Rhabdomyolysis: Cola-Coloured Urine After Extreme Exertion or Injury

The myoglobin pathway: muscle to kidney

Skeletal muscle cells contain myoglobin, an oxygen-carrying protein structurally similar to haemoglobin in red blood cells. Myoglobin is normally confined to muscle. When muscle cells break down (rhabdomyolysis literally means muscle dissolution), myoglobin spills into the bloodstream along with potassium, phosphate, uric acid, and creatine kinase. Plasma rapidly becomes saturated, and myoglobin is filtered through the kidneys into urine.

Myoglobin is dark red-brown when concentrated and gives urine a cola, tea, or dark brown appearance. Crucially, myoglobin causes urine dipsticks to read positive for blood (because the dipstick chemistry detects haem groups in both haemoglobin and myoglobin), even though there are no actual red blood cells in urine. This is one of the diagnostic clues: a urine dipstick positive for blood with no red cells on microscopy in someone with a relevant exertion or injury history strongly suggests rhabdomyolysis. The Cleveland Clinic rhabdomyolysis reference describes this diagnostic pathway.

Myoglobin is directly toxic to renal tubular cells, producing acute kidney injury through a combination of tubular obstruction by myoglobin casts, ischaemia from intense renal vasoconstriction, and direct toxicity from haem-iron. The result is acute tubular necrosis. The kidneys can recover fully if appropriate IV fluid resuscitation is started promptly, but delayed treatment carries higher rates of dialysis-requiring AKI.

Common triggers

Exertional rhabdomyolysis follows extreme physical activity, particularly in untrained or unaccustomed individuals. The leading patterns are:

• -Marathons and ultra-endurance events, particularly in hot conditions
• -Novel high-intensity workouts (CrossFit, spin classes, hot yoga in untrained beginners)
• -Heavy eccentric exercise (downhill running, novel weight training)
• -Military basic training, especially in heat
• -Sustained fast running of long distances

Non-exertional rhabdomyolysis includes:

• -Crush injury (road traffic accidents, building collapse, prolonged compression)
• -Prolonged immobilisation after a fall, especially in older adults
• -Seizures (prolonged or recurrent)
• -Electrical injury, burns, hyperthermia, malignant hyperthermia
• -Heavy alcohol or recreational drug use (cocaine, amphetamines, MDMA)
• -Certain medications (statins at high dose, certain antibiotics in combination)
• -Inherited muscle metabolism disorders (McArdle disease, others)
• -Severe infection or sepsis

The StatPearls rhabdomyolysis chapter on NCBI covers the comprehensive trigger list and the underlying mechanisms.

The classic triad and the diagnostic workup

The classic clinical triad of rhabdomyolysis is muscle pain, muscle weakness, and dark urine, although the full triad is present in only a minority of cases. Muscle pain is often disproportionate to the activity and may involve the muscles that did the work (thighs after running, shoulders after weight training). Muscle weakness can be subtle or marked. Dark urine is the cardinal sign and is what brings many patients to attention.

The diagnostic blood test is creatine kinase (CK), an enzyme that leaks from damaged muscle. Normal CK is below about 200 U/L. Rhabdomyolysis is typically defined as a CK above 1,000 U/L; the level can rise into tens of thousands or even hundreds of thousands in severe cases. Other relevant blood tests include kidney function (urea, creatinine, eGFR), electrolytes (especially potassium, which can rise dangerously), phosphate, calcium, and uric acid. Urine dipstick positive for blood with no red cells on microscopy is the urine clue.

Severity assessment combines the CK level, the trend over time, kidney function, potassium, and the underlying trigger. Severe rhabdomyolysis with established AKI, hyperkalaemia, or compartment syndrome may need intensive care management.

Treatment in hospital

The mainstay of rhabdomyolysis treatment is aggressive IV fluid resuscitation, typically starting with 1-2 litres per hour of normal saline in the first few hours, then titrated to maintain a high urine output (often targeting 200-300 ml per hour). The aim is to flush myoglobin through the kidneys before it can produce sustained tubular damage. Some centres add bicarbonate to alkalinise urine, although the evidence base for this is debated.

Hyperkalaemia (high potassium) is the immediate life-threat and is treated with insulin-dextrose, salbutamol nebulisers, calcium gluconate (cardiac membrane stabilisation), and dialysis if severe. Compartment syndrome (severely swollen muscles producing dangerous pressure on nerves and vessels) may need fasciotomy. Established AKI is managed with renal replacement therapy where needed; most cases recover kidney function over days to weeks with appropriate management.

Statin-associated muscle symptoms and rhabdomyolysis

Statins are widely prescribed for cardiovascular risk reduction. Mild muscle symptoms (aches, mild weakness) are common and usually do not represent rhabdomyolysis. Severe statin-induced rhabdomyolysis is rare. The NHS statins guidance and the BNF lipid-regulating drugs reference describe the muscle adverse effect spectrum.

Risk is higher with high doses, certain drug combinations (statin plus fibrate, statin plus certain macrolide antibiotics), in the elderly, in people with hypothyroidism, in those with kidney impairment, and in some inherited variants of the metabolising enzymes. New severe muscle pain on a statin should prompt a CK check; significant elevation warrants stopping the statin and discussion with the prescribing clinician.

Frequently asked questions