Abstract
SECONDARY parathyroid hyperplasia resulting from long standing renal insufficiency is a well described entity whose characteristics have been described by Castleman and Mallory1 and others.2 , 3 Moreover, clinical hyperparathyroidism due to such hyperplasia has been the subject of several reviews4 5 6 and case reports7 8 9 10 11 emphasizing the variety of complications that may ensue.However, despite suggestions that such secondarily stimulated hyperparathyroidism may become autonomous12 13 14 convincing data regarding such a possibility are not available, owing to the great excess of complexing anions in the blood that are an invariable consequence of significant uremia.The case reported below, therefore, is of considerable importance because it . . .
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