Abstract

SummaryBackgroundDue to the lack of diagnostic efficiency of serum creatinine in acute kidney injury (AKI), there is a pressing need to develop novel diagnostic markers. Therefore, in this study, we evaluated myo–inositol oxygenase (MIOX), neutrophil gelatinase-associated lipocalin (NGAL) and cystatin C in terms of their applicability in the diagnosis of AKI.MethodsWe enrolled a total of 39 AKI patients and 38 healthy controls in the study. We compared the levels of serum MIOX, NGAL and cystatin C between the two groups.ResultsWe found that the concentrations of serum creatinine, blood-urea nitrogen, MIOX and cystatin C were higher in the AKI group. According to the receiver operating characteristic analysis, the area under the curve (AUC) values were 0.694 (95% CI 0.579-0.794) for MIOX and 0.976 (95% CI; 0.912-0.997) for cystatin C. For MIOX, when the cut-off concentration was set to 77.3 pg/mL, the diagnostic sensitivity and specificity were found to be 53.8% (95% CI; 37.2-69.9) and 81.5 (95% CI; 65.7-92.3), respectively. For cystatin C, at the cut-off value of 14 mg/L, the diagnostic sensitivity and specificity were 94.8% (95% CI; 82.7-99.4) and 94.7 % (95% CI 82.3-99.4), respectively.ConclusionThe measurement of serum MIOX and cystatin C levels is valuable for the diagnosis of AKI. Further research is needed for the evaluation of the potential use of MIOX as a kidney-specific enzyme in the early diagnosis of AKI.

Highlights

  • Acute kidney injury (AKI) is a serious clinical problem due to its high morbidity and mortality [1]

  • We found that the concentrations of serum creatinine, blood-urea nitrogen, myo-inositol oxygenase (MIOX) and cystatin C were higher in the acute kidney injury (AKI) group

  • Some markers that have been suggested to date are neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver-type fatty acid–binding protein (L-FABP), interleukin 18 (IL-18), insulin-like growth factor binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinase 2 (TIMP-2), and calprotectin (S100A8/9) [3]

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Summary

Introduction

Acute kidney injury (AKI) is a serious clinical problem due to its high morbidity and mortality [1]. A diagnosis of AKI is based on the level of the plasma creatinine. Creatinine is an insensitive and non-specific marker that is affected by several variables such as age, gender, muscle density and hepatic functions. An increase in the level of creatinine is only observable days after a kidney injury and when 50% or more of the kidney functions are affected [2]. The search for alternative markers for early diagnosis of AKI has been increasing. Some markers that have been suggested to date are neutrophil gelatinase-associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1), liver-type fatty acid–binding protein (L-FABP), interleukin 18 (IL-18), insulin-like growth factor binding protein 7 (IGFBP7), tissue inhibitor of metalloproteinase 2 (TIMP-2), and calprotectin (S100A8/9) [3]

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