Contrast-induced nephropathy: pharmacology, pathophysiology and prevention

Modern iodinated contrast media (CM) consist of one or two tri-iodobenzene rings. They differ from each other in the composition of the side chains, creating different molecules and thus different brand substances. After intravascular administration, all CM are distributed rapidly into intravascular and extracellular fluids. They are eliminated solely by glomerular filtration. In patients with normal renal function, CMs are eliminated within 24 h. The pathophysiology of contrast-induced nephropathy (CIN) is based on three distinct but interacting mechanisms: medullary ischaemia, formation of reactive oxygen species and direct tubular cell toxicity. The contribution of each of these mechanisms to the development of CIN in the individual patient remains unclear. CIN prevention is extensively described in guidelines, such as the recently updated guideline from the Contrast Media Safety Committee (CMSC) of the European Society of Urogenital Radiology (ESUR). The recent update is briefly discussed. Furthermore, it remains unclear if volume expansion with either NaCl 0.9 % or NaHCO3 1.4 % is superior. Teaching points • After intravascular injection, CM are distributed over intravascular and extracellular fluids. • CM are eliminated by glomerular filtration in patients with normal kidney function. • CIN pathophysiology is based on medullary ischaemia, formation of reactive oxygen species (ROS) and tubular cell toxicity. • It remains unclear if volume expansion with either NaCl 0.9 % or NaHCO 3 1.4 % is superior.