ArticleCureus2022
Glomerular Endotheliosis in COVID-19-Associated Acute Kidney Injury.
Article in Cureus, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed, 3 citations in OpenAlex.
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) has been seen in patients hospitalized with a SARS-CoV-2 (COVID-19) infection,but the pathophysiology of glomerular injury is not yet fully understood. We present a case of COVID-19-related "glomerular endotheliosis" in which a 51-year-old female with a 13-year history of class IV lupus nephritis was admitted for COVID-19 pneumonia. Her lupus nephritis had been in complete renal remission for the past 10 years with a baseline serum creatinine level of 1.3 mg/dL and no proteinuria. Her serological workup, including complement levels, was unremarkable. Due to the worsening renal function and persistent proteinuria, she underwent a kidney biopsy that revealed diffuse glomerular endothelial cell swelling, also known as glomerular endotheliosis. Her clinical course unfortunately deteriorated and she succumbed to acute respiratory distress syndrome. As circulating anti-angiogenic factors may contribute to the pathogenesis of endothelial dysfunction leading to glomerular endotheliosis, we propose that a similar circulating antiangiogenic factor may have been triggered by COVID-19 and played a role in our patient's progressive renal failure.
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Registered trials
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