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Journal of Clinical Endocrinology & Metabolism Vol. 66, No. 5 896-902
doi:10.1210/jcem-66-5-896
Copyright © 1988 by the Endocrine Society.
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Response to Parathyroid Hormone in Normal Human Kidney Donors Before and After Uninephrectomy*

MIRIAM A. FRIEDLANDER and GINO V. SEGRE

Department of Internal Medicine, University of Iowa Hospitals and Clinics Iowa City, Iowa 52242
the Endocrine Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School Boston, Massachusetts 02114

Address requests for reprints to: Dr. Miriam A. Friedlander, Department of Medicine, Division of Nephrology, Case-Western Reserve University School of Medicine, 2065 Adelbert Road, Cleveland, Ohio 44106.

Normal human kidney donors represent a unique model of loss of renal mass without progressive disease. We studied such individuals to define the changes in mineral metabolism and renal responses to PTH that occur in mild renal insufficiency. PTH was infused for 24 h [0.132 µU/kg· (0.475 U/kg·h) synthetic human PTH, 1–34 fragment] before and after uninephrectomy in nine donors. Plasma 1,25-dihydroxyvitamin D levels were lower after uninephrectomy. However, the percent change from the preinfusion baseline was not different before and after uninephrectomy. With loss of a kidney, there was increased per nephron excretion of phosphate, calcium, and magnesium. Although serum carboxy-terminal levels were elevated after uninephrectomy, no changes in endogenous aminoterminal PTH levels were found. However, the levels of infused human PTH-(1–34) were higher after surgery because the MCR was lower. Serum carboxy-terminal PTH levels decreased in parallel with increased whole blood ionized calcium during PTH infusion, indicating appropriate parathyroid gland responsiveness. At this level of renal insufficiency, renal compensatory changes, rather than changes in parathyroid function, are the predominant factors in the maintenance of mineral homeostasis.

* This work was supported by a grant from Hoffman-LaRoche, Inc., and Grant RR-59 from the General Clinical Research Center.

Received June 24, 1986.







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Copyright © 1988 by The Endocrine Society