Urinary semaphorin 3A as an early biomarker to predict contrast-induced acute kidney injury in patients undergoing percutaneous coronary intervention.

Li Ning,Haiyan Chen,Dawei Wu,Zhiguo Li,Yanchun Wang,Chao Yang,Dianjun Wei,Jingwei Zhang

doi:10.1590/1414-431x20176487

Abstract

Contrast-induced acute kidney injury (CI-AKI) is a serious complication of diagnostic coronary angiograph and percutaneous coronary intervention (PCI). However, the exact pathophysiological mechanisms underlying CI-AKI development are largely unknown. The present study examined whether urinary semaphorin 3A levels predict the development of CI-AKI in patients undergoing PCI. This study enrolled 168 patients with stable angina undergoing elective PCI. Serial urine samples, obtained at baseline and 2, 6, 12, 24, 36, and 48 h post-PCI were analyzed by semaphorin 3A and neutrophil gelatinase-associated lipocalin (NGAL) ELISA kit. AKI was defined as an increase in serum creatinine beyond 50% according to the RIFLE classification system. Receiver operator characteristic (ROC) curve analyses identified optimal semaphorin 3A and NGAL values for diagnosing CI-AKI. CI-AKI occurred in 20 of 168 patients. There were no significant differences in the baseline clinical characteristics and angiographic findings between non-AKI patients group and AKI patients group. Both urinary semaphorin 3A and NGAL levels significantly increased at 2 and 6 h post-PCI. ROC analysis showed that the cut-off value of 389.5 pg/mg semaphorin 3A at 2 h post-PCI corresponds to 94% sensitivity and 75% specificity and the cut-off value of 94.4 ng/mg NGAL at 2 h post-PCI corresponds to 74% sensitivity and 82% specificity. Logistic regression showed that semaphorin 3A levels at 2 and 6 h post-PCI were the significant predictors of AKI in our cohort. Urinary semaphorin 3A may be a promising early biomarker for predicting CI-AKI in patients undergoing PCI.

Highlights

Contrast-induced acute kidney injury (CI-AKI) is a serious complication of diagnostic coronary angiography and percutaneous coronary intervention (PCI) [1]
The endpoint used for evaluating the patients was the appearance of AKI, defined as an increase in serum creatinine beyond 50% according to the RIFLE classification system
There were no significant differences in the clinical characteristics for age, gender, body mass index, serum creatinine, estimated GFR (eGFR), hemoglobin, hemoglobin A1c, left ventricular ejection fraction rate, fasting plasma glucose levels, brain natriuretic peptide level, percentage of hypertension, incidence of diabetes mellitus, and percentage of patients taking diuretics

Summary

Introduction

Contrast-induced acute kidney injury (CI-AKI) is a serious complication of diagnostic coronary angiography and percutaneous coronary intervention (PCI) [1]. Studies have proposed that the processes of CI-AKI involve immunologic reactions, ischemic injury, and tubular epithelial cell toxicity [3]. Many risk factors have been suggested to play an important role in the development of CI-AKI. The change of serum creatinine level was well-documented as a risk factor for CI-AKI [5]. The serum creatinine level does not elevate until glomerular filtration rate (GFR) has decreased by at least 50%, assessment of renal dysfunction according to serum creatinine is not reliable [6]. As far as we know, the renal markers such as cystatin C, neutrophil gelatinase-associated lipocalin (NGAL), liver fatty acidbinding protein (L-FABP), kidney injury molecule 1 (KIM-1) and interleukin 18 (IL-18) are proposed as potential

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Conclusion