Enalapril-Associated Anemia in a Patient with IgA Nephropathy and Hypertension

J.W. van der Pijl, MD, Renal Unit, Department of Medicine, Academic Medical Centre, Room F4-215, University of Amsterdam, Meibergdreef 9, NL-1105 AZ Amsterdam (The Netherlands) Fig. 1. Time course of hemoglobin and creatinine in relation to antihy-pertensive treatment in the male, 45-year-old patient. Although anemia is often not mentioned as a possible side-effect of CEI [6], we conclude that the existence of enalapril-associated anemia must be considered when this complication develops during enalapril treatment. References Griffing GT, Melby JC: Enalapril (MK-421) and the white cell count and haematocrit. Lancet 1982;i:1361. Loftus WK, lerino F, Mathew TH: Enalapril and anaemia. Med J Aust 1988;148:209-210. Dear Sir, Enalapril has been associated with minor decreases in hematocrit in a small group of volunteers [1], and a few reports have focused attention on a reduction in hematocrit in renal transplant recipients [2,3] and also in patients on chronic hemodialysis [4]. We report enalapril-associated anemia in a patient known to have IgA nephropathy. A 45year-old white male attended the outpatient clinic in August 1990 because of severe hypertension. Laboratory investigations showed a hemoglobin level of 13.4 g/dl and a plasma creatinine of 179 μmol/l. Enalapril, furosemide and nifedipine were prescribed and later on adjusted according to blood pressure and complaints of orthostatic hypotension. A normochromic, normocytic anemia was found in November 1990 (fig. 1). No explanation of this anemia was found: WBC and platelets were within the low normal range, reticulocytes 2%, haptoglobin 0.3 g/l, ferritin, folic acid, vitamin B,2, lactate dehy-drogenase and bilirubin were also normal. Antinuclear antibodies were positive, without a positive LE cell phenomenon nor positive antibodies to dsDNA. A bone marrow aspiration and biopsy showed a normocellular aspect. After discontinuation of enalapril, hemoglobin rose to normal values. A rechal-lenge with a lower dose, given after 3 months, provoked anemia again. Animal studies [5] have pointed out that the ischemic response elicited by angiotensin II might be an important stimulus for the production of erythropoietin, which could be overruled by giving an angiotensin-convert-ing enzyme inhibitor (CEI). The observations [4] done in chronic hemodialysis patients offer also support for this finding, because strong