ACTA ENDOCRINOLOGICA (BUC)

Context. We propose that the underlying etiology of renal calcium leak is complex and involves defects in renal handling and parathyroid sensing of ambient calcium concentration in the tubular fluid and blood. Therefore, treatment of such a patient requires both decreasing the parathyroid mass and inhibiting calcium sensing receptors that are present in the parathyroid and kidney. However, a combined treatment strategy of three-gland parathyroidectomy and calcimimetic therapy has not been formally studied to date. Objective. To present a patient with renal calcium leak causing secondary hyperparathyroidism presenting as primary hyperparathyroidism. There are a two year followup period. Results. A patient with mild hypercalcemia, hypercalciuria, musculoskeletal pain, and recurrent kidney stones underwent a three gland parathyroidectomy and had persistent hypercalciuria post-operatively. She was subsequently treated with thiazide diuretic that caused dramatic decrease in hypercalciuria, but overt hypercalcemia. She was then treated with Cinacalcet with normalization of intact PTH, serum calcium and serum phosphate. Conclusion. Patients with hypercalciuria and mild hypercalcemia may have secondary hyperparathyroidism. Renal calcium leak drives hyperparathyroidism and is unresponsive to parathyroidectomy or thiazide diuretic alone. In our patient, three gland parathyroidectomy plus calcium –sensing mimetic agent, Cinacalcet, normalized serum calcium, PTH, and phosphorus. Defects in calcium sensing in the parathyroid gland and kidney might be responsible for this form of secondary hyperparathyroidism.