R Y Aoki1, S T Saad. 1. Department of Internal Medicine and Hemocentro, State University of Campinas, SP. Brazil.
Abstract
PURPOSE: To evaluate the effects of enalapril, an angiotensin-converting enzyme inhibitor, on albuminuria associated with sickle cell anemia. PATIENTS AND METHODS: Two males and 6 females, mean age 22.8 +/- 5.5 years, with sickle cell anemia and albuminuria, received enalapril for 6 months. Before entry into the study, all had a urinary albumin concentration above 30 mg/L as determined by radioimmunoassay documented on three separate occasions at intervals of 15 to 30 days. Samples were collected before 10 AM after an oral water load of 10 mL/kg. RESULTS: Enalapril reduced 6 patients' pretreatment hyperalbuminuria to normal. One patient whose levels did not reach normal values experienced a reduction of 70%. Fractional excretion of sodium, potassium, and lithium did not change during the treatment. Mean arterial pressure decreased by 8.6 +/- 0.42 mm Hg. Two years after enalapril was discontinued, there were no changes in sodium, potassium, or creatinine levels of 7 patients who had received enalapril or in their mean arterial pressures. Urinary albumin concentration increased relative to pretreatment levels in 2 individuals, returned to pretreatment levels in 2, and remained below 30 mg/L in 2. CONCLUSION: Our results demonstrate that enalapril reduces albuminuria in patients with sickle cell anemia. After discontinuation of the drug, however, the albuminuria may increase to pretreatment levels or higher. Whether the reduction in urinary albumin concentration by angiotensin-converting enzyme inhibitors can delay the development of progressive renal failure in sickle cell anemia patients remains to be established.
PURPOSE: To evaluate the effects of enalapril, an angiotensin-converting enzyme inhibitor, on albuminuria associated with sickle cell anemia. PATIENTS AND METHODS: Two males and 6 females, mean age 22.8 +/- 5.5 years, with sickle cell anemia and albuminuria, received enalapril for 6 months. Before entry into the study, all had a urinary albumin concentration above 30 mg/L as determined by radioimmunoassay documented on three separate occasions at intervals of 15 to 30 days. Samples were collected before 10 AM after an oral water load of 10 mL/kg. RESULTS:Enalapril reduced 6 patients' pretreatment hyperalbuminuria to normal. One patient whose levels did not reach normal values experienced a reduction of 70%. Fractional excretion of sodium, potassium, and lithium did not change during the treatment. Mean arterial pressure decreased by 8.6 +/- 0.42 mm Hg. Two years after enalapril was discontinued, there were no changes in sodium, potassium, or creatinine levels of 7 patients who had received enalapril or in their mean arterial pressures. Urinary albumin concentration increased relative to pretreatment levels in 2 individuals, returned to pretreatment levels in 2, and remained below 30 mg/L in 2. CONCLUSION: Our results demonstrate that enalapril reduces albuminuria in patients with sickle cell anemia. After discontinuation of the drug, however, the albuminuria may increase to pretreatment levels or higher. Whether the reduction in urinary albumin concentration by angiotensin-converting enzyme inhibitors can delay the development of progressive renal failure in sickle cell anemiapatients remains to be established.
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