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Burn-Induced Acute Kidney Injury-Two-Lane Road: From Molecular to Clinical Aspects. | LitMetric

AI Article Synopsis

  • * Factors like hypovolemia, inflammatory response, and sepsis contribute to the development of AKI in burn victims, highlighting the need for quick recognition and intervention.
  • * Researchers are exploring various renal biomarkers (e.g., NGAL, cystatin C) for early detection of burn-induced AKI to help prevent progression and reduce the risk of chronic kidney disease.

Article Abstract

Severe burn injuries lead to acute kidney injury (AKI) development, increasing the mortality risk up to 28-100%. In addition, there is an increase in hospitalization days and complications appearance. Various factors are responsible for acute or late AKI debut, like hypovolemia, important inflammatory response, excessive load of denatured proteins, sepsis, and severe organic dysfunction. The main measure to improve the prognosis of these patients is rapidly recognizing this condition and reversing the underlying events. For this reason, different renal biomarkers have been studied over the years for early identification of burn-induced AKI, like neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule-1 (KIM-1), tissue inhibitor of metalloproteinase-2 (TIMP-2), interleukin-18 (IL-18), and insulin-like growth factor-binding protein 7 (IGFBP7). The fundamental purpose of these studies is to find a way to recognize and prevent acute renal injury progression early in order to decrease the risk of mortality and chronic kidney disease (CKD) onset.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9368898PMC
http://dx.doi.org/10.3390/ijms23158712DOI Listing

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