A Rare Reason for Severe Hypocalcemia Following Kidney Transplant: Denosumab Treatment

Deviations of calcium, phosphate, parathyroid hormone, and vitamin D levels are the basis for the diagnosis of calcium-phosphate metabolism disorders. The plasma concentration of the biologically active form known as free calcium is regulated in a harmonious manner by its exchange in the bones and reabsorption by the kidneys. These steps take place under the control of parathyroid hormone and calcitriol. In the process of chronic kidney disease, the kidney cannot synthesize adequate calcitriol, and the resulting hypocalcemia and hyperphosphatemia cause the development of secondary hyperparathyroidism. Osteoporosis is a metabolic bone disease and is essentially the consequence of osteoclastogenesis-induced bone resorption that exceeds bone formation. Osteoporosis is common after kidney transplant. However, hypocalcemia following kidney transplant is rare. The hungry bone syndrome after parathyroidectomy is often responsible for this condition in the pretransplant period. Denosumab is a human monoclonal antibody developed against the receptor activator of nuclear factor kappa-B ligand (known as RANKL). Denosumab exerts an antiresorptive effect on bones by reducing differentiation into osteoclasts. It is an effective treatment option for osteoporosis in the general population. There is insufficient scientific data regarding the use of denosumab in kidney transplant patients. Here, we present the case of a kidney transplant recipient who developed severe hypocalcemia (serum calcium 4.7 mg/dL) after denosumab treatment for osteoporosis.