Which Comes First in Contrast-Induced Nephropathy? Inflammation or Thrombus Formation?

Abstract

We read with interest the study entitled “Can Thrombus Burden Predict Contrast Induced Nephropathy in Patients with ST-Segment Elevation Myocardial Infarction?”. Contrast-induced nephropathy (CIN) is an important complication of cardiovascular interventions with an incidence of approximately 0.6% to 20% after procedures. Direct cytotoxicity to renal tubular cells, increased oxidative stress, increased blood, and renal tubular viscosity are some of the proposed causes of CIN. The study reported a relationship between thrombus burden and CIN. The authors state that a large thrombus burden can result in a high level of reactive oxygen radicals and lipid peroxidation, and this is the main reason for the association between thrombus burden and CIN. We partially agree but we would like to express our opinion about these results. Firstly, myocardial infarction is a complex acute event resulting in the activation of both the thrombotic and the inflammatory pathways. Initially, plaque rupture can occur with activation of the inflammatory pathway. Then, platelet activation, cytokines, and reactive oxygen radicals are triggered. This process adversely affects myocyte viability. In this context, the question is “Which comes first? Inflammation or thrombus formation?”. We think that there is an association between thrombus burden and CIN. But the reason is not that high thrombus burden results with cytokine activation. It is because some patients (eg, those with diabetes mellitus or active inflammation as well as the aged) have an excessive cytokine response. In these patients, acute myocardial infarction results in a high thrombus burden and increased risk of CIN. We think that the relationship between thrombus burden and CIN also involves inflammatory pathway activation.