Instructor University of Illinois at Chicago Chicago, Illinois, United States
Introduction : Calcium dyshomeostasis is a distinct electrolyte disturbance in rhabdomyolysis (RBD) in that both hypo- and hypercalcemia can occur during the course of disease. The hypercalcemic phase can be life-threatening and challenging to treat in some cases.
Case(s) Description : A 57-year-old female was admitted due to sepsis of an unclear source. Her hospital course was complicated by shock requiring pressors, atrial fibrillation requiring amiodarone, and acute kidney injury requiring continuous renal replacement therapy. Within two weeks, she had recovered from sepsis but had developed acute-onset bilateral lower extremity weakness that coincided with rising aspartate aminotransferase levels and markedly elevated creatine kinase levels. A diagnosis of statin-induced RBD was established. During that time, she was persistently oliguric on intermittent hemodialysis.
Immediately following the diagnosis of RBD, she developed hypocalcemia for several days, with a nadir total calcium of 7.3 mg/dL, corrected for albumin. As RBD resolved, she developed severe hypercalcemia with corrected total calcium peaking at 16.1 mg/dL and undetectably high ionized calcium levels ( > 8.0 mg/dL). Other labs were remarkable for hyperphosphatemia (9.0 mg/dL), low 25-vitamin D (8.0 ng/mL), low 1, 25-vitamin D (< 5.0 pg/mL), and low-normal PTH (18 pg/mL). A malignancy workup was unremarkable. Her hypercalcemia was presumed to be a complication of RBD. She received 360 units of calcitonin every 12 hours for four doses with minimal response. She was simultaneously initiated on cinacalcet 30 mg BID, which was subsequently escalated to 60 mg BID given suspicion of an element of hyperparathyroidism, but with no significant response. She received daily hemodialysis for hypercalcemia with minor transient improvement in calcium levels. Ultimately, she was given denosumab at a dose of 60 mg subcutaneously with normalization of serum calcium within a week.
Discussion : The initial events in RBD and release of intracellular muscle contents produce hyperphosphatemia and subsequent hypocalcemia from precipitation of calcium-phosphate deposits in muscle. With resolution of RBD, dissolution of these deposits and their subsequent release into the circulation is thought to produce the hypercalcemic phase of RBD. With minimal efficacy of treatment modalities and only a transient response to dialysis, denosumab was a late resort in our patient with persistent renal failure. A previous report demonstrated safe and effective use of denosumab in RBD at a dose of 120 mg. In our case, denosumab at a dose of 60 mg appeared to be safe and effective. Close monitoring for development of hypocalcemia is crucial.
