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Biochemical Markers in the Prediction of Contrast-induced Acute Kidney Injury

期刊

CURRENT MEDICINAL CHEMISTRY
卷 28, 期 6, 页码 1234-1250

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BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/0929867327666200502015749

关键词

Contrast-induced acute kidney injury; contrast CT; percutaneous coronary angioplasty; Kidney Injury Molecule 1 (KIM-1); Neutrophil Gelatinase Lipocalin (NGAL); Percutaneous Coronary Intervention (PCI)

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The search for a simple diagnostic tool to assess the risk of acute kidney injury (AKI) caused by contrast procedures continues, with Kidney Injury Molecule 1 (KIM-1) and Neutrophil Gelatinase Lipocalin (NGAL) showing potential as predictive markers. However, clinical trials have yielded conflicting results, highlighting the need for further research in this area.
For many years clinicians have been searching for kidney troponin- a simple diagnostic tool to assess the risk of acute kidney injury (AKI). Recently, the rise in the variety of contrast-related procedures (contrast computed tomography (CT), percutaneous coronary intervention (PCI) and angiography) has resulted in the increased number of contrast-induced acute kidney injuries (CI-AKI). CI-AKI remains an important cause of overall mortality, prolonged hospitalisation and it increases the total costs of therapy. The consequences of kidney dysfunction affect the quality of life and they may lead to disability as well. Despite extensive worldwide research, there are no sensitive and reliable methods of CI-AKI prediction. Kidney Injury Molecule 1 (KIM-1) and Neutrophil Gelatinase Lipocalin (NGAL) have been considered as kidney-specific molecules. High concentrations of these substances before the implementation of contrast-related procedures have been suggested to enable the estimation of kidney vulnerability to CI-AKI and they seem to have the predictive potential for cardiovascular events and overall mortality. According to other authors, routine determination of known inflammation factors (e.g., CRP, WBC, and neutrophil count) may be helpful in the prediction of CIAKI. However, the results of clinical trials provide contrasting results. The pathomechanism of contrast-induced nephropathy remains unclear. Due to its prevalence, the evaluation of the risk of acute kidney injury remains a serious problem to be solved. This paper reviews pathophysiology and suggested optimal markers facilitating the prediction of contrast-induced acute kidney injury.

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