Correspondence Address:
Maryam Sharifian
Nemazee Hospital Organ Transplantation Unit, Shiraz University of Medical Sciences, Shiraz, Iran

Full Text

To the Editor,

Contrast Induced Nephropathy (CIN) is com­monly defined as acute renal failure occurring within 48 hours of exposure to intravenous radiographic contrast that is not attributable to other causes. [1] It is the third most common cause of hospital-acquired acute renal failure, after surgery and hypotension. [2] In most cases it is preventable with sufficient fluid adminis­tration, however an irreversible damage to the kidney might occur.

Ideally, serial creatinine clearances should be measured, but is neither practical nor cost­effective and therefore literature describes the use of isolated measurements of serum crea­tinine levels, even though less sensitive. Con­trast induced acute renal failure has been variably defined as a minimum increase in serum creatinine level from baseline values of 25%-50% or an absolute increase from 0.5 mg/dL to 1.0 mg/dL. (44 to 88 µmol/L). [3]

The exact underlying mechanisms of CIN remain elusive. Experimental studies suggest combination of renal ischemia and direct tubu­lar epithelial cell toxicity as its pathogenesis. Inhibition of renal prostaglandins and nitric oxide synthesis. [4],[5] and contrast media causing oxidative stress and free radical release as possible mechanisms responsible for CIN. [6]

Apart from general agreement on the value of adequate hydration prior to the contrast injec­tion; conflicting and inconsistent reports exist as to the efficacy and safety of different phar­macologic interventions. In a recent meta­analysis, Kelly et al, reviewed effectiveness of different drugs for preventing CIN and could only show overall beneficial effects of N­acetylcysteine and theophylline [7] . They sugges­ted, N-acetylcysteine to be more reno-protec­tive than hydration alone.

Pentoxifylline (PTX) is a methyl-xanthine derivative with multiple haematologic proper­ties. It is commonly used to treat peripheral vascular diseases. PTX improves oxygen deli­very to ischemic tissues through effects of in­creasing intracellular cyclic-AMP in red blood cells, increasing cyclic-AMP in polymorph nuclear cells and decreasing oxygen free radi­cals production. [8],[9] There has been some evi­dence of PTX having free radical-scavenging properties besides limiting the inflammatory response with a reduction in cellular activa­tion, phagocytosis and endothelium adhesion. There are evidences that PTX also reduces the nitric oxide destruction. [9]

Accordingly it could be hypothesized that PTX may have a protective effect on deve­lopment of CIN.

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