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ROBERT T. COCHRAN, Jr., MD

Arch Intern Med. 1963;112(2):222-225.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

An impairment of renal concentrating power has been described as a common accompaniment of both sickle cell anemia and sickle cell trait. The mechanism by which this complication occurs has remained obscure. The demonstration that urine osmolarity rises after exchange transfusion in children with sickle cell disease has suggested that a specific tubular dysfunction results from such influences as anoxia or chronic S hemoglobinuria, both of which are presumably reversed by exchange transfusion. The role of such factors in the nonanemic patient with sickle cell trait is questionable, however. It is noteworthy, too, that alterations in urinary osmolarity following transfusion do not occur simultaneously with changes in the hematocrit. The rise in osmolarity reaches a maximum only after the hematocrit has been maintained at normal levels for up to two months; the return of the osmolarity to previous levels occurs at a comparable interval after the hematocrit has fallen to . . . [Full Text PDF of this Article]

Author Affiliations
GALVESTON, TEXAS

From the Department of Internal Medicine, University of Texas Medical Branch.

Footnotes
Received for publication Oct 8, 1962; accepted Feb 14, 1963.

Present address: Duke University Hospital, Durham, NC.

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