ReviewThe Egyptian journal of internal medicine2021
Acute kidney injury and COVID-19.
Review in The Egyptian journal of internal medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 20 citations in OpenAlex.
- Hyaluronidase inhibitor sHA2.75 alleviates ischemia-reperfusion-induced acute kidney injury.Cell cycle (Georgetown, Tex.) · 2024Article
- SARS-CoV-2 infection and dysregulation of nuclear factor erythroid-2-related factor 2 (Nrf2) pathway.Cell stress & chaperones · 2023Review
- Insights on Covid-19 with superimposed pulmonary histoplasmosis: The possible nexus.Immunity, inflammation and disease · 2023Review
- Mixed storm in SARS-CoV-2 infection: A narrative review and new term in the Covid-19 era.Immunity, inflammation and disease · 2023Review
- A perspective study of the possible impact of obeticholic acid against SARS-CoV-2 infection.Inflammopharmacology · 2023Review
- The potential link between Covid-19 and multiple myeloma: A new saga.Immunity, inflammation and disease · 2022Review
- Pirfenidone and post-Covid-19 pulmonary fibrosis: invoked again for realistic goals.Inflammopharmacology · 2022Review
- Pathophysiology of Post-COVID syndromes: a new perspective.Virology journal · 2022Review
- A raising dawn of pentoxifylline in management of inflammatory disorders in Covid-19.Inflammopharmacology · 2022Review
- The crucial role of prolactin-lactogenic hormone in Covid-19.Molecular and cellular biochemistry · 2022Review
- Neutrophil Extracellular Traps (NETs) and Covid-19: A new frontiers for therapeutic modality.International immunopharmacology · 2022Review
- Mitochondrial Targeted Antioxidant SKQ1 Ameliorates Acute Kidney Injury by Inhibiting Ferroptosis.Oxidative medicine and cellular longevity · 2022Article
- Changes in the Blood Viscosity in Patients With SARS-CoV-2 Infection.Frontiers in medicine · 2022Review
- Selinexor and COVID-19: The Neglected Warden.Frontiers in pharmacology · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCoronavirus 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.
conclusionCOVID-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.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.