Rhabdomyolysis is a syndrome due to a damage of skeletal muscle and the leakage of intracellular
contents into the extracellular fluid and the circulation. Several causes may induce rhabdomyolysis
and the major one is the crush syndrome. Most cases of non-traumatic rhabdomyolysis are related
to drugs. Many molecules are subject to hepatic metabolism and the concomitant use of drugs, as
statins, with other medications acting as substrates of the same isoenzymes can interact and increase
the risk of myopathy.
Subclinical rise of creatine kinase may be the expression of rhabdomyolysis that can present as a
medical emergency such as acute kidney injury (AKI), compartment syndrome, cardiac dysrhythmias and disseminated
The main pathophysiological mechanisms of myoglobinuric-related AKI are renal vasoconstriction, formation of intraluminal
casts and direct cytotoxicity promoted by heme-protein.
The aim of this review is to analyze the pathophysiology of myolysis, the causes of rhabdomyolysis and especially the
link between the liver and the kidney, which can represent the connecting element for the development of the syndrome.