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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Participation of the renin-angiotensin system in the captopril-induced worsening of anemia in chronic hemodialysis patients.

The study was aimed to show whether the renin-angiotensin system acts on erythropoiesis in chronic renal failure patients with hemodialysis, since captopril leads to the worsening of anemia in such patients. The average dose of captopril in 13 cases studied was 19.3 mg per day and duration of the administration was 48 days. Blood-pressure fall by captopril was accompanied with the worsening of anemia. There were significant decreases in hemoglobin (8.3%), hematocrit (7.3%), red blood cell count (7.6%) and reticulocyte count (43.7%). Angiotensin II was significantly decreased (15.7%) with significant reductions of plasma aldosterone concentration (15.2%) and angiotensin-I converting enzyme (45.7%), and with significant increases in plasma renin activity (158.6%) and in angiotensin I (238.3%). However, plasma erythropoietin concentration remained unchanged. Serum iron concentration was slightly but significantly increased after captopril. Reticulocyte count was significantly correlated with AII either before (r = 0.716, p less than 0.01) or after captopril (r = 0.658, p less than 0.05). There was significant correlation between angiotensin II and red blood cell count before captopril (r = 0.710, p less than 0.01). It is concluded from the present study that the reduction of angiotensin II by captopril might contribute to the worsening of anemia seen in chronic hemodialysis patients.[1]

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