Acute kidney injury and COVID-19
Abstract Background Coronavirus disease 2019 (COVID-19) is a recent pandemic infectious disease caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2). COVID-19 may lead to acute kidney injury (AKI). Main text SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) and dipeptidyl peptid...
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| Format: | Article |
| Language: | English |
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SpringerOpen
2021-10-01
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| Series: | The Egyptian Journal of Internal Medicine |
| Subjects: | |
| Online Access: | https://doi.org/10.1186/s43162-021-00064-x |
| _version_ | 1818689353667313664 |
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| author | Hayder M. Al-kuraishy Ali I. Al-Gareeb |
| author_facet | Hayder M. Al-kuraishy Ali I. Al-Gareeb |
| author_sort | Hayder M. Al-kuraishy |
| collection | DOAJ |
| description | Abstract Background Coronavirus disease 2019 (COVID-19) is a recent pandemic infectious disease caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2). COVID-19 may lead to acute kidney injury (AKI). Main text SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) and dipeptidyl peptidase 4(DPP4) as entry point receptors in the alveolar type II cell of the lung. However, the expression of ACE2 is 100-fold higher in kidney tissue than the lung, though the potential entry point of SARS-CoV-2 for renal tissue and induction of AKI remains undefined. Therefore, reduction of ACE2 and high circulating angiotensin II in COVID-19 may together participate in the induction of AKI. Thereby, direct ACE2 activator is under investigation to be used as an effective therapy in the management COVID-19-induced AKI. Besides, the direct effect via invasion of SARS-CoV-2 may lead to glomerulopathy and renal proximal tubular necrosis. Conclusion COVID-19 may associate with AKI due to direct effect of SARS-CoV-2 through ACE2 and DPP4 receptors or indirectly through the development of cytokine storm. Both ACE2 and DPP4 are interacted mutually in the pathogenesis of AKI. Thus, DPP4 inhibitors or ACE2 activators could reverse early AKI in COVID-19. Therefore, emerging of clinical trials is warranted to confirm the role of ACE2 and DPP4 modulators in COVID-19-induced AKI. |
| first_indexed | 2024-12-17T12:08:46Z |
| format | Article |
| id | doaj.art-7c57adad5976495c95704e0be4f53089 |
| institution | Directory Open Access Journal |
| issn | 1110-7782 2090-9098 |
| language | English |
| last_indexed | 2024-12-17T12:08:46Z |
| publishDate | 2021-10-01 |
| publisher | SpringerOpen |
| record_format | Article |
| series | The Egyptian Journal of Internal Medicine |
| spelling | doaj.art-7c57adad5976495c95704e0be4f530892022-12-21T21:49:31ZengSpringerOpenThe Egyptian Journal of Internal Medicine1110-77822090-90982021-10-013311510.1186/s43162-021-00064-xAcute kidney injury and COVID-19Hayder M. Al-kuraishy0Ali I. Al-Gareeb1Department of Clinical Pharmacology, Medicine and Therapeutic, Medical Faculty, College of Medicine, Al-Mustansiriya UniversityDepartment of Clinical Pharmacology, Medicine and Therapeutic, Medical Faculty, College of Medicine, Al-Mustansiriya UniversityAbstract Background Coronavirus disease 2019 (COVID-19) is a recent pandemic infectious disease caused by severe acute respiratory syndrome coronavirus (SARS-CoV-2). COVID-19 may lead to acute kidney injury (AKI). Main text SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2) and dipeptidyl peptidase 4(DPP4) as entry point receptors in the alveolar type II cell of the lung. However, the expression of ACE2 is 100-fold higher in kidney tissue than the lung, though the potential entry point of SARS-CoV-2 for renal tissue and induction of AKI remains undefined. Therefore, reduction of ACE2 and high circulating angiotensin II in COVID-19 may together participate in the induction of AKI. Thereby, direct ACE2 activator is under investigation to be used as an effective therapy in the management COVID-19-induced AKI. Besides, the direct effect via invasion of SARS-CoV-2 may lead to glomerulopathy and renal proximal tubular necrosis. Conclusion COVID-19 may associate with AKI due to direct effect of SARS-CoV-2 through ACE2 and DPP4 receptors or indirectly through the development of cytokine storm. Both ACE2 and DPP4 are interacted mutually in the pathogenesis of AKI. Thus, DPP4 inhibitors or ACE2 activators could reverse early AKI in COVID-19. Therefore, emerging of clinical trials is warranted to confirm the role of ACE2 and DPP4 modulators in COVID-19-induced AKI.https://doi.org/10.1186/s43162-021-00064-xCOVID-19SARS-CoV-2Acute kidney injury |
| spellingShingle | Hayder M. Al-kuraishy Ali I. Al-Gareeb Acute kidney injury and COVID-19 The Egyptian Journal of Internal Medicine COVID-19 SARS-CoV-2 Acute kidney injury |
| title | Acute kidney injury and COVID-19 |
| title_full | Acute kidney injury and COVID-19 |
| title_fullStr | Acute kidney injury and COVID-19 |
| title_full_unstemmed | Acute kidney injury and COVID-19 |
| title_short | Acute kidney injury and COVID-19 |
| title_sort | acute kidney injury and covid 19 |
| topic | COVID-19 SARS-CoV-2 Acute kidney injury |
| url | https://doi.org/10.1186/s43162-021-00064-x |
| work_keys_str_mv | AT haydermalkuraishy acutekidneyinjuryandcovid19 AT aliialgareeb acutekidneyinjuryandcovid19 |