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Evidence has accumulated suggesting that the state of secondary hyperparathyroidism and the elevated blood levels of parathy- roid hormone (PTH) in uremia participate in the genesis of many uremic manifestations. The present study examined the role of PIH in glucose intolerance of chronic renal failure (CRF). Intravenous glucose tolerance tests (IVGTI) and eu- glycemic and hyperglycemic clamp studies were performed in dogs with CRF with (NPX) and without parathyroid glands (NPX-PTX). There were no significant differences among the plasma concentrations of electrolytes, degree of CRF, and its duration. The serum levels of PTH were elevated in NPX and undetectable in NPX-PTX.
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Akmal et al. (1985) studied this question.
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