Relationship between monocyte to high-density lipoprotein ratio and contrast-induced nephropathy in patients with non-st elevation myocardial infarction

Amac: Kontrast madde kullanimina bagli nefropati (KBN) gelisimi perkutan koroner girisim (PKG) yapilan ST elevasyonu olmayan miyokard enfarktusu (NON-STEMI) geciren hastalarda sik gorulmekte olup artmis mortalite ve morbidite ile ilisklidir. KBN acisindan yuksek riskli hastalarin onceden tespiti ve tedavisi, klinik sonuclarin iyilesmesinde etkili olacaktir. Monosit yuksek dansiteli lipoprotein (HDL) orani ( MHO) klinikte yeni tanimlanan inflamasyon belirteclerinden biridir. Calisamizda islem oncesi MHO’ nin PKG yapilmis NON-STMI hastalarinda KBN gelisimi arasidaki iliski arastirilmistir. Gerec ve Yontemler: Calismamizda retrospektif olarak NON-STEMI tanisiyla PKG yapilan hastalar incelenmistir. Hastaneye basvurusunda alinan orneklerden MHO oranin hesaplanmis ve KBN; islemden 48-72 saat sonra bakilan serum kreatininde bazal degere gore % 25 ya da 0,5 mg/dl artis olarak tanimlanmistir. Bulgular: Toplam 370 (200, %54.1 erkek ) hasta geriye donuk incelenmis, 25 (%6.7) hastada KBN gelistigi saptanmistir. Ayrica hastalarin 104’unde (%28.1) Diabetes Mellitus (DM) oldugu gorulmistur. MHO; KBN gelilsen grupta gelismeyen gruba gore anlamli olarak yuksek saptandi (sirasiyla 0.014± 0.004 ve 0.011± 0.006, p: 0.017). Ek olarak MHO ile PKG sonrasi kreatinin degerleri arasinda pozitif korelasyon saptandi (r:0,104, p: 0.047). Beklendigi gibi KBN gelisen hastlarin yatislari sirasinda daha cok komplikasyon oldugu goruldu. Ayrica; kilo ve MHO degerleri KBN gelisimi icin bagimsiz risk faktorleri olarak bulundu. Sonuc: MHO ucuz, basit ve kolay sekilde saptanabilen inflamasyon belirteci olup, PKG yapilan NON-STEMI hastlarinda KBN’nin saptanmasinda ve tedavinin yonlendirilmesinde faydali olabilir.


Introduction
Contrast-induced nephropathy(CIN), is afrequent complication of contrast use, after coronary procedures such as percutaneous coronary interventions (PCI) in patients with acute coronary syndromes (ACS) including non-ST elevation myocardial infarction (NSTEMI) and strongly associated with high mortality and morbidity (1)(2)(3)(4)(5)(6).The aetiology of CIN is not clearly clarified.Although many risk factors for the development of CIN have been demonstrated such as chronic kidney disease (CKD), diabetes mellitus (DM), reduced left ventricular systolic function, nephrotoxic drugs and age over 70 years (6)(7)(8), the main pathophysiology of CIN is still underinvestigation.
Recently studies have shown that The platelet to-lymphocyte ratio (PLR), elevated preprocedural high sensitive-C-reactive protein (Hs-Crp), and the neutrophil-to-lymphocyte ratio (NLR) have been shown to be associated with increased risk of CIN levels were associated with CIN in patients with ACS (11)(12)(13).
Monocyte to high density lipoprotein cholesterol (HDL-C) ratio (MHR)has been entered a new inflammatory marker and several studies have shown that there is strongcorrelation between MHR various adverse cardiovascular events (14)(15)(16).
Although the relationship between the risk of developing CIN and MHR was demonstratedin small sized patients with STsegment elevation myocardial infarction(STEMI) (17), whether there is a relationship between MHR and CIN in the patient with NSTEMIis still unclear. Thus, the aim of this study was to assess whether there is a relationship MHR and CIN after urgent PCI in patients with NSTEMI.

Results
A total of 370(200, 54.1% men) patients were included in this studyand 104 (28.1%) of them had DM. 25 (6.7%) of patients had CIN. There was not significant difference between the patients with and without CIN in terms of weight, age and gender.General risk factors that DM, smoking and hypertension were same in both groups. Additionally; previous medications, Grace scores, HbA1c, peak troponin levels, left ventricular ejection fraction(LVEF), contrast volume, numbers of PCI and CABG rates were not differed between two groups. The baseline clinical and procedural characteristics of patients were shown in Table I and II. MHR, PLR, NLR and high sensitive C reactive protein (Hs-Crp) were significantly higher in patients with CIN ( Table II) (Figure 1 and 2). MHR was also significantly correlated with creatinine levels after PCI (r:0,104, p: 0.047). Additionally,patients developed CIN experienced a more complicated in-hospital clinical course (Table II) ( Figure  3) and weight and MHRwere detected as independent risk factors of CIN in logistic regression analysis (Table III).     Contrast-induced nephropathy during the course of NSTEMI is associated with increased morbidity and mortality (18).
Inflammation may also play an important role in the initiation and extension phases of CIN (19). Early identification of patients with a high CIN risk plays critical role to allow the necessary interventions. Many of these biomarkers cannot be done in several centers at the time of admission. Therefore markers that can be used before the procedure and are widely available in many centers are needed. Monocytes account for the major source of pro-inflammatory and prooxidant factors, and they interact with endothelial cells and platelets leading to inflammation, thrombosis, and endothelial dysfunction (20,21). On the other hand, HDL-C has anti-inflammatory, antioxidant, and antithrombotic effects (22). So increased the MHR reflects the inflammatory process. MHR is also an important marker that reflect the inflammatory status in patients with atherosclerosis and has been demonstrated to predict the cardiovascular events in patients with ACS (14).
As an inflammatory marker, the MHR has many advantages of being obtainable before the procedure. We observed that admission MHR was an independent predictor for CIN development. A recent study also revealed admission MHR as a risk factor for CIN in patients with STEMI and ACS (19).
Preprocedural MHR measurement may help to identify patients with high risk of CIN and to take protective preventions such as reducing contrast volume and increasing fluid administration.
Contrast volume is an important risk factor for CINand dose minimization, on the background of a known baseline reduced renal function, may serve as an important strategy to limit the incidence of CIN (8).However, we used a relatively small amount of contrast, and we did not find significant difference in terms of dose of contrast used in all patients with and without CIN. We suggested that other factors, such as impaired renal function and DM, age and weight might contribute more to the development of CIN than contrast volume. Also in our study; PLR, NLR and Hs-CRP were significantly higher in patients with CIN which were concordant with the previous studies (18,(23)(24)(25). We also found that CIN was associated with increased incidence of adverse events during hospitalization.
This study has some limitations. First, it is a single-center study. Second, the number of patients studied with CIN was relatively small, which could limit the number of independent predictors identified. However, we found some important results, consistent with the literature. Also, we only calculated MHR before the procedure. Serum HDL-C level and monocyte count may change with time; thus, single measurements of these parameters may not reflect any trend.

Conclusion
MHR is a risk factor for the development of CIN in patients with NSTEMI. The MHR is a simple marker of inflammation that can easily be obtained on admission and can be used to predict CIN risk.