Contrast-induced nephropathy (CIN) primarily results from direct tubular epithelial cell toxicity caused by contrast agents, leading to cellular injury. Additionally, renal vasoconstriction reduces renal blood flow, causing medullary ischemia and exacerbating tubular damage. These combined effects disturb renal function, manifesting as an acute decline in glomerular filtration rate. Immune-mediated or obstructive mechanisms are not the primary causes in CIN. Understanding this pathophysiology is crucial for prevention and management strategies.

Reference: Harrison's Principles of Internal Medicine, Kasper et al., 20th Edition.