SUN-803 Profound Hypercalcemia After Recovery of Rhabdomyolysis Associated Acute Kidney Injury and Hypocalcemia Requiring Dialysis

Abstract Disclosure: Y. Kim: None. E.Y. Lee: None. R.J. Weber: None. S. Kim: None. J.E. Kim: None. E. Murphy: None. S. Patzek: None. D.M. Shoback: None. C. Liu: None. Developing hypercalcemia (H-Ca) after rhabdomyolysis-induced acute kidney injury (RIAKI) is rare. We report 3 cases of profound H-Ca after RIAKI. A 76-year-old (y/o) man(M) was admitted for RIAKI and hypocalcemia (L-Ca) with an ionized calcium (iCa) of 0.79 mmol/L [1.14 – 1.34] and albumin-corrected calcium (C-Ca) of 8.7 mg/dL [8.4 – 10.5], requiring 5 days of CRRT followed by 23 days of intermittent hemodialysis (iHD) with a high calcium (Ca) bath and 101.5 g of intravenous Ca (IV-Ca). He was discharged with oral Ca and vitamin D. Four weeks later, he presented with iCa > 1.8 mmol/L and C-Ca 20.9 mg/dL. PTH and 1,25-OH vitamin D (1-25-D) were low, and 25-OH Vitamin D (25-D) and PTHrP were normal. Ca deposits throughout his chest walls and the buttock area were noted incidentally. iCa slowly improved over the following 18 days with fluids, diuretics, calcitonin, and 1 dose of denosumab, to 1.5 mmol/L when a second dose of denosumab was given. iCa normalized 2 days later. A 30 y/o M was admitted after an opioid overdose and bilateral lower extremity compartment syndrome. He was found to have RIAKI and L-Ca with iCa of 0.89 mmol/L [1.12 – 1.32] and C-Ca of 7.9 mg/dL [8.3 – 10.6], requiring 4 days of CRRT followed by 8 days of iHD with a high Ca bath and 35g of IV-Ca. iCa normalized to 1.2 mmol/L 18 days later. A week later, the patient developed acute H-Ca in 1 day with a peak iCa of 2.27 mmol/L and C-Ca of 17.1mg/dL 4 days later. PTH and 1-25-D were low with normal 25-D and high PTHrP (4.2 pmol/L [0-2.3]). Imaging revealed Ca deposits in his lower extremities. C-Ca decreased by 2 points over 2 days with fluids and calcitonin but plateaued for 4 days. It normalized 3 days after a dose of 90 mg of pamidronate. A 60 y/o M was admitted for presumed alcohol withdrawal seizure, RIAKI, and L-Ca. A duodenal ulcer was also found, requiring multiple surgeries. Worsening RIAKI and L-Ca were noted 3 months after admission, with iCa of 0.82 mmol/L [1.12 – 1.32] and C-Ca of 6.6 mg/dL [8.3 – 10.6], requiring 28 days of CRRT followed by 18 days of iHD with a high Ca bath and 50.2g of IV-Ca. Ca normalized on day 102. C-Ca started rising on day 125, and H-Ca (C-Ca of 10.8 mmol/L) developed on day 127 with a peak iCa of 1.33 mmol/L and C-Ca of 15.8 mg/dL on day 140. PTH and 1-25-D were low, with normal 25-D and high PTHrP (8.7 pmol/L [0-2.3]). A Ca deposit in his right external iliac vein was incidentally noted. Ca remained high after fluids and calcitonin and normalized 2 days after 4 mg of IV zoledronate on day 157. Life-threatening H-Ca can develop days to weeks after recovery of RIAKI and L-Ca. All our patients received dialysis and IV-Ca during the hypocalcemic phase and the usual care during the hypercalcemic phase. Mobilization of Ca deposits has been hypothesized as an important mechanism. Clinicians should be aware of this potential complication and cautiously replete Ca as aggressive repletion may exacerbate H-Ca. Presentation: Sunday, July 13, 2025