Contrast-induced nephropathy; an update on pathophysiology

Abstract

Contrast-induced nephropathy (CIN) is a well-known complication of contrast media administration for diagnostic and therapeutic purposes. The incidence of CIN has increased with the widespread use of diagnostic imaging and contrast media. CIN is a pathological condition that typically occurs within 48 hours of exposure to contrast material and results in an increase in serum creatinine levels of more than 44 µmol/L (0.5 mg/dL) or 25% above baseline or an increase in serum creatinine of more than 1.5 times the baseline level within 7 days of exposure to contrast material or a reduction in urine output to less than 0.5 mL/h for at least 6 hours after exposure to contrast material. The mechanism of CIN is not fully understood, but it is thought to involve direct nephrotoxic effects of contrast particles, hemodynamic changes, hypoxia and oxidative stress, apoptosis, inflammation, and immune responses. Prevention of CIN involves identifying the risk factors and taking appropriate measures to mitigate them. Currently, there is no definitive treatment for CIN, and treatment is mainly symptomatic, with supportive care being the mainstay. Experimental treatments such as renal replacement therapy, extracorporeal blood purification, and stem cell therapy are being investigated, but their clinical efficacy is yet to be established.

Keywords: Contrast-induced nephropathy, Glomerular filtration rate, Acute tubular necrosis, Iodine-containing contrast media, Reactive oxygen species, Apoptosis, Oxidative stress, Serum creatinine