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The effect of Losartan on insulin resistance and beta cell function in chronic hemodialysis patients

S Fishman1, M J Rapoport, J Weissgarten

  • 1Department of Internal Medicine A, Assaf Harofeh Medical Center, Zerifin, Israel. sigal001@bezeqint.net

Renal Failure
|December 1, 2001
PubMed

Insights

Losartan treatment in hemodialysis patients may negatively impact glucose control by reducing beta cell function, despite not affecting blood pressure. This suggests potential risks for glucose homeostasis in this population.

Area of Science:

  • Nephrology
  • Endocrinology
  • Cardiovascular Medicine

Background:

  • Insulin resistance (IR) is common in hemodialysis patients and contributes to atherosclerosis, a leading cause of death.
  • Antihypertensive drugs that improve IR may offer cardiovascular benefits in hemodialysis patients.
  • The effect of angiotensin II receptor antagonists on glucose metabolism in this population requires further investigation.

Purpose of the Study:

  • To investigate the impact of Losartan on insulin resistance and beta cell function in hypertensive, non-diabetic chronic hemodialysis patients.
  • To assess potential alterations in glucose homeostasis following short-term Losartan administration.

Main Methods:

  • A preliminary study involving five hypertensive, non-diabetic chronic hemodialysis patients.
  • Losartan (50 mg) administered for six weeks after a two-week washout period.
  • Fasting blood glucose and insulin levels measured pre- and post-treatment; IR and beta cell function calculated using HOMA.

Main Results:

  • No significant changes in systolic or diastolic blood pressure were observed.
  • Fasting blood glucose levels increased significantly post-Losartan treatment (p < 0.01).
  • Beta cell function significantly decreased (p < 0.016), while insulin levels and IR showed no significant change.

Conclusions:

  • Short-term Losartan treatment may have a detrimental effect on glucose homeostasis in hypertensive, non-diabetic hemodialysis patients.
  • This adverse effect appears to be mediated by a reduction in beta cell function.
  • Further research is warranted to explore the long-term implications and mechanisms involved.

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