Radiographic contrast media (RCM) are excreted mainly by the kidneys following intravascular administration. However, these agents can cause significant reduction in renal function in patients with pre-existing renal impairment. The pathophysiology of contrast media-induced renal impairment involves activation of the tubuloglomerular feedback (TGF) mechanism and the modulation of intrarenal production of vasoactive mediators such as prostaglandins, nitric oxide, endothelin and adenosine. The TGF response is osmolality-dependent and accounts for about 50% of the acute functional effects of high osmolar RCM on the kidney. Reduction in the synthesis of the endogenous vasodilators nitric oxide and prostaglandins increases the nephrotoxicity of RCM. The release of endothelin and adenosine plays a crucial role in mediating the reduction in renal function induced by RCM.

Vacuolisation of the cells of the proximal tubules and necrosis of those of the medullary ascending limbs of loops of Henle are the main structural effects of RCM in the kidney.

Contrast media induced renal impairment could be minimised by the use of low osmolar RCM and adequate hydration. The prophylactic administration of calcium channel blockers and adenosine antagonists such as theophylline may also offer some protective effect.