Severe anemia: a risk factor for glomerular injury in sickle cell disease

• Published in: Journal of the National Medical Association 1995-03, Vol.87 (3), p.209-213
• Main Authors: FAULKNER, M, TURNER, E. A, DEUS, J, PHILLIPS, K, WEAVER, C, TAIWO, O, OMITOWOJU, O
• Format: Article
• Language: English
• Subjects: Adult; Albuminuria - etiology; Albuminuria - physiopathology; Anemia, Sickle Cell - physiopathology; Anemias. Hemoglobinopathies; Biological and medical sciences; Diseases of red blood cells; Female; Glomerulonephritis - diagnosis; Glomerulonephritis - etiology; Hematologic and hematopoietic diseases; Humans; Kidney Function Tests; Male; Medical sciences; Risk Factors
• ISSN: 0027-9684; 1943-4693

Approximately 15% to 20% of patients with sickle cell disease have proteinuria. Proteinuria, particularly albuminuria, is the hallmark of glomerular injury. This study examines risk factors for glomerular injury as indicated by urinary albumin excretion (UAE) 30 microgram/minute, directly related to sickle cell disease. A total of seven patients were enrolled between September 1992 and March 1993. Fasting blood chemistries, complete blood cell count, 24-hour urine for protein and creatinine clearance, and glomerular filtration rate determined by 125 I-iothalamate were obtained for each patient. The results indicated that the lower the hematocrit, the higher the UAE rate. Low hematocrits have served as a protective mechanism in sickle cell disease by reducing blood viscosity and thus decreasing the number of vaso-occlusive crises. However, severe anemia appears to have an indirect adverse effect on the kidney in sickle cell disease.