MANAGEMENT OF ACUTE RENAL FAILURE WITH DELAYED HYPERCALCEMIA SECONDARY TO SARCOCYSTIS NEURONA-INDUCED MYOSITIS AND RHABDOMYOLYSIS IN A CALIFORNIA SEA LION (ZALOPHUS CALIFORNIANUS).

A 3-yr-old captive-born California sea lion (Zalophus californianus) developed Sarcocystis neurona-induced myositis and rhabdomyolysis that led to acute renal failure. The sea lion was successfully managed with fluid therapy, antiprotozoals, antibiotics, anti-inflammatories, antiemetics, gastroprotectants, and diuretics, but developed severe delayed hypercalcemia, a syndrome identified in humans after traumatic or exertion-induced rhabdomyolysis. Treatment with calcitonin was added to the management, and the individual recovered fully. The case emphasizes that animals with rhabdomyolysis-induced renal failure risk developing delayed hypercalcemia, which may be life threatening, and calcium levels should be closely monitored past the resolution of renal failure.

Case Report: Plasmodium knowlesi Infection with Rhabdomyolysis in a Japanese Traveler to Palawan, the Philippines.

Skeletal muscle is known to be damaged by falciparum malaria via sequestration of infected erythrocytes. We present a case of rhabdomyolysis caused by Plasmodium knowlesi infection. The patient had fever, myalgia, and muscle weakness 5 days after returning to Japan from Palawan, the Philippines. Blood test revealed thrombocytopenia and an elevated creatine kinase level. Although rhabdomyolysis resolved with fluid therapy, fever of 24-hour cycle continued and thrombocytopenia intensified. On day 7 of illness, Giemsa-stained thin blood smear revealed malaria parasites, with a parasite count of 2,380/µL, which were morphologically indistinguishable between P. knowlesi and Plasmodium malariae. Rapid diagnostic test showed a negative result. The pathogen was later confirmed to be P. knowlesi by nested polymerase chain reaction (PCR). The patient was successfully treated with artemether/lumefantrine. This case suggests that knowlesi malaria might be able to cause skeletal muscle damage.

Severe rhabdomyolysis caused by Plasmodium vivax malaria in the Brazilian Amazon.

Severe rhabdomyolysis (creatine phosphokinase = 29,400 U/L) developed in a 16-year-old boy from Manaus, Brazil, after he started treatment with chloroquine for infection with Plasmodium vivax. Treatment led to myoglobinuria and acute renal failure. After hemodialysis, the patient improved and a muscle biopsy specimen showed no myophosphorylase or deaminase deficiency. This case of rhabdomyolysis associated with P. vivax infection showed no comorbidities. The pathogenesis is still unclear. Although rhabdomyolysis is generally reported as a complication of Plasmodium falciparum malaria, leading to metabolic and renal complications,1 it has been reported in a patient with P. vivax infection with myoadenylate deaminase deficiency.2 We report a case in a patient without typical muscle enzyme deficiencies in which severe rhabdomyolysis developed while the patients was being treated with chloroquine for a confirmed P. vivax infection.