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Myoglobinuria Clinical Presentation

  • Author: Prasad Devarajan, MD, FAAP; Chief Editor: Craig B Langman, MD  more...
Updated: Oct 07, 2015


The classical triad of symptoms of rhabdomyolysis includes myalgia, muscle weakness, and dark urine. The typical history may include drug use, coma, trauma, or strenuous exercise. Patients who use diuretics and develop severe potassium deficiency may be predisposed to rhabdomyolysis.

  • Some patients may provide a history of viral illnesses, fever, convulsions, electric shock, burns, crush injuries, or trauma of any type. Patients may have a history of sepsis, especially sepsis that affects muscle tissue, such as gas gangrene. Others may give a history of participation in organized athletics during the summer or in strenuous exercise during athletic events, such as bicycle races or mountain climbing.
  • The use of some prescription drugs, such as azidothymidine (AZT) or lovastatin, or the ingestion of ethylene glycol may predispose individuals to myoglobinuria. Other drugs associated with myoglobinuria include heroin, codeine, barbiturates, amphetamines, licorice, diazepam, amphotericin-B, phencyclidine, and some dietary supplements.
  • Acute tumor lysis syndrome may be associated with myoglobinuria.
  • Snakebites, bites from recluse spiders, and multiple insect stings can cause muscle necrosis.
  • Ingestion of quail can precipitate myoglobinuria.
  • Autoimmune vesiculitis, such as dermatomyositis, may destroy muscle tissue.
  • Recurrent myoglobinuria was reported in a 14-year-old girl with Becker muscular dystrophy.[8]


See the list below:

  • Physical examination reveals generalized muscle weakness, often with painful muscle groups, trauma, and/or areas of ischemic pressure necrosis when the patient has laid down for extended periods.
  • Expect any patient with extensive trauma to have some myoglobinuria.
  • The volume status of the patient should be carefully and quickly determined because volume depletion necessitates rapid correction in order to prevent acute renal failure.


See the list below:

  • Trauma and compression: Trauma is one of the most common cause of myoglobinuria. Patients who experience crush injuries, such as those that occur when individuals are buried after earthquakes, have rhabdomyolysis and myoglobinuria. Volume depletion from fluid sequestration in damaged tissues and poor fluid intake accentuate the possibility of acute renal insufficiency. Electric shock can cause enough muscle damage to precipitate myoglobinuria.
  • Exertion: Exertional myoglobinuria occurs in most athletes but rarely becomes symptomatic unless combined with poor training, inadequate oral intake, dehydration, and heat exhaustion. Trauma from repeated blows to the muscle always releases myoglobin into the system. The treatment is prevention, which includes plentiful fluid, limited exercise during particularly hot periods, and avoiding muscle trauma. Athletes have more myoglobin in their muscles than other individuals and are prone to symptoms when small amounts of muscle tissue are damaged.[9, 10]
  • Viral myositis: Viral infections from a wide variety of organisms can cause myositis and myoglobinuria. Viral myositis is one of the most common causes of rhabdomyolysis in children.[11] Influenza is the predominant viral agent associated with rhabdomyolysis. The patient usually presents with generalized weakness and myalgias, particularly in the back and proximal extremities. Children with influenza A and influenza B viral infections can present with tenderness in calves and lower extremities.[12]
  • Electrolyte disorders: Metabolic diseases, particularly those involving muscle metabolism, may be associated with myoglobinuria. Males are affected more often, and symptomatology is exacerbated by exercise and heat injuries. Potassium depletion has been particularly associated with myoglobinuria.
  • Toxins, drugs, and diet
    • Snakebites and other venoms can cause muscle necrosis and myoglobinuria.
    • Some drugs predispose individuals to rhabdomyolysis, including AZT (used to treat acquired immunodeficiency syndrome [AIDS]) and lovastatin (used to treat hypercholesterolemia). However, statin-induced rhabdomyolysis is rare and occurs in less than 0.1% of all users.
    • Alcohol, cocaine, amphetamines, phencyclidine, ecstasy, and some dietary supplements can lead to myoglobinuria.[13]
    • Ingestion of ethylene glycol, isopropyl alcohol, and phencyclidine has been associated with myoglobinuria.
    • Overindulgence in quail can also cause myoglobinuria in some patients.
  • Infection or sepsis syndromes: Syndromes involving muscle destruction include gas gangrene, tetanus, Legionnaire disease, or shigellosis. Coxsackie viral infections with myositis may be the most common cause of mild myoglobinuria.
  • Endocrine disorders: Diabetic ketoacidosis, myxedema, and nonketotic hyperosmolar comas can disrupt muscle energy.
  • Malignant hyperthermia and high fevers: These may be contributors.
  • Hereditary myopathies
    • Hereditary myopathies, such as McArdle syndrome and muscular dystrophy, can precipitate myoglobinuria.
    • The differential diagnosis for myoglobinuria must include metabolic myopathies. This diverse and complex list of disorders is long, with new additions each year.
    • In general, patients with myopathies report exercise intolerance, muscle pain, and cramps rather than weakness. Patients with some types of muscular dystrophy or inflammatory myositis (eg, dermatomyositis, polymyositis) may present with progressive weakness.
  • Metabolic disorders
    • Patients with defects of carbohydrate metabolism (eg, myophosphorylase, phosphofructokinase, phosphohexoisomerase deficiency) have symptoms of easy fatigability or cramping induced by dynamic isometric exercise, such as heavy lifting, or prolonged exercise, such as swimming or running. Acute muscle breakdown can lead to myoglobinuria. These patients typically present after participating in high-intensity exercise, such as weight lifting.
    • Defects in lipid metabolism include carnitine deficiency, beta-oxidation enzyme deficiency, or disorders of fatty acid transport. Prolonged fasting or prolonged activity induces muscle pain and myoglobinuria. Fever, sepsis, and exposure to cold can also induce muscle fatigue in this set of disorders. These patients typically develop symptoms after prolonged low-intensity exercise, such as walking.
    • Patients with mitochondrial disorders (beta-oxidation disorders) usually present with static and progressive muscular weakness. Failure to thrive, floppy-baby syndrome, and generalized muscle weakness are present in most of these children. Patients usually present with chronic muscle cramping and weakness rather than episodic muscle cramping and weakness. Patients with some types of muscular dystrophy or inflammatory myositis may present with progressive weakness.
    • A case study reinforced the idea that myoglobinuria should be considered a manifestation of a primary sarcoglycanopathy, even as the only recognizable sign at the debut of the disease.[14]
  • Heat exhaustion and cold exposure: These conditions induce abnormal muscle metabolism by means of various mechanisms, including poor perfusion and decreased oxygenation, acidosis, rhabdomyolysis, or glucose and/or glycogen depletion.[15] Reye syndrome may also be included in this group. Patients with recurrent exercise-induced myoglobinuria may have defective carnitine palmitoyltransferase activity.[16]
Contributor Information and Disclosures

Prasad Devarajan, MD, FAAP Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of the Nephrology Fellowship Program, Medical Director of the Kidney Stone Center, Co-Director of the Institutional Office of Pediatric Clinical Fellowships, Director of Clinical Nephrology Laboratory, CEO of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine

Prasad Devarajan, MD, FAAP is a member of the following medical societies: American Heart Association, American Society of Nephrology, American Society of Pediatric Nephrology, National Kidney Foundation, Society for Pediatric Research

Disclosure: Received none from Coinventor on patents submitted for the use of NGAL as a biomarker of kidney injury for none.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Frederick J Kaskel, MD, PhD Director of the Division and Training Program in Pediatric Nephrology, Vice Chair, Department of Pediatrics, Montefiore Medical Center and Albert Einstein School of Medicine

Frederick J Kaskel, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, Eastern Society for Pediatric Research, Renal Physicians Association, American Academy of Pediatrics, American Pediatric Society, American Physiological Society, American Society of Nephrology, American Society of Pediatric Nephrology, American Society of Transplantation, Federation of American Societies for Experimental Biology, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Sigma Xi, Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

Craig B Langman, MD The Isaac A Abt, MD, Professor of Kidney Diseases, Northwestern University, The Feinberg School of Medicine; Division Head of Kidney Diseases, The Ann and Robert H Lurie Children's Hospital of Chicago

Craig B Langman, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, International Society of Nephrology

Disclosure: Received income in an amount equal to or greater than $250 from: Alexion Pharmaceuticals; Raptor Pharmaceuticals; Eli Lilly and Company; Dicerna<br/>Received grant/research funds from NIH for none; Received grant/research funds from Raptor Pharmaceuticals, Inc for none; Received grant/research funds from Alexion Pharmaceuticals, Inc. for none; Received consulting fee from DiCerna Pharmaceutical Inc. for none.

Additional Contributors

Laurence Finberg, MD Clinical Professor, Department of Pediatrics, University of California, San Francisco, School of Medicine and Stanford University School of Medicine

Laurence Finberg, MD is a member of the following medical societies: American Medical Association

Disclosure: Nothing to disclose.


Watson C Arnold, MD Director, Department of Pediatric Nephrology, Cook Children's Medical Center

Watson C Arnold, MD is a member of the following medical societies: American College of Medical Quality, American Federation for Medical Research, American Society for Nutritional Sciences, American Society of Nephrology, American Society of Pediatric Nephrology, International Society of Nephrology, Sigma Xi, Southern Society for Pediatric Research, Texas Medical Association, and Texas Pediatric Society

Disclosure: Nothing to disclose.

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Model of helical domains in myoglobin.
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