Effects of ACE Inhibitor on Renal Anemia in Predialysis Patients
Author(s) -
Shinsuke Nomura,
Tamaki Sasaki,
Yuichi Kitano,
Gengo Osawa
Publication year - 1996
Publication title -
nephron
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.951
H-Index - 72
eISSN - 1423-0186
pISSN - 0028-2766
DOI - 10.1159/000189073
Subject(s) - medicine , anemia , ace inhibitor , kidney disease , urology , angiotensin converting enzyme , blood pressure
Shinsuke Nomura, MD, Nephrology Division, Department of Medicine, Kawasaki Medical School, Kurashiki, Okayama 70101 (Japan) Dear Sir, The role of angiotensin-converting enzyme inhibitors (ACEI) in inducing anemia has been reported in people with normal renal function [1], in patients with chronic renal failure on hemodialysis [2] and in kidney transplant patients [3, 4]. Several mechanisms of ACEI-induced anemia have been hypothesized. ACEI may decrease angioten-sin II, which stimulates erythropoietin production. They may decrease renal tissue hyp-oxia due to their property for increasing renal blood flow. Or, by decreasing renin levels, they may diminish one likely precursor of erythropoietin [2, 5]. The association between renal anemia and ACEI in patients at the predialysis stage has not been well discussed. Therefore, we carried out a retrospective analysis of 39 predialysis patients checking their medical records during the follow-up period at our outpatient clinic. Among patients in whom regular renal replacement therapy had been initiated from 1984 to 1993 at Kawasaki Medical School Hospital, 39 Japanese patients (23 males) were entered into the study with the following restrictive criteria: (1) age 30-65; (2) followed up by us from when serum creatinine level had been less than 2.0 mg/dl to the initiation of renal replacement therapy; (3) never showed microcytic hypochromic anemia during the period; (4) had no malignancies, liver cirrhosis, or collagen diseases, (5) no anabolic steroid, recombinant human erythropoietin (rhEpo) or transfusion was given during the period. Patients with diabetic ne-phropathy and polycystic kidney disease were excluded from the study. Twenty of them had chronic glomerulonephritis or nephrosclerosis diagnosed by renal biopsy. When their serum creatinine level increased to over 3.0 mg/dl (phase A) and over 7.0 mg/dl (phase B), the patients were divided into three groups according to the medication they were taking for hypertension: group 1 (no antihypertensive agents was prescribed): group 2 (ACEI was prescribed for at least over 2 months), and group 3 (other antihypertensive agent(s) was prescribed, such as calcium antagonists, α-and ß-blockers). Most of the prescribed ACEI were capto-pril or enalapril. Patients in whom ACEI was prescribed in combination with other agents were put into group 2. As shown in figure 1 ‚ the hematocrit level of group 2 at phase B was significantly lower than in group 1, while no difference was found at phase A (unpaired t test). There was no difference in
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