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Long-Term Effects of Severe Burns on the Kidneys: Research Advances and Potential Therapeutic Approaches

Overview
Journal J Inflamm Res
Publisher Dove Medical Press
Date 2023 May 8
PMID 37152866
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Abstract

Burns are a seriously underestimated form of trauma that not only damage the skin system but also cause various complications, such as acute kidney injury (AKI). Recent clinical studies have shown that the proportion of chronic kidney diseases (CKD) in burn patients after discharge is significantly higher than that in the general population, but the mechanism behind this is controversial. The traditional view is that CKD is associated with hypoperfusion, AKI, sepsis, and drugs administered in the early stages of burns. However, recent studies have shown that burns can cause long-term immune dysfunction, which is a high-risk factor for CKD. This suggests that burns affect the kidneys more than previously recognized. In other words, severe burns are not only an acute injury but also a chronic disease. Neglecting to study long-term kidney function in burn patients also results in a lack of preventive and therapeutic methods being developed. Furthermore, stem cells and their exosomes have shown excellent comprehensive therapeutic properties in the prevention and treatment of CKD, making them increasingly the focus of research attention. Their engineering strategy further improved the therapeutic performance. This review will focus on the research advances in burns on the development of CKD, illustrating the possible mechanism of burn-induced CKD and introducing potential biological treatment options and their engineering strategies.

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References
1.
Hsu C, Hsu R, Yang J, Ordonez J, Zheng S, Go A . Elevated BP after AKI. J Am Soc Nephrol. 2015; 27(3):914-23. PMC: 4769190. DOI: 10.1681/ASN.2014111114. View

2.
Xu M, Zhao M, Zheng D . Effect of IGF-1C domain-modified nanoparticles on renal ischemia-reperfusion injury in mice. Ren Fail. 2022; 44(1):1376-1387. PMC: 9389927. DOI: 10.1080/0886022X.2022.2098773. View

3.
Calzavacca P, May C, Bellomo R . Glomerular haemodynamics, the renal sympathetic nervous system and sepsis-induced acute kidney injury. Nephrol Dial Transplant. 2014; 29(12):2178-84. DOI: 10.1093/ndt/gfu052. View

4.
Wu G, Xiao Y, Wang C, Hong X, Sun Y, Ma B . Risk Factors for Acute Kidney Injury in Patients With Burn Injury: A Meta-Analysis and Systematic Review. J Burn Care Res. 2016; 38(5):271-282. DOI: 10.1097/BCR.0000000000000438. View

5.
Baligand C, Qin H, True-Yasaki A, Gordon J, von Morze C, DeLos Santos J . Hyperpolarized C magnetic resonance evaluation of renal ischemia reperfusion injury in a murine model. NMR Biomed. 2017; 30(10). PMC: 5618802. DOI: 10.1002/nbm.3765. View