Extensive investigations of the parathyroid glands were instigated by the cure of generalized osteitis fibrosa cystica by surgical removal of a parathyroid adenoma by Mandl (1) in 1925. It was early noted that renal calculi were often found in cases of parathyroid tumor (2). Later work showed that these stones consisted chiefly of calcium phosphate and that the tendency to their formation was definitely decreased when the urine was made more acid (3). Removal of the parathyroid tumor. resulted in the disappearance of this tendency to calculus formation and of the alkalinity of the urine.Albright, Baird, Cope, and Bloomberg (4), in their discussion of 83 cases of parathyroid tumor with hyperparathyroidism, brought out the fact that 43 of these showed clinical evidence of renal damage. These kidney lesions were attributed to damage resulting from the deposition of calcium in the renal parenchyma or to the formation of calculi in the pelves, such calcium depositions being manifestations of primary hyperparathyroidism. However, these authors suggested the possibility that parathyroid enlargement may be secondary to renal impairment: " It seems conceivable therefore that a chronic renal insufficiency with phosphate retention and a high inorganic phosphorus level might likewise cause hyperplasia of all parathyroid tissue which might go on to multiple tumor formation" and later, "In these cases the kidney damage may be the cause and not the result of the parathyroid tumors."p Bergstrand (5) studied the parathyroid glands in an extensive series of autopsies, and in most of the cases where he found them enlarged, there was also some damage to the kidneys. Pappenheimer and Wilens (6) carefully weighed the parathyroid glands from a large series of necropsies. They found the parathyroids taken from unselected nephritics to average more than 50 per cent greater in weight than those taken from non-nephritic controls. Seven severe nephritics showed an increase of 109 per cent over the same control series. The enlargement was diffusely hyperplastic in character, resembling the enlargement which has been reported in rickets (7,8), and which may exist in pregnancy (9, 10). Adenomata were found in only three of 56 nephritics and in two of 74 controls. Jarrett, Peters, and Pappenheimer (11) report that they have induced a similar enlargement of the parathyroids by producing chronic renal insufficiency in rats.In previous reports from this laboratory evidence of functional hyperactivity of the parathyroid glands in rickets (12) and in pregnancy (13) has been presented. We have used the same approach in our investigation of parathyroid activity in the present series of nephritic patients,' to determine whether the hyperplasia noted by Pappenheimer and Wilens (6) is accompanied by a hyperfunction. The patients were selected on the basis of elevation of the blood urea nitrogen, most of them having chronic rather than acute renal insufficiency. The controls were thirtyeight normal persons-thirty women and eight men. Determinations of ca...