Post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury

Abstract

Background: Acute kidney injury (AKI) is a common cause of morbidity and mortality. It mainly targets the renal tubular epithelium with pathological changes, referred to as acute tubular injury. The latter is followed by a regenerative response that is difficult to visualize on routine hematoxylin and eosin (H&E) stains. In this study, we examined the regenerative capacity of renal tubules by correlating vimentin (VIM) immunohistochemical (IHC) expression and pathological findings of AKI and renal tubular regeneration (RTR) on H&E. Methods: We reviewed 23 autopsies performed in the clinical setting of AKI and RTR. VIM expression was scored in the renal cortical tubular epithelium using a statistical cutoff ≥ 3% for high expression and < 3% for low expression. Results: Of the 23 kidney tissues examined, seven (30.4%) had low VIM expression, and 16 (69.6%) had high VIM expression. Kidney tissues with evidence of AKI and RTR had significantly higher VIM expression. Renal peritubular microenvironment features showing regenerative changes on H&E were associated with high VIM expression. In the univariate model, kidney tissues with RTR were 18-fold more likely to have high VIM expression. Conclusions: In conclusion, our findings suggest that VIM could serve as an IHC marker for RTR following AKI. However, correlation with H&E findings remains critical to excluding chronic tubular damage. Collectively, our preliminary results pave the way for future studies including a larger sample size to validate the use of VIM as a reliable biomarker for RTR.

Myocardial infarction injury is exacerbated by nicotine in vape aerosol exposure

“…88 Similar findings for vimentin as a marker of regeneration were also reported in the kidney. 89 Accrual of vimentin immunofluorescence in Vape alone myocardial tissue sections (Fig. 4) is unlikely to represent the acute inflammatory wave of cellular infiltrates responding to infarction injury since the hearts were harvested well after the peak inflammatory response occurring days after injury.…”