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April 1959

The Nephropathies of Sickle-Cell Disease

Author Affiliations

Washington, D. C.

From the Renal Laboratory, Georgetown Division, District of Columbia General Hospital, and the Department of Medicine, Georgetown University Medical Center. Director, Renal Laboratory, Georgetown Division, District of Columbia General Hospital, Post-doctoral Fellow, National Heart Institute (Dr. Berman); Resident in Medicine, Georgetown Division, District of Columbia General Hospital (Dr. Tublin).

AMA Arch Intern Med. 1959;103(4):602-606. doi:10.1001/archinte.1959.00270040088011

Many of the complications of sickle-cell anemia have been well described and may be readily diagnosed, e. g., the pulmonary and cardiac manifestations.1,2 In contrast, the functional and morphological renal changes associated with hemoglobin S have received little intensive study until the past few years. Margolies, in a clinical and pathologic review of the subject in 1951, mentioned albuminuria, hematuria, cylindruria, frequent urinary infections, fixed specific gravities, uremia and renal thromboses, and infarctions as complications of sicklecell disease and trait.3 The nephropathies thus far described in detail include gross hematuria,4 hyposthenuria,5 fat embolism,6 and the nephrotic syndrome.7

The referral of a patient with homozygous hemoglobin S and massive proteinuria provided the opportunity to observe many of these renal defects in the same subject and to study their response to corticotropin (ACTH).

Report of Case  The patient was a 9-year-old Negro boy with eight hospital admissions preceding the present one.

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