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Background <p>Rhabdomyolysis is a clinical syndrome that follows destruction of skeletal muscles releasing a number of toxic substances and electrolytes causing hyperkalemia, hyperphosphatemia, and hypocalcemia. However, hypercalcemia may arise during the recovery phase of rhabdomyolysis and can be life-threatening.</p> Case presentation <p>A 31-year-old previously healthy Egyptian man was admitted to the surgical unit in the teaching hospital for 4-day history of peri-anal pain, fever, vomiting, and diarrhea. He was found to have peri-anal abscess for which he underwent multiple sessions of surgical debridement. His kidney function deteriorated rapidly in the first few days with hyperkalemia resistant to medical therapy and oliguria requiring hemodialysis. His serum calcium during the period of acute kidney injury was low as expected with high serum phosphorus and elevated myoglobin and creatine kinase (CK) indicating rhabdomyolysis. However, he developed severe hypercalcemia during recovery phase peaking at 5.62 mmol/L (23 mg/dl). Plasma levels of PTH hormone, 25-hydroxy-vitamin D, and 1,25 hydroxy-vitamin D were low&#xa0;whilePTH-related peptide (PTHrP) was normal&#xa0;&#xa0;. Twenty four-hour urinary calcium level was high. Serum PTH-related peptide (PTHrP) was normal 0.7 pmol/L. Workup for hypercalcemia was unrevealing. Rhabdomyolysis was suggested as the cause of hypercalcemia.</p> Conclusion <p>Massive degree of hypercalcemia can be the result of rhabdomyolysis and may be persistent and resistant to the conventional treatment of hypercalcemia. Although hypocalcemia is the immediate sequelae of rhabdomyolysis, marked hypercalcemia can follow the recovery phase of AKI due to rhabdomyolysis as a result of release of calcium that was sequestered in the damaged muscles. However, normocalcemia ultimately ensues. Clinicians should anticipate rebound hypercalcemia in rhabdomyolysis recovery, and resistant cases may require advanced therapy.</p>

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Severe resistant hypercalcemia complicating rhabdomyolysis: a case report and review of the literature

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月20日

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  • Ali Ibrahim Ali Rahil,
  • Ahmed El-Bardissy,
  • Ahmed Elmudathir Osman,
  • Munir Abu Ageila,
  • Nada H. Soliman,
  • Razan Rahil

摘要

Background

Rhabdomyolysis is a clinical syndrome that follows destruction of skeletal muscles releasing a number of toxic substances and electrolytes causing hyperkalemia, hyperphosphatemia, and hypocalcemia. However, hypercalcemia may arise during the recovery phase of rhabdomyolysis and can be life-threatening.

Case presentation

A 31-year-old previously healthy Egyptian man was admitted to the surgical unit in the teaching hospital for 4-day history of peri-anal pain, fever, vomiting, and diarrhea. He was found to have peri-anal abscess for which he underwent multiple sessions of surgical debridement. His kidney function deteriorated rapidly in the first few days with hyperkalemia resistant to medical therapy and oliguria requiring hemodialysis. His serum calcium during the period of acute kidney injury was low as expected with high serum phosphorus and elevated myoglobin and creatine kinase (CK) indicating rhabdomyolysis. However, he developed severe hypercalcemia during recovery phase peaking at 5.62 mmol/L (23 mg/dl). Plasma levels of PTH hormone, 25-hydroxy-vitamin D, and 1,25 hydroxy-vitamin D were low whilePTH-related peptide (PTHrP) was normal  . Twenty four-hour urinary calcium level was high. Serum PTH-related peptide (PTHrP) was normal 0.7 pmol/L. Workup for hypercalcemia was unrevealing. Rhabdomyolysis was suggested as the cause of hypercalcemia.

Conclusion

Massive degree of hypercalcemia can be the result of rhabdomyolysis and may be persistent and resistant to the conventional treatment of hypercalcemia. Although hypocalcemia is the immediate sequelae of rhabdomyolysis, marked hypercalcemia can follow the recovery phase of AKI due to rhabdomyolysis as a result of release of calcium that was sequestered in the damaged muscles. However, normocalcemia ultimately ensues. Clinicians should anticipate rebound hypercalcemia in rhabdomyolysis recovery, and resistant cases may require advanced therapy.