Abstract: SA-PO514
Hypercalcemia: A Harbinger of Recovery From Rhabdomyolysis?
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports
November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders
- 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical
Authors
- Maldonado, Dawn, Mount Sinai Health System, New York, New York, United States
- Guadalupe, Joseph, Mount Sinai Health System, New York, New York, United States
- Ediale, Temi-Ete I., Mount Sinai Health System, New York, New York, United States
- Ogbolu, Cora O., Mount Sinai Health System, New York, New York, United States
- Brown, Maritza, Mount Sinai Health System, New York, New York, United States
- Stern, Aaron S., Mount Sinai Health System, New York, New York, United States
Introduction
Hypercalcemia occasionally develops following renal recovery from rhabdomyolysis. We describe a case of hypercalcemia developing just prior to renal recovery. This case suggests that not only can hypercalcemia develop after rhabdomyolysis, but that it can sometimes be a sign of imminent recovery.
Case Description
We present a case of a 65-year-old man with a past medical history of hepatitis C who was brought to the emergency department after prolonged cold exposure. He was hypothermic at 30.4 Celsius and had frostbite of multiple digits. Laboratory results were significant for a markedly elevated serum creatine kinase level >22,000 units/L and serum creatinine 4 mg/dL with unknown baseline. He did not respond to aggressive fluid resuscitation; hence dialysis was initiated. Corrected serum calcium was 5.8 mEq/L on hospital day 2, and remained low until it started to rise beyond normal levels on hospital day 28, peaking at 14.4 meq/L on hospital day 41 (table 1). Therapy was initiated with calcitonin and lower calcium dialysate. On hospital day 43 he began making urine, so dialysis was held. Hypercalcemia work-up revealed parathyroid hormone 9.9 pg/mL, vitamin D-25 9 ng/mL, vitamin D1-25 <5 ng/mL, fractional excretion of calcium 0.05, parathyroid-related hormone <2 pg/mL, and alkaline phosphatase 79 U/L – thus ruling out more common causes of hypercalcemia. N-telopeptide/creatinine ratio was 54 (normal 0-62), which ruled out hypercalcemia of immobilization. These results led us to the conclusion that the hypercalcemia was due to recovery from rhabdomyolysis.
Discussion
Hypercalcemia can be seen in the setting of recovery from rhabdomyolysis. The mechanism remains unclear, but it is postulated that it is from mobilization of calcium deposits that are sequestered in damaged muscle tissue. We present a case where the patient started developing hypercalcemia shortly before other signs of kidney recovery. Our case suggests that hypercalcemia may at times be the first indication of renal recovery from rhabdomyolysis.