Crush-related acute kidney injury (acute renal failure)
- Raymond Vanholder, MD, PhD
Raymond Vanholder, MD, PhD
- Professor Emeritus of Medicine
- University Hospital, Ghent, Belgium
- Mehmet S Sever, MD
Mehmet S Sever, MD
- Professor of Medicine
- Istanbul School of Medicine
Following rhabdomyolysis, several pathogenetic mechanisms can cause heme pigment-associated acute tubular necrosis (ATN), which results in an abrupt rise in serum creatinine, or acute kidney injury (AKI) [1-4]. (See "Definition and staging criteria of acute kidney injury (acute renal failure)".)
Rhabdomyolysis may be due to either traumatic or nontraumatic muscle injury. Much of our knowledge on rhabdomyolysis-associated ATN derives from observations of traumatic rhabdomyolysis that forms the basis for development of the crush syndrome resulting from large-scale, natural or manmade disasters .
Treatment of both acute and chronic kidney diseases after disasters deserves special mention because it almost always requires complex technology and equipment. Crush syndrome-related AKI is the most frequent acute kidney problem after mass disasters .
The clinical features and prevention of AKI due to traumatic rhabdomyolysis will be reviewed here. ATN due to nontraumatic rhabdomyolysis and hemolysis and general overviews of rhabdomyolysis, hemolysis, and drug-induced myopathies are discussed in detail separately. (See "Clinical features and diagnosis of heme pigment-induced acute kidney injury (acute renal failure)" and "Clinical manifestations and diagnosis of rhabdomyolysis" and "Diagnosis of hemolytic anemia in the adult" and "Drug-induced myopathies".)
DEFINITIONS AND EPIDEMIOLOGY
Systemic manifestations that are induced by crush injury are often referred to as crush syndrome. Crush syndrome develops in 30 to 50 percent of cases of traumatic rhabdomyolysis and is frequently seen after catastrophic earthquakes. According to some estimates, the incidence of crush syndrome ranges between 2 and 5 percent of all injured victims of catastrophic earthquakes [7-10]. All disaster victims, irrespective of whether they are mildly or severely injured, should be considered at increased risk.
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- Gibney RT, Sever MS, Vanholder RC. Disaster nephrology: crush injury and beyond. Kidney Int 2014; 85:1049.
- Sever MS, Lameire N, Van Biesen W, Vanholder R. Disaster nephrology: a new concept for an old problem. Clin Kidney J 2015; 8:300.
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- Hatamizadeh P, Najafi I, Vanholder R, et al. Epidemiologic aspects of the Bam earthquake in Iran: the nephrologic perspective. Am J Kidney Dis 2006; 47:428.
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- Sever MS, Erek E, Vanholder R, et al. Renal replacement therapies in the aftermath of the catastrophic Marmara earthquake. Kidney Int 2002; 62:2264.
- DEFINITIONS AND EPIDEMIOLOGY
- CLINICAL MANIFESTATIONS
- Compartment syndrome
- Dark urine
- Renal insufficiency
- Other clinical problems
- BIOCHEMICAL ABNORMALITIES
- DIFFERENTIAL DIAGNOSIS
- Before and during extrication
- - Evidence
- After extrication
- - Use of bicarbonate
- - Use of mannitol
- - Prevention of hyperkalemia
- - Urine output goal
- - Total volume administered
- - Calcium
- - Loop diuretics
- TREATMENT OF ESTABLISHED ACUTE KIDNEY INJURY
- SOCIETY GUIDELINE LINKS
- INFORMATION FOR PATIENTS
- SUMMARY AND RECOMMENDATIONS