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1/4. medullary sponge kidney and renal-leak hypercalciuria. A link to the development of parathyroid adenoma?

    The pathogenesis of the association of medullary sponge kidney and hyperparathyroidism from parathyroid adenoma remains obscure. This unusual case of medullary sponge kidney and secondary hyperparathyroidism due to renal-leak hypercalciuria gives insight into a possible mechanism for the occurrence of medullary sponge kidney with parathyroid adenoma. Suppressible hyperparathyroidism due to renal calcium wasting could represent an intermediate stage in the development of unsuppressible parathyroid hormone secretion. Thus, parathyroid adenoma occurring with medullary sponge kidney may represent a consequence of disordered renal calcium excretion rather than a primary abnormality.
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2/4. Prolonged fever associated with primary hyperparathyroidism.

    A 36-year-old woman presented with hypercalcemia, hypercalciuria, elevated serum parathyroid hormone levels and prolonged fever. Surgical removal of the hyperplastic and adenomatous parathyroid glands led to reversal of the biochemical abnormalities as well as return of her temperature to normal.
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3/4. Normocalcemic hyperparathyroidism.

    10 patients with normocalcemic secondary hyperparathyroidism due to renal hypercalciuria and 1 patient with normocalcemic primary hyperparathyroidism are presented. The diagnostic criteria of both manifestations of disturbed calcium metabolism are outlined. Successful therapeutic approach depends on the exact discrimination between each form of normocalcemic hyperparathyroidism.
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4/4. Pathogenesis of renal calculi in distal renal tubular acidosis. Possible role of parathyroid hormone.

    Elevated circulating levels of immunoreactive parathyroid hormone (PTH), hypercalciuria and renal calculi were found in 3 patients with distal renal tubular acidosis (RTA). Treatment with alkali resulted in a fall of PTH toward normal and a reduction in urinary calcium, but the frequency of urolithiasis was unchanged. In one patient in whom prolonged follow-up was possible, a subtotal parathyroidectomy was performed. This was followed by virtual cessation of stone formation despite persistence of the acidification defect. This study suggests that RTA may be associated with secondary hyperparathyroidism and that the consequent elevation in PTH may play a contributory role in the pathogenesis of renal calculi.
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