دالات كيموحيويـة اخرى كعوامـل خطـورة لاصابــات الكلــيتين نتيجــة التعرض لمواد التصوير الضليلي

Interleukin-18 and Tumor Necrosis Factor Gene Polymorphisms and other Biochemical Markers as Risk Factors for Contrast Induced Nephropathy

Contrast-induced nephropathy is a significant complication of angiographic procedures caused by contrast media injection, and considered as third most frequent cause of hospital-acquired acute renal failure which represents about 12% of the cases. Contrast-induced nephropathy is defined as an increase in serum creatinine of 0.5 mg/dL (44 µmol/L), or a relative 25 % increase from the baseline value, within a period of 24 hours following intravascular administration of contrast media. Despite being a widespread disease, the pathophysiology of contrast-induced nephropathy is still incompletely understood and developed at a rate of about 14.5%. In-hospital mortality for patients with contrast-induced nephropathy was 7.1% in those who did not require dialysis and 35.7% in those who did, compared to 1.1% for patients with no contrast-induced nephropathy.
The aim of the present study is to investigate the impacts of contrast media following therapeutic coronary angiography on interleukins-18 and tumor necrosis factor alpha serum levels. To investigate the role of both genotypes (rs1946518) interleukin-18 and (rs361525) tumor necrosis factor alpha gene polymorphisms as susceptible markers after percutaneous coronary intervention.
The study was conducted in cardiac catheterization unit at Karbala Center of Cardiology, and Al-Kafeel super specialty hospital, Karbala health directorates, Kerbala, Iraq. The study included 60 patients (47 males, 13 females) who underwent elective or emergency coronary angiography. Clinical examination and laboratory investigations were done before and 24 hours after interventions. These investigations include: serum creatinine, blood urea, estimated glomerular filtration rate, serum tumor necrosis factor alpha and serum interleukin-18. Molecular analysis: interluekine-18 tag SNPs (rs1946518) and tumor necrosis factor alpha tag SNPs (rs361525) were analyzed by Allele-specific PCR. Patients with incomplete data, those who underwent diagnostic coronary angiography only, and those who have other causes of acute kidney injury were excluded from this study.

The contrast agent has a risk to induce acute kidney injury represented by a significant rises in serum creatinine and blood urea (p ˂0.001) 24 hours after coronary angiography. Past history of type 2 diabetes mellitus, and ischemic cardiac failure had a statistically significant adverse effect on the prevalence of contrast induced acute kidney injury (p=0.001, 0.003 and 0.008) respectively. There were a significant rising of interleukin-18 serum level after contrast media exposure (p = 0.001), while no significant deference was found in tumor necrosis factor alpha. When compared to (no contrast-induced nephropathy) controls, the (+ contrast-induced nephropathy) patients showed increased frequencies of CA+ AA (rs1946518) genotypes in interleukin-18 (OR =0.8 (1.020-622.737), p = 0.048; OR = 1.029 (1.026-1.029), p = <0.001, respectively). Significant different rates of serum creatinine and estimated glomerular filtration rate after percutaneous coronary intervention in (rs1946518) genotypes interleukin-18 (p = 0.014, 0.024, respectively).
In conclusion, there was an elevation of interleukine-18 after therapeutic coronary interventions as a key factor behind contrast agent induced acute kidney injury. Gene polymorphisms of (rs1946518) interleukin-18 is associated with contrast-induced nephropathy risk and renal outcome after percutaneous coronary intervention.