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Net renal tubular reabsorption of zinc in healthy man and impaired handling in sickle cell anemia
Author(s) -
YuzbasiyanGurkan Vilma A.,
Brewer George J.,
Vander Arthur J.,
Guenther Michael J.,
Prasad Ananda S.
Publication year - 1989
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.2830310203
Subject(s) - zinc , excretion , medicine , endocrinology , renal function , reabsorption , sickle cell anemia , creatinine , urine , zinc deficiency (plant disorder) , renal physiology , anemia , urinary system , chemistry , kidney , disease , organic chemistry
Zinc deficiency is a significant clinical finding in sickle cell anemia (SCA) and abnormalities of zinc handling such as hyperzincuria are present. The cause of increased urinary zinc excretion in SCA is not clear. To define the renal handling of zinc in SCA and in healthy subjects, we measured zinc (total and ultrafilterable plasma zinc, urine zinc) and creatinine clearance in eight healthy and seven SCA subjects. Ultrafilterable zinc in plasma was assessed by equilibration of plasma with 65 Zn followed by filtration through Amicon Cetriflo CF25 cones. While the mean filtered load of zinc was not significantly different between the two groups, the mean zinc excretion rate was approximately threefold higher in patients (1.73 ± 0.96 vs. 0.63 ± 0.39 μg/min, P <.05). In controls, zinc excreted was significantly less than zinc filtered ( P <.005), the fractional excretion of zinc averaging 0.49 ± 0.31, indicating net reabsorption. This was not the case for the SCA patients. We conclude that there is impaired renal tubular handling of zinc in SCA.