Rhabdomyolysis-Induced Kidney Injury is a form of acute kidney injury caused by extensive skeletal muscle breakdown and release of intracellular contents into the bloodstream, particularly myoglobin. This condition is an important and potentially preventable cause of AKI encountered in emergency departments and hospitals across the UAE, especially following trauma, extreme exertion, heat exposure, or drug toxicity.

When muscle cells are damaged, large quantities of myoglobin, potassium, phosphate, and other intracellular substances enter the circulation. Myoglobin is filtered by the kidneys and, under conditions of dehydration or acidic urine, precipitates within the renal tubules. This leads to tubular obstruction, oxidative injury, and direct toxicity to tubular epithelial cells, resulting in impaired filtration and acute renal failure.

Common triggers of rhabdomyolysis include crush injuries, prolonged immobilization, intense physical activity, heat stroke, seizures, severe infections, and certain medications or illicit substances. Patients with dehydration or pre-existing kidney disease are at particularly high risk of developing renal complications.

Clinically, patients may present with muscle pain, swelling, weakness, and dark or tea-colored urine. However, classic symptoms may be absent, and kidney injury may be the first indication of rhabdomyolysis. Laboratory findings include markedly elevated creatine kinase (CK) levels, rising serum creatinine, hyperkalemia, hyperphosphatemia, and metabolic acidosis. These metabolic abnormalities can be life-threatening if not promptly addressed.

Diagnosis is based on clinical suspicion supported by laboratory testing. Early recognition is essential, as kidney injury can develop rapidly and progress to severe AKI. Urinalysis may show myoglobinuria, often without significant red blood cells, and imaging is used selectively to assess complications.

Management centers on early and aggressive intravenous fluid therapy to dilute myoglobin concentration, maintain urine output, and prevent tubular obstruction. Electrolyte abnormalities are closely monitored and corrected. In severe cases, alkalinization of urine may be considered to reduce myoglobin toxicity. Renal replacement therapy may be required if complications such as refractory hyperkalemia, acidosis, or fluid overload occur.

With timely intervention, many patients recover kidney function completely. Delayed treatment significantly increases the risk of permanent renal damage and mortality. Patients who experience rhabdomyolysis-related AKI require follow-up to assess renal recovery and prevent recurrence through risk factor modification.