Myoglobinuria Workup

  • Author: Prasad Devarajan, MD; Chief Editor: Craig B Langman, MD   more...
 
Updated: Jan 4, 2010
 

Laboratory Studies

  • The most important laboratory test is measurement of creatine kinase (CK) levels to assess for rhabdomyolysis.
    • Myoglobin is the first enzyme that increases, but it returns to normal levels within the first 24 hours after the onset of symptoms. This is because myoglobin is rapidly cleared from the serum into the urine. However, serum CK levels may remain elevated after serum and urine test results for myoglobin have become negative. Serum CK levels typically peak about 3 days after the onset of symptoms, and remain elevated for several days. Thus, although the detection of myoglobin in the serum is considered pathognomonic for rhabdomyolysis, the serum CK level is a more useful marker for the diagnosis and assessment of severity because of its delayed clearance from the plasma.
    • A CK level of more than 1000 U/L is characteristically seen in patients with rhabdomyolysis.[4, 9]
    • Levels of other muscle enzymes, such as aldolase, lactate dehydrogenase (LDH), or serum glutamic-oxaloacetic transaminase (SGOT), may also be elevated.
  • Electrolyte abnormalities may cause or result from rhabdomyolysis, including hyperkalemia and hyperphosphatemia from the damaged muscle cells.
    • Hypocalcemia may develop from the hyperphosphatemia or as result of calcium deposition in the damaged muscles.
    • Uric acid values may be elevated, and metabolic acidosis may develop.
  • Acute renal insufficiency (elevated BUN and creatinine levels) is a consequence of severe myoglobinuria in which the globulin precipitates and blocks the urinary tubules.
    • Creatinine levels may be elevated out of proportion to BUN levels due to excessive leak of creatine from damaged muscle cells.
    • Alkalinization of the urine and increased urine flow facilitates myoglobin excretion.
  • Although both myoglobinuria and hemoglobinuria may cause a tea-colored appearance of the urine, and although both cause positive results on the urine dipstick for blood, myoglobinuria may be differentiated from hemoglobinuria by performing a series of simple tests.
    • Myoglobinuria is brown, and often only a few RBCs are present in the urine.
    • Hematuria produces a reddish sediment in spun urine samples.
    • Red or brown urine with a negative dipstick result for blood indicates a dye in the urine.
    • Hemoglobin produces a reddish or brown coloration in the spun serum, whereas myoglobin does not discolor the serum.
    • CK levels are markedly elevated in myoglobinuria.
    • Results of radioimmunoassays for the specific measurement of serum or urine myoglobin can be delayed by several days and are not useful in immediate diagnosis and treatment.
  • Other electrolytic abnormalities associated with rhabdomyolysis result from the extrusion of intracellular contents into the plasma and include hyperkalemia, hypercalcemia or hypocalcemia, hyperphosphatemia, and hyperuricemia.
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Imaging Studies

  • Imaging studies are rarely of use in this metabolic disorder.
  • Intravenous (IV) pyelograms may reveal a dense renogram, but most are normal.
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Other Tests

  • Tests for sickle cell disease (eg, sickle preparations, hemoglobin electrophoresis) may reveal patients who are prone to rhabdomyolysis.
  • A drug and metabolic screen of the urine, blood, or both may indicate illicit drug use.
  • Complements and antinuclear antibodies may help in differentiating autoimmune polymyositis from other conditions.
  • In patients with acute renal insufficiency due to myoglobinuria, fractional excretion of sodium (FENa) is less than 1%, probably because tubular obstruction and damage is the cause of oliguria rather than glomerular damage.
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Procedures

  • Muscle biopsy may be of use when a metabolic myopathy is suspected.
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Contributor Information and Disclosures
Author

Prasad Devarajan, MD  Louise M Williams Endowed Chair in Pediatrics, Professor of Pediatrics and Developmental Biology, Director of Nephrology and Hypertension, Director of Clinical Nephrology Laboratories, Chief Executive Officer of Dialysis Unit, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine

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

Disclosure: Nothing to disclose.

Coauthor(s)

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.

Specialty Editor Board

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

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

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine

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 Academy of Pediatrics, American Association for the Advancement of Science, American Pediatric Society, American Physiological Society, American Society of Nephrology, American Society of Pediatric Nephrology, American Society of Transplantation, Eastern Society for Pediatric Research, Federation of American Societies for Experimental Biology, International Society of Nephrology, National Kidney Foundation, New York Academy of Sciences, Renal Physicians Association, Sigma Xi, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Howard Trachtman, MD  Program Director, Pediatrics Research, Schneider Children's Hospital, Department of Pediatrics, Division of Nephrology, Professor, Albert Einstein College of Medicine

Howard Trachtman, MD is a member of the following medical societies: American Society of Hypertension, American Society of Nephrology, American Society of Pediatric Nephrology, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Chief Editor

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

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

Disclosure: Amgen Grant/research funds None; Altus Pharmaceuticals Grant/research funds None; Genzyme Grant/research funds None; Merck Grant/research funds None; NIH Grant/research funds None

References

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  17. Kilfoyle D, Hutchinson D, Potter H, George P. Recurrent myoglobinuria due to carnitine palmitoyltransferase II deficiency: clinical, biochemical, and genetic features of adult-onset cases. N Z Med J. Feb 25 2005;118(1210):U1320. [Medline].

  18. Lin AC, Lin CM, Wang TL, Leu JG. Rhabdomyolysis in 119 students after repetitive exercise. Br J Sports Med. Jan 2005;39(1):e3. [Medline].

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Model of helical domains in myoglobin.
 
 
 
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