SARS-CoV-2 renal tropism associates with acute kidney injury

SARS-CoV-2-mediated acute kidney injury might be explained by indirect factors (eg, cytokine-mediated injury) and by direct viral infection and replication in kidney epithelial cells.4 We isolated SARS-CoV-2 from an autopsied kidney, which produced a 1000-times increase in viral RNA after 48 h of ce...

Celý popis

Uložené v:
Podrobná bibliografia
Vydané v:The Lancet (British edition) Ročník 396; číslo 10251; s. 597 - 598
Hlavní autori: Braun, Fabian, Lütgehetmann, Marc, Pfefferle, Susanne, Wong, Milagros N, Carsten, Alexander, Lindenmeyer, Maja T, Nörz, Dominik, Heinrich, Fabian, Meißner, Kira, Wichmann, Dominic, Kluge, Stefan, Gross, Oliver, Pueschel, Klaus, Schröder, Ann S, Edler, Carolin, Aepfelbacher, Martin, Puelles, Victor G, Huber, Tobias B
Médium: Journal Article
Jazyk:English
Vydavateľské údaje: England Elsevier Ltd 29.08.2020
Elsevier Limited
Predmet:
ISSN:0140-6736, 1474-547X, 1474-547X
On-line prístup:Získať plný text
Tagy: Pridať tag
Žiadne tagy, Buďte prvý, kto otaguje tento záznam!
Popis
Shrnutí:SARS-CoV-2-mediated acute kidney injury might be explained by indirect factors (eg, cytokine-mediated injury) and by direct viral infection and replication in kidney epithelial cells.4 We isolated SARS-CoV-2 from an autopsied kidney, which produced a 1000-times increase in viral RNA after 48 h of cell infection in vitro (figure; appendix p 1), thus confirming the presence of infective virus in the kidney, even under post-mortem conditions. Furthermore, we found that patient-derived SARS-CoV-2 replicates in non-human primate kidney tubular epithelial cells (the main cellular target of acute kidney injury) using indirect immunofluorescence imaging of SARS-CoV-2 non-structural protein 3, one of the SARS-CoV replicase cleaving products (appendix p 5).5 Our findings indicate that SARS-CoV-2 renal tropism is associated with disease severity (ie, premature death) and development of acute kidney injury. TBH reports grants from the German Research Foundation (CRC/1192, HU 1016/8-2, HU 1016/11-1, HU 1016/12-1), the Federal Ministry of Education and Research (STOP-FSGS-01GM1518C), and the European Research Council (grant 616891) during the study; grants and personal fees from Fresenius Medical Care; grants from Amicus Therapeutics and Sanofi Genzyme; and personal fees from Boehringer Ingelheim, Goldfinch Bio, Novartis Pharma, DaVita Germany, and Bayer Vital, unrelated to this Correspondence.
Bibliografia:SourceType-Scholarly Journals-1
ObjectType-Correspondence-1
content type line 14
ObjectType-Article-2
content type line 23
ISSN:0140-6736
1474-547X
1474-547X
DOI:10.1016/S0140-6736(20)31759-1