2022 Volume 29 Issue 2 Pages 141-145
Delayed hypercalcemia sometimes occurs in the diuretic phase of rhabdomyolysis-induced acute kidney injury (AKI), and may be caused by the absorption of heterotopic calcifications in injured muscles. A 60s-year-old woman with perforated peritonitis was admitted to our ICU. She developed oliguric AKI due to septic shock and rhabdomyolysis, and was treated with renal replacement therapy (RRT) for 30 days after admission to the ICU. Although she developed hyperphosphatemia from day 16 of admission during weaning from RRT, it spontaneously improved on day 43 of admission. She subsequently developed mild drowsiness and nausea, and laboratory tests revealed severe hypercalcemia, with a maximum serum ionized calcium level of 1.63 mmol/L on day 59 of admission. Her hypercalcemia and symptoms improved after treatment with a diuretic agent and fluid infusion. Serial CT images showed worsening muscle calcifications that resolved prior to the onset of hypercalcemia. These findings strongly support the hypothesis that the absorption of heterotopic calcifications in injured muscles caused hypercalcemia in this case. This case also suggests that hyperphosphatemia in the subacute phase of rhabdomyolysis-induced AKI may exacerbate heterotopic calcification and subsequent hypercalcemia.
