This is the first confirmed report of exertional rhabdomyolysis in a non-hu
man primate. The monkey was singly housed and presented with anorexia and r
eluctance to move. There was no external evidence of trauma. Clinicopatholo
gic findings included mild azotemia, marked elevation in serum creatine pho
sphokinase (CPK), alanine aminotransferase, aspartate aminotransferase, and
myoglobinuria. Two days post-incident, the peripheral skeletal muscle had
marked multifocal myonecrosis and fibrillar disruption without an inflammat
ory reaction. Treatment included diuresis and pain relief, and urinary outp
ut was monitored. The monkey recovered over the next two weeks. The major s
ignificance of skeletal muscle damage is the potential of released myoglobi
n to cause acute renal failure in the presence of other co-factors such as
hypovolemia, acidosis, or ischemia. CPK levels can be highly variable and a
re inconsistent with the degree of muscle damage; however, CPK is thought t
o be the most sensitive enzyme marker for muscle necrosis. Because of the p
otential life-threatening sequelae, exertional rhabdomyolysis should be inc
luded as a differential diagnosis when similar clinical and pathological si
gns are observed.