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Neutrophil Gelatinase-Associated Lipocalin as a Biomarker of Allograft Function After Renal Transplantation: Evaluation of the Current Status and Future Insights.

Maria Laura CappuccilliIrene CapelliGiorgia ComaiGiuseppe CiancioloGaetano La Manna
Published in: Artificial organs (2017)
Neutrophil gelatinase-associated lipocalin (NGAL), a protein belonging to the lipocalin superfamily initially found in activated neutrophils, is expressed by several cell types, including kidney tubule. The increase in NGAL production and release from tubular cells in response to various insults has been proven to predict acute kidney injury (AKI). For this reason, it has emerged as a valuable noninvasive biomarker of AKI in clinical nephrology. Also in the renal transplant setting, different studies have indicated NGAL as a valuable tool, especially in the early postoperative period, since the currently available clinical and laboratory parameters remain poorly sensitive to monitor immediate posttransplant graft function. This is an analysis of the recent literature to assess the utility of plasma and urinary NGAL, exosomal mRNA for NGAL, and NGAL levels in the perfusate of machine-perfused kidneys for the prediction of graft function recovery in the early postsurgery phase after renal transplantation. We found that NGAL appears as a promising troponin-like biomarker to detect short-term impairment of graft function after renal transplant, but there are still some limitations in its clinical application, essentially related to its low specificity. Moreover, comparing NGAL assayed in serum, urine, machine-perfusate, or as exosomal mRNA, each one has shown limitations and benefits in terms of predictive performance for DGF, according to various existing studies, feasibly due to different cut-off levels, designs and patient sample sizes.
Keyphrases
  • acute kidney injury
  • systematic review
  • cardiac surgery
  • induced apoptosis
  • binding protein
  • machine learning
  • patients undergoing
  • mesenchymal stem cells
  • cell therapy
  • endoplasmic reticulum stress
  • cell death