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Crush injury-related acute tubular necrosis

INTRODUCTION

High circulating plasma myoglobin levels secondary to rhabdomyolysis can cause heme pigment-associated acute tubular necrosis (ATN), which results in an abrupt rise in serum creatinine, or acute kidney injury (AKI) [1-5]. (See "Definition of acute kidney injury (acute renal failure)".)

Rhabdomyolysis may be due to either traumatic or non-traumatic muscle injury. Much of our knowledge of rhabdomyolysis-associated ATN derives from observations of rhabdomyolysis that occurs as part of the crush syndrome resulting from large scale natural or man-made disasters.

The clinical features and prevention of AKI due to traumatic rhabdomyolysis will be reviewed here. ATN due to nontraumatic rhabdomyolysis (due to exertion, coma-induced immobility, and toxins) and hemolysis and general overviews of rhabdomyolysis, hemolysis, and drug-induced myopathies are discussed in detail separately. (See "Clinical features and prevention of heme pigment-induced acute tubular necrosis" and "Rhabdomyolysis" and "Approach to the diagnosis of hemolytic anemia in the adult" and "Drug-induced myopathies".)

DEFINITIONS AND EPIDEMIOLOGY

Crush injury complicated by AKI is often referred to as crush syndrome. Crush syndrome may include hypovolemic shock, sepsis, electrolyte disturbances (of which hyperkalemia is the most important), heart failure, arrhythmias, acute respiratory distress syndrome, disseminated intravascular coagulation, bleeding, psychological trauma, and heme pigment-induced ATN, although all of these components need not be present for the term crush syndrome to be used [6-8].

Crush syndrome develops in 30 to 50 percent of cases of traumatic rhabdomyolysis and, thus, is frequently seen after catastrophic earthquakes [6,7]. According to some estimates, the incidence of crush syndrome ranges between 2 and 5 percent of all injured victims of catastrophic earthquakes [9-11].
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