tetano
Editor, Senior Moderator
J Am Soc Nephrol
. 2021 Jun 4;ASN.2021010059.
doi: 10.1681/ASN.2021010059. Online ahead of print.
High SARS-CoV-2 Viral Load in Urine Sediment Correlates with Acute Kidney Injury and Poor COVID-19 Outcome
Paulo Caceres[SUP] 1 [/SUP], Gina Savickas[SUP] 2 [/SUP], Shannon Murray[SUP] 3 [/SUP], Kausik Umanath[SUP] 4 [/SUP], Junior Uduman[SUP] 5 [/SUP], Jerry Yee[SUP] 6 [/SUP], Tang-Dong Liao[SUP] 7 [/SUP], Steven Bolin[SUP] 8 [/SUP], Albert Levin[SUP] 9 [/SUP], Moomal Khan[SUP] 10 [/SUP], Sarah Sarkar[SUP] 11 [/SUP], Jamie Fitzgerald[SUP] 12 [/SUP], Dipak Maskey[SUP] 13 [/SUP], Adrian Ormsby[SUP] 14 [/SUP], Yuvraj Sharma[SUP] 15 [/SUP], Pablo Ortiz[SUP] 16 [/SUP]
Affiliations
Abstract
Background Acute kidney injury (AKI) is a complication of coronavirus disease 2019 (COVID-19) that is associated with high mortality. Despite documented kidney tropism of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), there are no consistent reports of viral detection in urine or correlation with AKI or COVID-19 severity. Here we hypothesize that quantification of SARS-CoV-2 viral load in urine sediment from COVID-19 patients correlates with occurrence of AKI and mortality. Methods SARS-CoV-2 viral load in urine sediments (U-viral load) was quantified by qRT-PCR in 52 patients with PCR-confirmed COVID-19 diagnosis, hospitalized between March 15th and June 8th, 2020. Immunolabeling of SARS-CoV-2 proteins Spike and Nucleocapsid was performed in two COVID-19 kidney biopsies and urine sediments. Viral infectivity assays were performed from 32 urine sediments. Results Twenty COVID-19 patients (39%) had detectable SARS-CoV-2 U-viral load, of which 17 (85%) developed AKI with an average U-viral load 4-times higher than non-AKI COVID-19 patients. U-viral load was highest (7.7-fold) within two weeks after AKI diagnosis. A higher U-viral load correlated with mortality but not with albuminuria or AKI stage. SARS-CoV-2 proteins partially colocalized with the viral receptor ACE2 in kidney biopsies in tubules and parietal cells, and in urine sediment cells. Infective SARS-CoV-2 was not detected in urine sediments. Conclusion Our results further support SARS-CoV-2 kidney tropism. A higher SARS-CoV-2 viral load in urine sediments from COVID-19 patients correlated with increased incidence of AKI and mortality. Urinary viral detection could inform medical care of COVID-19 patients with kidney injury to improve prognosis.
. 2021 Jun 4;ASN.2021010059.
doi: 10.1681/ASN.2021010059. Online ahead of print.
High SARS-CoV-2 Viral Load in Urine Sediment Correlates with Acute Kidney Injury and Poor COVID-19 Outcome
Paulo Caceres[SUP] 1 [/SUP], Gina Savickas[SUP] 2 [/SUP], Shannon Murray[SUP] 3 [/SUP], Kausik Umanath[SUP] 4 [/SUP], Junior Uduman[SUP] 5 [/SUP], Jerry Yee[SUP] 6 [/SUP], Tang-Dong Liao[SUP] 7 [/SUP], Steven Bolin[SUP] 8 [/SUP], Albert Levin[SUP] 9 [/SUP], Moomal Khan[SUP] 10 [/SUP], Sarah Sarkar[SUP] 11 [/SUP], Jamie Fitzgerald[SUP] 12 [/SUP], Dipak Maskey[SUP] 13 [/SUP], Adrian Ormsby[SUP] 14 [/SUP], Yuvraj Sharma[SUP] 15 [/SUP], Pablo Ortiz[SUP] 16 [/SUP]
Affiliations
- PMID: 34088853
- DOI: 10.1681/ASN.2021010059
Abstract
Background Acute kidney injury (AKI) is a complication of coronavirus disease 2019 (COVID-19) that is associated with high mortality. Despite documented kidney tropism of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), there are no consistent reports of viral detection in urine or correlation with AKI or COVID-19 severity. Here we hypothesize that quantification of SARS-CoV-2 viral load in urine sediment from COVID-19 patients correlates with occurrence of AKI and mortality. Methods SARS-CoV-2 viral load in urine sediments (U-viral load) was quantified by qRT-PCR in 52 patients with PCR-confirmed COVID-19 diagnosis, hospitalized between March 15th and June 8th, 2020. Immunolabeling of SARS-CoV-2 proteins Spike and Nucleocapsid was performed in two COVID-19 kidney biopsies and urine sediments. Viral infectivity assays were performed from 32 urine sediments. Results Twenty COVID-19 patients (39%) had detectable SARS-CoV-2 U-viral load, of which 17 (85%) developed AKI with an average U-viral load 4-times higher than non-AKI COVID-19 patients. U-viral load was highest (7.7-fold) within two weeks after AKI diagnosis. A higher U-viral load correlated with mortality but not with albuminuria or AKI stage. SARS-CoV-2 proteins partially colocalized with the viral receptor ACE2 in kidney biopsies in tubules and parietal cells, and in urine sediment cells. Infective SARS-CoV-2 was not detected in urine sediments. Conclusion Our results further support SARS-CoV-2 kidney tropism. A higher SARS-CoV-2 viral load in urine sediments from COVID-19 patients correlated with increased incidence of AKI and mortality. Urinary viral detection could inform medical care of COVID-19 patients with kidney injury to improve prognosis.