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Sickle-Cell Nephropathy

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Emory University School of Medicine, Atlanta, Ga.

Ann Intern Med. 1970;73(3):488-489. doi:10.7326/0003-4819-73-3-488
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Patients with sickle-cell anemia have a defect in renal concentrating ability. This abnormality has been characterized functionally as an inability to attain normal maximum osmolality levels in response to water deprivation, despite normal tubular water reabsorption during solute diuresis, and a normal diluting mechanism (1, 2). This unique pathophysiologic alteration of the countercurrent mechanism suggests that the defect is due to an abnormality in trapping of solute in the renal papilla. The mechanism of this supposed abnormality in solute trapping by the medulla has been attributed to a poorly defined disorder of vasa recta hemodynamics caused by the presence of


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