High SARS-CoV-2 Viral Load in Urine Sediment Correlates with Acute Kidney Injury and Poor COVID-19 Outcome

Authors

Paulo S. Caceres, Henry Ford HealthFollow
Gina Savickas, Henry Ford HealthFollow
Shannon L. Murray, Henry Ford HealthFollow
Kausik Umanath, Henry Ford HealthFollow
Junior Uduman, Henry Ford HealthFollow
Jerry Yee, Henry Ford HealthFollow
Tang-Dong Liao, Henry Ford HealthFollow
Steven Bolin
Albert M. Levin, Henry Ford HealthFollow
Moomal Khan, Henry Ford Health
Sarah Sarkar, Henry Ford HealthFollow
Jamie Fitzgerald, Henry Ford HealthFollow
Dipak Maskey, Henry Ford HealthFollow
Adrian Ormsby, Henry Ford HealthFollow
Yuvraj Sharma, Henry Ford HealthFollow
Pablo A. Ortiz, Henry Ford HealthFollow

Recommended Citation

Caceres P, Savickas G, Murray S, Umanath K, Uduman J, Yee J, Liao TD, Bolin S, Levin A, Khan M, Sarkar S, Fitzgerald J, Maskey D, Ormsby A, Sharma Y, and Ortiz P. High SARS-CoV-2 Viral Load in Urine Sediment Correlates with Acute Kidney Injury and Poor COVID-19 Outcome. J Am Soc Nephrol 2021.

Document Type

Article

Publication Date

6-4-2021

Publication Title

Journal of the American Society of Nephrology : JASN

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.

PubMed ID

34088853

ePublication

ePub ahead of print