Journal
KIDNEY INTERNATIONAL
Volume 65, Issue 4, Pages 1435-1439Publisher
ELSEVIER SCIENCE INC
DOI: 10.1111/j.1523-1755.2004.00524.x
Keywords
plasma renin activity; plasma angiotensin II concentration; vascular injury; sodium; potassium
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Funding
- NCRR NIH HHS [M01RR02635] Funding Source: Medline
- NHLBI NIH HHS [5P50HL55000, T32HL07609] Funding Source: Medline
- NIDDK NIH HHS [1R01DK5466804] Funding Source: Medline
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Background. Vascular injury at the microvascular and macrovascular levels plays a crucial role in the patient with diabetes mellitus. Evidence for renin-system activation in many patients with type 1 diabetes mellitus has raised the possibility that aldosterone-widely recognized as a contributor to vascular injury-could play a role. Methods. We examined the state of the renin-angiotensin-aldosterone system (RAAS) in 58 subjects with type 1 diabetes mellitus and 64 age-matched normal control subjects. All studies were performed on a fixed sodium (200 mmol/day) and potassium (100 mmol/day intake), and samples were drawn at 8: 00 a. m. to avoid the influence of circadian rhythms. Results. The patient with diabetes mellitus showed an increase in plasma renin activity (PRA) (P < 0.01), plasma angiotensin II concentration (P < 0.01), and plasma aldosterone concentration (P < 0.001). A striking influence of the angiotensin receptor blocker, candesartan, on plasma aldosterone concentration in the patients with diabetes mellitus suggested strongly that renin-system activation is responsible for the elevated plasma aldosterone concentration. Conclusion. Pharmacologic interruption of the effects of aldosterone at the tissue level could be especially useful in patients with diabetes mellitus. The dose of agents that block the renin-angiotensin system (RAS) should be adjusted to maximize the fall in plasma aldosterone concentration.
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