Systemic Immune-Inflammation Index Is a Predictor of Contrast-Induced Nephropathy in Patients With ST-Segment Elevation Myocardial Infarction

Abstract

We evaluated the predictive value of admission systemic immune-inflammation index (SII) for the risk of contrast-induced nephropathy (CIN) in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). The neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and SII (platelet × NLR) levels were calculated in 1621 consecutive patients with STEMI. The relationship of these parameters with CIN development within 72 hours of pPCI was analyzed. Of the study population, 343 (21.1%) cases developed CIN. The frequency of CIN was 11.1% in the first SII quartile, 11.6% in the second SII quartile, 26.8% in the third SII quartile, and 35% in the fourth SII quartile, which differed significantly between groups ( P < .01). Age, baseline glomerular filtration rate, contrast media volume, hypertension, C-reactive protein levels, and the quartiles of SII were independent predictors of CIN. Patients in the third SII quartile versus first SII quartile (OR: 2.906, 95% CI, 1.903-4.437; P < .001), and fourth SII quartile versus first SII quartile (OR: 4.168, 95% CI, 2.754-6.313; P < .001) had a significantly higher risk for CIN in the multivariable model. The SII may be a promising inflammatory parameter to predict CIN after pPCI.

The Utility of Systemic Immune-Inflammation Index for Predicting Contrast-Induced Nephropathy in Patients with ST-Segment Elevation Myocardial Infarction Undergoing Primary Percutaneous Coronary Intervention

“…They reported that the patients with CIN had increased hsCRP, glucose, total cholesterol, NLR, and SII levels compared with the patients without CIN and SII was an independent predictor of CIN [51]. Recently, Ozturk et al [25] have concluded that SII was markedly elevated in patients with STEMI undergoing primary PCI and independently predicted CIN. Also, CRP, eGFR, and baseline creatinine were associated with CIN in their study [25].…”

“…Recently, Ozturk et al [25] have concluded that SII was markedly elevated in patients with STEMI undergoing primary PCI and independently predicted CIN. Also, CRP, eGFR, and baseline creatinine were associated with CIN in their study [25]. In addition, Bagcı et al [52] conducted a novel study to assess the relationship between SII and development of CIN in patients with STEMI who underwent primary PCI.…”

“…The relationship between SII and cardiovascular diseases such as coronary artery disease (CAD), HF, pulmonary embolism, acute myocardial infarction, and calcific aortic stenosis has been demonstrated subsequently [19][20][21][22][23]. Recently, SII has been shown to be a predictive indicator of CIN in patients with different ACS manifestations undergoing PCI [24,25]. Our study sought to evaluate the utility of SII to predict CIN in patients with ST-segment elevation myocardial infarction (STEMI) who underwent primary PCI.…”

Systemic Immune-Inflammation Index as a Predictor of Microvascular Dysfunction in Patients With Cardiac Syndrome X

“…31,32 The prognostic value of SII in many clinical conditions such as cancer, contrastinduced nephropathy, pulmonary embolism, and coronary artery disease has been demonstrated. 14,[33][34][35] Esenboga et al determined the relationship between no-reflow and SII in patients who underwent primary percutaneous coronary intervention (PCI) due to ST-elevation myocardial infarction (STEMI). 36 Yang et al showed an association between increased SII values and poor CV outcomes after PCI in coronary artery disease.…”

C-Reactive Protein/Albumin Ratio as a Novel Predictor of Contrast Induced Nephropathy in Patients With Stable Angina Pectoris

“…7,9,17 In addition to CRP, cystatin-C, procalcitonin, NLR, PLR, MPVLR, and systemic immune-inflammation index may be independent predictors of CIN. 7,10,[18][19][20] A recent study, which investigated the relationship between plasma endothelial microparticles and CIN in patients who underwent CAG, demonstrated that cystatin-C, high-sensitivity CRP, and uric acid were significantly higher in patients with CIN than ones without CIN. 8 The researchers found that elevated microparticles in CIN patients correlated with interleukin-6 and high-sensitivity CRP, and reported that high cystatin-C, uric acid, and N-terminal pro-brain natriuretic peptide were the predictors of CIN rather than high-sensitivity CRP.…”