Severe symptomatic hypocalcemia and prolonged heart failure after treatment of osteoporosis with denosumab in a peritoneal dialysis patient: A case report

Abstract

Patients with dialysis have a high risk of osteoporosis and fractures. However, the optimal treatment strategies for osteoporosis in dialysis patients remain unclear due to the complexity of chronic kidney disease (CKD)–mineral and bone disorder. This case report describes severe symptomatic hypocalcemia and prolonged heart failure following denosumab treatment in a peritoneal dialysis (PD) patient with secondary hyperparathyroidism and osteoporosis. A 70-year-old woman on PD for dialysis caused by diabetic nephropathy was diagnosed with osteoporosis (T score −2.5) during a routine checkup. Denosumab, a receptor activator of nuclear factor kappa-B ligand (RANKL) inhibitor, was administered following an increase in active vitamin D analog levels. One month later, she developed tetany, making it difficult to perform PD. Two days later, she was hospitalized with breathing difficulties and diagnosed with severe hypocalcemia and heart failure. Heart failure was attributed to mild fluid overload and reduced cardiac contractility due to hypocalcemia. Treatment with calcium supplementation and hemodialysis alleviated her symptoms and improved cardiac function. Denosumab is a promising option for osteoporosis in dialysis patients, but it poses a significant risk of severe hypocalcemia, especially in those with secondary hyperparathyroidism. Reports of such complications in PD patients are rare. Clinicians should carefully monitor serum calcium levels, implement preventive strategies, and promptly address complications when using denosumab in this population. In this case, cardiac function remained impaired for at least 6 months, suggesting prolonged heart failure following denosumab-associated hypocalcemia.