Urinary liver-type fatty acid binding protein is a biomarker reflecting renal damage and the ameliorative effect of drugs at an early stage of histone-induced acute kidney injury.
acute kidney injury (AKI)
heparin
histone
liver-type fatty acid binding protein (L-FABP)
phosphodiesterase 4 (PDE4) inhibitor
urinary biomarker
Journal
Nephrology (Carlton, Vic.)
ISSN: 1440-1797
Titre abrégé: Nephrology (Carlton)
Pays: Australia
ID NLM: 9615568
Informations de publication
Date de publication:
11 Nov 2023
11 Nov 2023
Historique:
revised:
31
10
2023
received:
02
08
2023
accepted:
01
11
2023
medline:
11
11
2023
pubmed:
11
11
2023
entrez:
11
11
2023
Statut:
aheadofprint
Résumé
Circulated histones play a crucial role in the pathogenesis of infectious diseases and severe trauma, and it is one of the potential molecular targets for therapeutics. Recently, we reported that histone is one of the causative agents for urinary L-FABP increase. However, the mechanism is still unclear, especially in severe cases. We further investigated the mechanism of urinary L-FABP increase using a more severe mouse model with histone-induced kidney injury. This study also aims to evaluate the therapeutic responsiveness of urinary L-FABP as a preliminary study. Human L-FABP chromosomal transgenic mice were administrated 30 mg/kg histone from a tail vein with a single dose. We also performed a comparative study in LPS administration model. For the evaluation of the therapeutic responsiveness of urinary L-FABP, we used heparin and rolipram. The histological change with cast formation as a characteristic of the models was observed in proximal tubules. Urinary L-FABP levels were significantly elevated and these levels tended to be higher in those with more cast formation. Heparin and rolipram had the ameliorative effect of the cast formation induced by histone and urinary L-FABP levels significantly decreased. Histone is one of the causative agents for the increase of urinary L-FABP at an early stage of AKI. In addition, it suggested that urinary L-FABP may be useful as a subclinical AKI marker reflecting kidney damage induced by histone. Furthermore, urinary L-FABP reflected the degree of the damage after the administration of therapeutic agents such as heparin and PDE4 inhibitor.
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Japan Agency for Medical Research and Development
ID : JP20fk0108302
Informations de copyright
© 2023 Asian Pacific Society of Nephrology.
Références
Kawai C, Kotani H, Miyao M, et al. Circulating extracellular histones are clinically relevant mediators of multiple organ injury. Am J Pathol. 2016;186(4):829-843.
de Vries F, Huckriede J, Wichapong K, Reutelingsperger C, Nicolaes GAF. The role of extracellular histones in COVID-19. J Intern Med. 2023;293(3):275-292.
Xu J, Zhang X, Pelayo R, et al. Extracellular histones are major mediators of death in sepsis. Nat Med. 2009;11:1318-1321.
Okubo K, Kurosawa M, Kamiya M, et al. Macrophage extracellular trap formation promoted by platelet activation is a key mediator of rhabdomyolysis-induced acute kidney injury. Nat Med. 2018;24(2):232-238.
Nakazawa D, Kumar SV, Marschner J, et al. Histones and neutrophil extracellular traps enhance tubular necrosis and remote organ injury in ischemic AKI. J Am Soc Nephrol. 2017;28(6):1753-1768.
Sato E, Kamijo-Ikemori A, Oikawa T, et al. Urinary excretion of liver-type fatty acid-binding protein reflects the severity of sepsis. Renal Replacement Therapy. 2017;3(1):1-10.
Kamijo-Ikemori A, Kimura K. Clinical utility of tubular markers in kidney disease: a narrative review. J Lab Precis Med. 2022;7:27.
Ohata K, Sugaya T, Nguyen HN, et al. Urinary liver-type fatty acid binding protein is increased in the early stages of the disease with a risk of acute kidney injury induced by histone. Nephrology (Carlton). 2023;28(6):345-355.
Kusirisin P, Kaewdoungtien P, Thanapongsatorn P, Peerapornratana S, Srisawat N. Innovations in intensive care nephrology. In: da Silva B, Junior G, Nangaku M, eds. Innovations in Nephrology: Breakthrough Technologies in Kidney Disease Care. Springer Nature; 2022:P343-P363.
Noiri E, Doi K, Negishi K, et al. Urinary fatty acid-binding protein 1: an early predictive biomarker of kidney injury. Am J Physiol Renal Physiol. 2009;296(4):F669-79.
Negishi K, Noiri E, Doi K, et al. Monitoring of urinary L-type fatty acid-binding protein predicts histological severity of acute kidney injury. Am J Pathol. 2009;174(4):1154-1159.
Katayama M, Miyazaki T, Ohata K, et al. Temporal changes in urinary excretion of liver-type fatty acid binding protein (L-FABP) in acute kidney injury model of domestic cats: a preliminary study. J Vet Med Sci. 2019;81(12):1868-1872.
Katagiri D, Ishikane M, Asai Y, et al. Evaluation of coronavirus disease 2019 severity using urine biomarkers. Crit Care Explor. 2020;2(8):e0170.
Katagiri D, Asai Y, Ohmagari N, et al. Urinary L-type fatty acid-binding protein predicts oxygen demand of COVID-19 in initially mild cases. Crit Care Explor. 2023;5(3):e0873.
Fukao Y, Nagasawa H, Nihei Y, et al. COVID-19-induced acute renal tubular injury associated with elevation of serum inflammatory cytokine. Clin Exp Nephrol. 2021;25(11):1240-1246.
Naruse H, Ishii J, Takahashi H, et al. Urinary liver-type fatty-acid-binding protein predicts long-term adverse outcomes in medical cardiac intensive care units. J Clin Med. 2020;9(2):482.
Ichikawa D, Kamijo-Ikemori A, Sugaya T, et al. Utility of urinary tubular markers for monitoring chronic tubulointerstitial injury after ischemia-reperfusion. Nephrology (Carlton). 2018;23(4):308-316.
Ikonomidis I, Pavlidis G, Kadoglou N, et al. Apremilast improves endothelial glycocalyx integrity, vascular and left ventricular myocardial function in psoriasis. Pharmaceuticals (Basel). 2022;15(2):172.
Wu JJ, Liu J, Thatiparthi A, Martin A, Egeberg A. The risk of COVID-19 in patients with psoriasis: a retrospective cohort study. J Am Acad Dermatol. 2022;87(6):1395-1398.
Holthoff JH, Wang Z, Patil NK, Gokden N, Mayeux PR. Rolipram improves renal perfusion and function during sepsis in the mouse. J Pharmacol Exp Ther. 2013;347(2):357-364.
Kamijo-Ikemori A, Sugaya T, Matsui K, Yokoyama T, Kimura K. Roles of human liver type fatty acid binding protein in kidney disease clarified using hL-FABP chromosomal transgenic mice. Nephrology (Carlton). 2011;16(6):539-544.
Ohata K, Kamijo-Ikemori A, Sugaya T, et al. Renoprotective effect of the xanthine oxidoreductase inhibitor Topiroxostat under decreased angiotensin II type 1a receptor expression. Eur J Pharmacol. 2017;815:88-97.
Akira S, Uematsu S, Takeuchi O. Pathogen recognition and innate immunity. Cell. 2006;124(4):783-801.
Doi K, Noiri E, Maeda-Mamiya R, et al. Urinary L-type fatty acid-binding protein as a new biomarker of sepsis complicated with acute kidney injury. Crit Care Med. 2010;38(10):2037-2042.
Doi K, Katagiri D, Negishi K, et al. Mild elevation of urinary biomarkers in prerenal acute kidney injury. Kidney Int. 2012;82(10):1114-1120.
Watanabe K, Okamoto T, Saitou T, et al. Increased urinary albumin leakage is related to injuries of glomerular glycocalyx and podocytes, and associated with tubular dysfunction in preeclampsia. Pregnancy Hypertens. 2023;32:1-6.
Kamijo A, Sugaya T, Hikawa A, et al. Urinary excretion of fatty acid-binding protein reflects stress overload on the proximal tubules. Am J Pathol. 2004;165(4):1243-1255.
Zhang D, Qi B, Li D, et al. Phillyrin relieves lipopolysaccharide-induced AKI by protecting against glycocalyx damage and inhibiting inflammatory responses. Inflammation. 2020;43(2):540-551.
Takaori K, Nakamura J, Yamamoto S, et al. Severity and frequency of proximal tubule injury determines renal prognosis. J Am Soc Nephrol. 2016;27(8):2393-2406.
Chang W, Chen J, Schlueter CF, Rando RJ, Pathak YV, Hoyle GW. Inhibition of chlorine-induced lung injury by the type 4 phosphodiesterase inhibitor rolipram. Toxicol Appl Pharmacol. 2012;263(2):251-258.
Miwa T, Mori A, Nakahara T, Ishii K. Intravenously administered phosphodiesterase 4 inhibitors dilate retinal blood vessels in rats. Eur J Pharmacol. 2009;602(1):112-116.
Land WG. Publisher correction: role of DAMPs in respiratory virus-induced acute respiratory distress syndrome - with a preliminary reference to SARS-CoV-2 pneumonia. Genes Immun. 2022;23(8):245.
Gao M, Wan X, Ma M, et al. Kidney injury induced by elevated histones in community-acquired pneumonia. Mol Cell Biochem. 2020;471(1-2):155-163.
van Smaalen TC, Beurskens DMH, Kox JJHFM, et al. Extracellular histone release by renal cells after warm and cold ischemic kidney injury: studies in an ex-vivo porcine kidney perfusion model. PloS One. 2023;18(1):e0279944.
Li Y, Chen Y, Yang T, et al. Targeting circulating high mobility group box-1 and histones by extracorporeal blood purification as an immunomodulation strategy against critical illnesses. Crit Care. 2023;27(1):77.
Pan HC, Yang SY, Chiou TT, et al. Comparative accuracy of biomarkers for the prediction of hospital-acquired acute kidney injury: a systematic review and meta-analysis. Crit Care. 2022;26(1):349.