The clinical crush syndrome occurs as a consequence of traumatic events, either accidents or disasters. In contrast to accidents, which affect only a limited number of individuals, disasters affect large numbers of victims simultaneously, thus provoking veritable crush syndrome epidemics, which often require supraregional assistance. As a result of muscular compression, myocytes are damaged, and this is followed by the release of intracellular constituents into the systemic circulation. This process is called rhabdomyolysis. One of the key compounds released is myoglobin, a 18 800 Da oxygen carrier similar to haemoglobin. In contrast to haemoglobin, however, it contains only one haeme moiety. Myoglobin is filtered by the glomeruli and reaches the tubules, where it provokes obstruction and failure of renal function [1]. Other intracellular components such as protons, phosphate, potassium, and nucleotides, i.e. precursors of uric acid, are released from the damaged muscles as well, and play an important role in crush‐associated pathophysiology. Finally, volume depletion of the victim is an important determinant of renal injury