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

Abstract

AbstractAimUrinary liver‐type fatty acid binding protein (L‐FABP) has potential utility as an early prognostic biomarker ahead of traditional severity scores in coronavirus disease 2019 and sepsis, however, the mechanism of elevated urinary L‐FABP in the disease has not been clearly elucidated. We investigated the background mechanisms of urinary L‐FABP excretion through non‐clinical animal model focusing on histone, which is one of the aggravating factors in these infectious diseases.MethodsMale Sprague–Dawley rats were placed in central intravenous catheters, and these rats were given a continuous intravenous infusion of 0.25 or 0.5 mg/kg/min calf thymus histones for 240 min from caudal vena cava.ResultsAfter the administration of histone, urinary L‐FABP and gene expression of an oxidative stress marker in the kidney increased in a histone dose‐dependent manner before increased serum creatinine. Upon further investigation, fibrin deposition in the glomerulus was observed and it tended to be remarkable in the high dose administrated groups. The levels of coagulation factor were significantly changed after the administration of histone, and these were significantly correlated with the levels of urinary L‐FABP.ConclusionsFirstly, it was suggested that histone is one of the causative agents for the urinary L‐FABP increase at an early stage of the disease with a risk of acute kidney injury. Secondly, urinary L‐FABP could be a marker reflecting the changes of coagulation system and microthrombus caused by histone in the early stage of acute kidney injury before becoming severely ill and maybe a guide to early treatment initiation.