Myoglobinuria

Myoglobinuria is the presence of myoglobin in urine, typically resulting from skeletal muscle injury or breakdown (rhabdomyolysis). It can follow traumatic injury, prolonged immobilization, strenuous or unaccustomed exercise, seizures, heat illness, or exposure to toxins and certain drugs, including some statins, cocaine, alcohol, and certain metabolic disorders. Clinically, it often presents with dark, tea- or reddish-brown urine and may be accompanied by muscle pain, weakness, swelling, and, in severe cases, signs of acute kidney injury.

Pathophysiology involves the release of myoglobin from damaged muscle into the bloodstream, followed by filtration by the kidneys. In large amounts, myoglobin can cause tubular obstruction and oxidative injury, contributing to nephrotoxicity. Electrolyte disturbances such as hyperkalemia and hypocalcemia may accompany rhabdomyolysis.

Diagnosis relies on a combination of history, examination, and laboratory tests. Urinalysis may show a positive dipstick for blood, but microscopic examination often reveals few or no red blood cells, indicating myoglobin or hemoglobin as the pigment source. Serum creatine kinase is typically markedly elevated, reflecting muscle breakdown. Renal function and electrolytes should be monitored; urine myoglobin testing is not routinely necessary but may be used if available.

Management centers on rapid restoration of intravascular volume with isotonic fluids to maintain urine output, avoidance of nephrotoxins, and correction of electrolyte abnormalities. In severe cases or persistent renal dysfunction, dialysis may be required. Urine alkalinization is used in some settings but has limited supporting evidence.

Prognosis depends on the extent of muscle injury and promptness of treatment; many patients recover renal function, but delayed treatment increases the risk of acute kidney injury and other complications. Prevention focuses on adequate hydration and gradual return to activity, particularly after intense exertion.