Systemic immune inflammation index: is it a new marker for contrast-induced nephropathy?

Abstract

Introduction: Worldwide, >200 million patients are affected by peripheral arterial disease (PAD) and endovascular interventional treatments are increasingly being applied. Contrast-induced nephropathy (CIN) is the third most common cause of renal failure in hospitals. However, factors such as renal vasoconstriction, decrease in renal blood flow, endothelial dysfunction, and oxidative stress have been suggested in the etiology of CIN. Studies are showing that inflammatory markers increase in CIN. Systemic immune inflammation index (SII), a newly defined parameter, is calculated by multiplying the platelet and lymphocyte counts and dividing by the neutrophil count. Studies are showing that this parameter influences prognosis in various cancer types. Considering that inflammation may play a role in CIN, we planned this study to investigate the role of SII in patients undergoing percutaneous peripheral vascular interventions. Material and Method: 300 patients who underwent percutaneous peripheral vascular interventions between August 2018-December 2021 due to peripheral arterial disease were included in the study. The data of the patients were scanned retrospectively from the patient files. The neutrophil-lymphocyte ratio (NLR) was calculated by dividing the neutrophil count by the lymphocyte count. SII was found by multiplying NLR with platelet count Results: Contrast-induced nephropathy developed in 41 (12.3%) patients. CIN(+) patients also, had higher CRP levels (5.1±0.7vs 2.4±0.4,P<0.05), NLR (4.07±1.07vs 2.65±0.84, P<.005), SII score (1778±627.57vs 867.14±491.88, P<.005.) the contrast media used was also higher in CIN(+) patients (176.19±48.44 vs 128.72±48.44;P<0.05) Multivariate logistic regression analysis demonstrated that a high SII score was an independent predictor of development of CIN (odds ratio [OR]: 1.002, 95% confidence interval [CI]: 1.001-1.002, P<.0005) together with high NLR (OR: 3.56, 95% CI: 1.905-6.675, P<.005) and CRP (OR: 1.002, 95% CI: 1.001-1.002, P<.005 Receiver operating characteristic curve analysis demonstrated that the best cutoff value of 1224 for SII to predict the development of CIN with 85% sensitivity and 72% specificity (area under ROC curve 0.904 [95% CI: 0.866-0.942], P<.005). Conclusion: Imbalance in inflammatory cells, the increase in neutrophils, and the decrease in lymphocytes play a role in developing kidney damage. Impaired immune functions due to lymphocytopenia contribute to the development of acute kidney injury. Oxidative stress exacerbates the inflammatory state by increasing inflammatory cell infiltration. AS a result, SII may be a powerful predictor of inflammation and can be used to determine the risk before interventional procedures.

Keywords

• contrast-induced nephropathy
• inflammation
• peripheral vascular interventions
• systemic immune inflammation index

References

1. Song P, Rudan D, Zhu Y, et al. Global, regional, and national prevalence and risk factors for peripheral artery disease in 2015: an updated systematic review and analysis. Lancet Glob Health 2019; 7: 1020–30.
2. Pucelikova T, Dangas G, Mehran R. Contrast-induced nephropathy. Catheter Cardiovasc Interv 2008; 71: 62-72.
3. Morcos R, Kucharik M, Bansal P, et al. Contrast-induced acute kidney injury: review and practical update. Clin Med Insights Cardiol 2019; 13: 1179546819878680.
4. James MT, Samuel SM, Manning MA, et al. Contrast-induce acute kidney injury and risk of adverse clinical outcomes after coronary angiography: a systematic review and meta-analysis. Circ Cardiovasc Interv 2013; 6: 37-43.
5. Caiazza A, Russo L, Sabbatini M, Russo D. Hemodynamic and tubular changes induced by contrast media. Biomed Res Int 2014; 2014: 578974.
6. Goldenberg I, Matetzky S. Nephropathy induced by contrast media: pathogenesis, risk factors and preventive strategies. CMAJ 2005; 172: 1461-71.
7. Kurtul A, Yarlioglues M, Duran M, Murat SN. Association of neutrophil-to lymphocyte ratio with contrast-induced nephropathy in patients with non-st-elevation acute coronary syndrome treated with percutaneous coronary intervention. Heart Lung Circ 2016; 25: 683-90.
8. Kaya A, Kaya Y, Topcu S, et al. Neutrophil-to-lymphocyte ratio predicts contrast-induced nephropathy in patients undergoing primary percutaneous coronary intervention. Angiology 2014; 65: 51-6.

9. Liu Y, Tan N, Zhou YL, et al. High-sensitivity C-reactive protein predicts contrast-induced nephropathy after primary percutaneous coronary intervention. J Nephrol 2012; 25: 332-40.
10. Kocas C, Yildiz A, Abaci O, et al. Platelet- to-lymphocyte ratio predicts contrast-induced nephropathy in patients with non-st segment elevation acute coronary syndrome. Angiology 2015; 66: 964-8.
11. .Ji Y, Wang H. Prognostic prediction of systemic immune inflammation index for patients with gynecological and breast cancers: a meta-analysis. World J Surg Oncol 2020; 18: 197.
12. Huang Y, Gao Y, Wu Y, Lin H. Prognostic value of systemic immune-inflammation index in patients with urologic cancers: a meta-analysis. Cancer Cell Int 2020; 12: 499
13. Zhang Y, Lin S, Yang X, Wang R, Luo L. Prognostic value of pretreatment systemic immune-inflammation index in patients with gastrointestinal cancers. J Cell Physiol 2019; 234: 5555-6
14. Kelesoglu S, Yilmaz Y, Elcık D, et al. Systemic immune inflammation index: a novel predictor of contrast-induced nephropathy in patients with non-st segment elevation myocardial infarction. Angiology 2021 Oct; 72: 889-95.
15. Mehran R, Aymong ED, Nikolsky E, et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention: development and initial validation. J Am Coll Cardiol 2004; 44: 1393-9.
16. Tsai TT, Patel UD, Chang TI, et al. Contemporary incidence, predictors, and outcomes of acute kidney injury in patients undergoing percutaneous coronary interventions: insights from the NCDR Cath-PCI registry. JACC Cardiovasc Interv 2014; 7: 1-9.
17. Davidson CJ, Hlatky M, Morris KG, et al. Cardiovascular and renal toxicity of a nonionic radiographic contrast agent after cardiac catheterization. A prospective trial. AnnIntern Med 1989; 110: 119-24
18. Eng J, Wilson RF, Subramaniam RM, et al. Comparative effect of contrast media type on the incidence of contrastinduced nephropathy: a systematic review and meta-analysis. Ann Intern Med 2016; 164: 417–24.
19. Wong PC, Li Z, Guo J, Zhang A. Pathophysiology of contrast-induced nephropathy. Int J Cardiol 2012; 158: 186– 92.
20. Brandes RP, Fleming I, Busse R. Endothelial aging. Cardiovasc Res 2005; 66: 286 94.
21. Jurado-Román A, Hernández-Hernández F, García-Tejada J, et al. Role of hydration in contrast-induced nephropathy in patients who underwent primary percutaneous coronary intervention. Am J Cardiol 2015; 115: 1174-8.
22. Morcos SK, Thomsen HS, Webb JA. Contrast-media-induced nephrotoxicity: A consensus report. Contrast media safety committee, European Society of Urogenital Radiology (ESUR). Eur Radiol 1999; 9: 1602-13.
23. Hoshi T, Sato A, Kakefuda Y, et al. Preventive effect of statin pretreatment on contrast-induced acute kidney injury in patients undergoing coronary angioplasty: propensity score analysis from a multicenter registry. Int J Cardiol 2014; 171: 243-9.
24. Kwasa EA, Vinayak S, Armstrong R. The role of inflammation in contrast-induced nephropathy. Br J Radiol 2014; 87; 20130738.
25. Lau A, Chung H, Komada T, et al. Renal immune surveillance and dipeptidase-1 contribute to contrast-induced acute kidney injury. J Clin Invest 2018; 128: 2894–913.
26. Lu Z, Cheng D, Yin Y, et al. Antithrombin iii protects against contrast-induced nephropathy, E Bio Medicine 2017; 17: 101–7.
27. Wang F, Yin J, Lu Z, et al. Limb ischemic preconditioning protects against contrast-induced nephropathy via renalase.E Bio Medicine 2016; 9: 356–65.
28. Sun SC. The non-canonical nf-κb pathway in immunity and inflammation, Nat Rev Immunol 2017; 17: 545–58.
29. Zhang Q, Lenardo MJ, Baltimore D. 30 years of nf-κb: a blossoming of relevance to human pathobiology. Cell 2017; 168: 37–57.
30. Machado RA, Constantino Lde S, Tomasi CD, et al. Sodium butyrate decreases the activation of nf-κb reducing inflammation and oxidative damage in the kidney of rats subjected to contrast-induced nephropathy. Nephrol Dial Transplant 2012; 27: 3136–40.
31. Furuichi K, Wada T, Iwata Y, et al. Interleukin-1- dependent sequential chemokine expression and inflammatory cell infiltration in ischemia-reperfusion injury. Crit Care Med 2006; 34: 2447–55.
32. Huang J, Zhang Q, Wang R, et al. Systemic immune-inflammatory index predicts clinical outcomes for elderly patients with acutemyocardial infarction receiving percutaneous coronary intervention. Med Sci Monit 2019; 25: 9690-701.
33. Yang YL, Wu CH, Hsu PF, et al. Systemic immune-inflammation index (SII) predicted clinical outcome in patients with coronary artery disease. Eur J Clin Invest 2020; 50: e13230.
34. Li B, Li W, Li X, Zhou H. Inflammation: A novel therapeutic target/direction in atherosclerosis. Curr Pharm Des 2017; 23: 1216-27.
35. Seo M, Yamada T, Morita T, et al. Prognostic value of systemic immune-inflammation index in patients with chronic heart failure. Eur Heart J 2018; 39: ehy564.P589.
36. Xu J, Hu S, Li S, et al. Systemic immuneinflammation index predicts postoperative acute kidney injury in hepatocellular carcinoma patients after hepatectomy. Medicine 2021; 100: e25335.
37. Bagci A, Aksoy F, Ba¸s HA. Systemic immune-inflammation index may predict the development of contrast-induced nephropathy in patients with ST-segment elevation myocardial infarction. Angiology 2022; 73: 218– 24.
38. Gok M, Kurtul A. A novel marker for predicting severity of acute pulmonary embolism: systemic immune-inflammation index. Scand Cardiovasc J 2021; 55: 91-6.