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Patients may complain of muscle pain, weakness, and dark urine. Serum creatine kinase levels are elevated.


  1. Direct trauma to the myocyte, or depletion of ATP within the cell, leads to increased intracellular calcium causing persistent contraction and eventual myocyte disintegration.

  2. Leakage of muscle cell contents (electrolytes, myoglobin, creatine kinase, other proteins) then occurs.

  3. Causes of rhabdomyolysis include

    1. Trauma (crush injury)

    2. Exertion (strenuous exercise, seizures, alcohol withdrawal syndrome)

    3. Muscle hypoxia (limb compression during prolonged immobilization, major artery occlusion)

    4. Infections (influenza, coxsackievirus, Epstein-Barr virus, HIV, Legionella, Streptococcus pyogenes, Staphylococcus aureus, Clostridium, tick-borne infections)

    5. Metabolic (hypokalemia, hypophosphatemia, hypocalcemia, diabetic ketoacidosis, nonketotic hyperosmotic conditions)

    6. Drugs/toxins (fibrates, statins, alcohol, heroin, cocaine)

    7. Body temperature changes (heat stroke, malignant hyperthermia, malignant neuroleptic syndrome, hypothermia)

    8. Genetic defects

    9. Idiopathic

  4. AKI is the most serious complication of rhabdomyolysis.

    1. Rhabdomyolysis causes 7–10% of cases of AKI in the United States.

    2. Incidence of AKI is 13–50% and is higher in patients who use illicit drugs or alcohol, or who have multiple causes of rhabdomyolysis.

    3. Survival in patients with rhabdomyolysis and AKI is about 80%, with most patients recovering kidney function.

    4. AKI occurs due to myoglobin-induced proximal tubule cytotoxicity, distal tubular obstruction from precipitation of myoglobin, and intrarenal vasoconstriction due to intravascular volume depletion and activation of renal vascular mediators.


  1. Weak correlation between peak creatine kinase and development of AKI

    1. Risk of AKI is low when the admission creatine kinase is < 15,000–20,000 units/L.

    2. AKI may occur with creatine kinase levels as low as 5000 units/L when coexisting conditions, such as sepsis, dehydration, or acidosis, are present.

  2. Urine findings include

    1. Pigmented granular casts

    2. A reddish-brown supernatant

    3. Dipstick testing positive for blood with no RBCs in the sedi­ment (sensitivity of 80% for the detection of rhabdomyolysis)

  3. BUN/creatinine ratio is often low.

  4. Oliguria is frequent, with occasional anuria.

  5. The FENa is < 1% due to the contribution of vasoconstriction to the AKI.

  6. Common electrolyte abnormalities include hyperkalemia, hyperphosphatemia, hyperuricemia, high anion gap metabolic acidosis, hypermagnesemia, and hypocalcemia.


  1. Aggressive fluid repletion is essential; some patients require up to 10 L/day.

  2. Comparative studies show that early and high-volume hydration is better than delayed hydration; there is no difference in outcomes regardless of which type of fluid is used (normal saline, lactated Ringer, sodium bicarbonate), and adding mannitol is not beneficial.

  3. However, massive infusions of normal saline can cause metabolic acidosis, so experts recommend alternating 1 L of 0.45 normal saline + bicarbonate with each liter of normal saline if the urine pH is < 6.5.

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