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REVIEW ARTICLE
Year : 2015  |  Volume : 2  |  Issue : 2  |  Page : 50-54

Myoglobinuria and Acute Kidney Injury


Department of Pediatrics and Neonatology, All India Institute of Medical Sciences, Raipur, Chhattisgarh, India

Correspondence Address:
Atul Jindal
Department of Pediatrics and Neonatology, All India Institute of Medical Sciences, Raipur - 492 099, Chhattisgarh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/2225-1243.155775

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Myoglobin is a heme protein present in muscle tissues and responsible for binding and delivery of oxygen in the muscle cells for oxidative metabolism. Whenever muscle tissue is injured, that is, rhabdomyolysis occurs free myoglobin enters into circulation along with other enzymes and electrolytes and myoglobinuria occurs when the renal threshold is crossed. There are many causes of rhabdomyolysis including physical damage, infective, inflammatory, toxic, and metabolic problems. Clinically, myoglobinuria presents as muscle pain, weakness, cola colored urine, and laboratory diagnosis is done by elevated serum creatine kinase, urine dipstick positive for blood without RBC in microscopy examination. These myoglobin molecules can cause renal injury by renal vasoconstriction, proximal tubular necrosis, and distal tubular obstruction. Early anticipation of myoglobinuria and aggressive fluid resuscitation during the initial stage of injury is the mainstay of management of myoglobinuric acute kidney injury (AKI). There is lesser role of forced alkaline diuresis and mannitol than diuresis by normal crystalloid solution in myoglobinuric AKI. Renal replacement therapy should be considered in cases with life-threatening dyselectrolytemia and acidosis.


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