Rhabdomyolysis is clinical syndrome characterized by breakdown of skeletal muscle and the release of muscle intracellular contents into the circulation. It is a type of pigment nephropathy. It was first reported in Germany in 1881. Bywaters and Beall described in detail after the London blitz during the second world war in 1941. They described the first association between crush injury and acute kidney injury (AKI). Details about the global incidence of rhabdomyolysis is limited. There are eight commonly reported causes of rhabdomyolysis. They are trauma, muscle exertion, muscle hypoxia, genetic defects, infections, body temperature changes, metabolic and electrolyte disorders, drugs and toxins and idiopathic causes. The causes of rhabdomyolysis are different depending on the age. The most commonly reported causes in adults are trauma, drugs and infections whereas in children it is trauma, viral infections, drugs and exercise aetiologies. Clinically patients commonly present with triad of symptoms such as myalgia, weakness, and myoglobinuria, classically described as brown-coloured or tea-coloured urine.

Systemic complications of rhabdomyolysis are acute kidney injury, hyperkalemia, hypocalcemia, disseminated intravascular coagulation, compartment syndrome and cardiac arrhythmias and cardiac arrest. Acute kidney injury is the most common systemic complication. AKI incidence in patients with rhabdomyolysis is between 10% to 55% and usually associated with poor outcome in the presence of multiorgan failure. There are three mechanisms postulated to explain rhabdomyolysis causing AKI: 1) intrarenal vasoconstriction, 2) direct and ischemic tubular injury and 3) tubular obstruction. This study evaluates eight patients with AKI associated with rhabdomyolysis and the relation of the latter to causes and outcome after treatment. The aim of the study is to report the varied aetiologies of rhabdomyolysis and to study their presentation, clinical profile and outcome in patients with AKI.

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