Author`s Reply

To the Editor,

We would like to thank the authors of the letter for their interest and criticism about our study, published in the September issue of The Anatolian Journal of Cardiology 2014; 14: 505-10 (1). They suggested an acute contrast-agent-induced reduction in renal function as an increase in serum creatinine concentration of at least 0.5 mg per deciliter after administration of the contrast agent, instead of a 25% increase in serum creatinine concentration from the baseline value, in patients with relatively well-preserved renal function. This recommendation seems to be sensible at first glance but in fact can actually lead to misinterpretations.

Contrast-induced nephropathy (CIN) is most commonly defined as acute renal failure occurring within 48 hours after exposure to intravascular radiographic contrast material that is not attributable to other causes (2). Ideally, the impairment of renal function should be measured by serial creatinine clearance, but because this step may not be practical or cost-effective in many centers, most of the literature describes the use of isolated measurements of serum creatinine levels, even though this parameter may be less sensitive in reflecting subtle early changes in renal function and may be slower to reach maximal sensitivity than creatinine clearance.

The rate of incidence of contrast-induced nephropathy as a complication of radiographic diagnostic and interventional studies varies markedly, depending on the definition used and on other variables, such as the type of radiology procedure performed, the dose and type of contrast agent administered, the differing patient populations in regard to number and type of risk factors, and the length of patient follow-up. An overall incidence of 14.5% was recently quoted in a large epidemiologic study, which is close to the rate in our study (defined as >25% increase in serum creatinine levels over baseline in the first 5 days), but rates may vary from 0% to 90%, depending on the presence of risk factors, most notably chronic renal insufficiency, diabetes mellitus, and high contrast volume administered (3-5). In our study, approximately 17% of the patients developed CIN as you marked and considered very high in the relatively well-preserved renal function of the study population. Baseline creatinine level is very important, as you indicated, but it is not the only factor that facilitates the development of contrast nephropathy.

Our study population was a heterogeneous group that consisted of patients with different diagnoses; for example, the study population had 74 diabetic patients. The incidence of CIN among patients with diabetes has been reported to be 9%-40% (3). Also, our study population was under the stress of ACS, in contrast to patients who had a diagnostic angiography, and most of our study patients had a coronary intervention, which extends the duration of coronary angiography with the usage of more contrast media compared to diagnostic coronary angiography.

In summary, even apparently small decreases in renal function can lead to excessive mortality rates, independent of other risk factors, given that small rises in serum creatinine levels actually represent a significant decline in GFR. So, in light of this fact, contrast-induced nephropathy has become most commonly defined as “a 25% increase in serum creatinine concentration from the baseline value or an absolute increase of at least 0.5 mg/dL (44.2 µmol/L), which appears within 48 hours after the administration of radiographic contrast media and is maintained for 2-5 days” (5).