Post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury
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 an...
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Korean Society of Pathologists & the Korean Society for Cytopathology
2021
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oai:doaj.org-article:7a965e6ac0334fc0a46c70c5fa532b882021-11-18T05:29:08ZPost-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury2383-78372383-784510.4132/jptm.2021.08.03https://doaj.org/article/7a965e6ac0334fc0a46c70c5fa532b882021-11-01T00:00:00Zhttp://www.jpatholtm.org/upload/pdf/jptm-2021-08-03.pdfhttps://doaj.org/toc/2383-7837https://doaj.org/toc/2383-7845Background 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.Juan Carlos Alvarez MorenoHisham F. BahmadChristopher A. Febres-AldanaAndrés PirelaAndres AzueroAli SalamiRobert PoppitiKorean Society of Pathologists & the Korean Society for Cytopathologyarticleacute kidney injuryacute tubular injuryrenal tubular regenerationvimentinbiomarkerimmunohistochemistryPathologyRB1-214ENKOJournal of Pathology and Translational Medicine, Vol 55, Iss 6, Pp 369-379 (2021) |
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acute kidney injury acute tubular injury renal tubular regeneration vimentin biomarker immunohistochemistry Pathology RB1-214 |
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acute kidney injury acute tubular injury renal tubular regeneration vimentin biomarker immunohistochemistry Pathology RB1-214 Juan Carlos Alvarez Moreno Hisham F. Bahmad Christopher A. Febres-Aldana Andrés Pirela Andres Azuero Ali Salami Robert Poppiti Post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury |
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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. |
format |
article |
author |
Juan Carlos Alvarez Moreno Hisham F. Bahmad Christopher A. Febres-Aldana Andrés Pirela Andres Azuero Ali Salami Robert Poppiti |
author_facet |
Juan Carlos Alvarez Moreno Hisham F. Bahmad Christopher A. Febres-Aldana Andrés Pirela Andres Azuero Ali Salami Robert Poppiti |
author_sort |
Juan Carlos Alvarez Moreno |
title |
Post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury |
title_short |
Post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury |
title_full |
Post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury |
title_fullStr |
Post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury |
title_full_unstemmed |
Post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury |
title_sort |
post-mortem assessment of vimentin expression as a biomarker for renal tubular regeneration following acute kidney injury |
publisher |
Korean Society of Pathologists & the Korean Society for Cytopathology |
publishDate |
2021 |
url |
https://doaj.org/article/7a965e6ac0334fc0a46c70c5fa532b88 |
work_keys_str_mv |
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