Severe Hypercalcemia Presenting During Recovery Phase of Rhabdomyolysis-Induced Acute Kidney Injury

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SAT 199-223-Disorders of Bone & Calcium Homeostasis: Case Reports
Clinical
Saturday, June 15, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SAT-202
Andy Cheng*1, Reza Bashtar1, Anthony Francis Firek2 and Kevin Anthony Codorniz1
1Loma Linda University Medical Center, Loma Linda, CA, 2Jerry L Pettis Veterans Administration, Loma Linda, CA
Background: Calcium abnormalities are common complications from rhabdomyolysis. Hypocalcemia is typically seen during the acute phase of rhabdomyolysis, thought to be caused by i) precipitation of calcium phosphate from hyperphosphatemia due to acute kidney injury and ii) dystrophic calcium deposition into damaged muscles. Hypercalcemia is less common and is seen during the recovery phase of rhabdomyolysis. Several etiologies for delayed hypercalcemia have been proposed, including mobilization of calcium deposits out of the recovering muscles, secondary hyperparathyroidism, increase in calcitriol, and resolution of hyperphosphatemia.

Purpose: We present a case that highlights mobilization of calcium deposits out of the recovering muscles as the principal mechanism for severe delayed hypercalcemia in a patient with rhabdomyolysis.

Hospital course: 23 year old male admitted after found down from suspected hit-and-run motor vehicle accident, with subsequent rhabdomyolysis, compartment syndrome (ultimately requiring amputation), intubation, cardiac arrest, and acute kidney injury requiring hemodialysis (HD) for 3 weeks. Renal function improved and the patient was taken off HD, but he then developed progressive hypercalcemia. Pt was started on calcitonin and then pamidronate with increasingly aggressive fluid resuscitation. Despite these measures, over the next several days calcium persistently increased to peak 17.1 mg/dL corrected (8.9-10.3 mg/dL). Pt experienced fatigue, nausea and vomiting but showed no other signs/symptoms of hypercalcemia, and EKG was unchanged. Labs measured at hypercalcemic peak included PTH < 2.5 pg/mL (10-65 pg/mL), Vit 1,25(OH)2D <8 (18-72 pg/mL) and phosphate 6.3 mg/dL (2.4-4.7 mg/dL). Technetium pyrophosphate scan discovered extensive calcium deposition in the left thigh muscles and left amputation stump. Calcium level normalized briefly with HD but then continued rising to 13.4 mg/dL, requiring a second day of HD. Hypercalcemia resolved several days later. The total episode of hypercalcemia was 16 days in duration.

Discussion: This case demonstrates that mobilization of calcium deposits out of recovering muscles is a primary mechanism for hypercalcemia during recovery phase of rhabdomyolysis-induced acute kidney injury. This mobilization phase may continue for over 2 weeks. Calcitonin and pamidronate are ineffective therapies for this syndrome since their mechanisms of action are unrelated to calcium release from recovering muscles.

Nothing to Disclose: AC, RB, AFF, KAC

*Please take note of The Endocrine Society's News Embargo Policy at http://www.endo-society.org/endo2013/media.cfm