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
COCHRAN RT. Hyposthenuria in Sickle Cell States. Arch Intern Med. 1963;112(2):222–225. doi:10.1001/archinte.1963.03860020120016
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