The pathophysiology of CIN is not clearly understood; however, several attempts have been made to explain the underlying mechanism.  It is generally agreed that CIN is due to a combination of several influences brought on by contrast-media infusion rather than a single process.  The most important mechanism thought to be involved in CIN is a reduction in renal perfusion and subsequent hypoxia.  This has been attributed to several alterations in the renal microenvironment including activation of the tubuloglomerular feeback, local vasoactive metabolites including adenosine, prostaglandin, NO, and endothelin as well as increased interstitial pressure.  Although sometimes considered controversial, studies have also proposed injury to renal tubular cells as another contributor both via a direct cytotoxic effect and via reactive oxygen species production.
Contrast induced nephropathy pathophysiology
Renal papillary necrosis pathophysiology
Acute tubular necrosis pathophysiology
Analgesic nephropathy pathophysiology
Contrast induced nephropathy risk factors
Interstitial nephritis pathophysiology
Renal artery stenosis pathophysiology
Membranous glomerulonephritis pathophysiology