Abstract #1406447: A Case of Severe Hypercalcemia After Recovery from Rhabdomyolysis that was Refractory to Hemodialysis

Abstract

Rhabdomyolysis (RBD) is severe skeletal muscle injury which often results in acute kidney injury (AKI) and significant electrolytes abnormalities. We herein describe a case of severe hypercalcemia that occurred during the recovery phase of RBD that was successfully treated with intravenous (IV) pamidronate. A 58-year-old male with history of cirrhosis, IgA nephropathy and chronic kidney disease presented with lower extremity weakness and was found to have AKI due to statin-induced RBD. Creatinine Kinase (CK) was > 30000 U/L [30-200], BUN 78 mg/dl [ 6-22], Creatinine 5.78 mg/dl [ 0.77-1.25], corrected Calcium (Ca) 7.0 mg/dl [8.6- 10.2], Ionized Ca 2.5 mg/dl [4.5- 5.3], Phosphorus 6.7 mg/dl [2.3-4.7], 25-OH Vitamin D 4.8 ng/ml [30 -80] and Parathyroid hormone (PTH) 333 ng/ml [8.7-77.1]. The patient received IV calcium gluconate, vitamin D supplementation and hemodialysis (HD) and was started on calcitriol 0.25 mg three times a week. He was discharged on calcitriol, calcium acetate and vitamin D with a corrected Ca of 9.1 mg/dl. One week later, the patient was readmitted with confusion and a corrected Ca of 15.3 mg/dl, phosphorus of 7 mg/dl, CK of 131 U/L, 25- OH vitamin D 10 ng/ml, PTH 11.4 ng/ml. Additional workup for hypercalcemia was unremarkable. His hypercalcemia persisted despite HD with low calcium baths, gentle IV hydration, and IV furosemide. Calcitonin 4 units/kg was initiated but his Ca remained 12.4mg/dl after 48 hours. IV pamidronate 30 mg was given and within 5 days, his Ca level was 9.4 mg/dl, reaching a nadir of 8.9 mg/dl. RBD is commonly associated with hypocalcemia in the acute phase. Hypercalcemia can also occur in the recovery phase, but few reports exist and the appropriate management has not been established. As in our case, overtreatment of hypocalcemia may exacerbate hypercalcemia. The pathophysiology of the hypercalcemia may be due to mobilization of Ca from injured muscles and soft tissue deposits. Secondary hyperparathyroidism can also contribute to a hypercalcemic response. Hypercalcemia due to RBD is usually self-limited but more severe cases can occur. Few have reported on the use of bisphosphonates for this condition. In our case, multiple treatments were not successful in lowering calcium. Despite concerns that bisphosphonates may not successfully lower calcium, since hypercalcemia was not mediated by bone turnover, calcium decreased after bisphosphonate therapy and no adverse effects were experienced. Therefore, bisphosphonate therapy can be considered in refractory post-rhabdomyolysis hypercalcemia.