis model assessment (HOMA-IR), fasting plasma glucose
(FPG), fasting plasma insulin, and blood pressure monitoring were measured during the study.
Results : At baseline, metabolic profiles did not significantly differ between the treatment and the control groups. After
12 weeks of treatment, the valsartan group significantly improved HOMA-IR from 2.60.9 to 2.30.7 (p = 0.041) and
significantly decreased FPG from 90.115.1 to 84.813.2 mg/dL (p = 0.008). In contrast, the control group was not associated
with any significant changes in HOMA-IR, FPG, and fasting insulin levels. At the end of 12-week treatment, HOMA-IR,
FPG, and fasting insulin levels were not significantly different between the two groups.
Conclusion : These results indicate that the antihypertensive action of valsartan improves glucose metabolism by improving
the peripheral insulin sensitivity in subjects with long-term dialysis.
Keywords : Insulin resistance, Glucose metabolism, Hemodialysis, Angiotensin II Receptor Blockers
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