Hyposthenuria and recurrent episodes of hema- turia are well-known complications of the sickle- cell disorders (1). Although it has been sug- gested that the defect in renal concentrating ability results from the presence of sickle hemoglobin within the circulating erythrocytes, there has been no satisfactory explanation for the special vulner- ability of the kidney to the presence of such cells.
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Perillie et al. (1963) studied this question.
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