Abstract
A 64 year old patient with non-metastatic renal carcinoma, hypercalcemia, and metabolic alkalosis was in-vestigated in an effort to determine the etiology of the hypercalcemia. Clinical evaluation revealed muscular weakness, polyuria, dysphagia, hypophosphatemia and elevated phosphate clearances consistent with marked tissue effects of hypercalcemia resulting from parathyroid hormone excess. Surgical removal of the tumor was associated with reversion to normal of the clinical and laboratory abnormalities; recurrence of the neoplasm was followed by reappearance of hyper-calcemia and metabolic alkalosis. Immunological analysis of the surgical specimen by quantitative complement fixation and inhibition of complement fixation revealed the presence of parathyroid hormone-like material in the tumor but not in the normal upper pole of the affected kidney. The results suggest that parathyroid hormone was secreted by the neoplasm into the circulation where it exerted its effects on peripheral tissues, resulting in a syndrome clinically indistinguishable from primary hyperparathyroidism.