Together with other factors, such as rhabdomyolysis-associated activation of the renin angiotensin aldosterone system (RAAS), volume depletion, and release of vascular mediators [for instance, endothelin-1 (ET-1) and TNF-α], this cascade of events promotes pathological remodeling on both endothelial and epithelial cells and leads to AKI.4 Here, TNF is linked to rhabdomyolysis.