Kidney Week

Abstract: SA-OR03

SARS-CoV-2 Detection in Urine Sediment Suggests Infection of Kidneys and Correlates with Risk of AKI and Poor COVID-19 Prognosis

Session Information

• Coronavirus: Research Abstracts
  October 24, 2020 | Location: Simulive
  Abstract Time: 05:00 PM - 07:00 PM

Category: Coronavirus (COVID-19)

• 000 Coronavirus (COVID-19)

Authors

• Caceres, Paulo S., Henry Ford Hospital, Detroit, Michigan, United States

Paulo S. Caceres, PhD



My research interests are in cellular mechanisms of polarity and solute transport in kidney epithelia, with particular emphasis in molecular interactions with surrounding tissues in health and disease.

• Savickas, Gina, Henry Ford Hospital, Detroit, Michigan, United States

Gina Savickas,

• Uduman, Junior, Henry Ford Hospital, Detroit, Michigan, United States

Junior Uduman,

• Umanath, Kausik, Henry Ford Hospital, Detroit, Michigan, United States

Kausik Umanath,

• Sharma, Yuvraj, Henry Ford Hospital, Detroit, Michigan, United States

Yuvraj Sharma,

• Yee, Jerry, Henry Ford Hospital, Detroit, Michigan, United States

Jerry Yee,

• Murray, Shannon, Henry Ford Hospital, Detroit, Michigan, United States

Shannon Murray,

• Sarkar, Sarah, Henry Ford Hospital, Detroit, Michigan, United States

Sarah Sarkar,

• Fitzgerald, Jamie, Henry Ford Hospital, Detroit, Michigan, United States

Jamie Fitzgerald,

• Maskey, Dipak, Henry Ford Hospital, Detroit, Michigan, United States

Dipak Maskey,

• Ormsby, Adrian, Henry Ford Hospital, Detroit, Michigan, United States

Adrian Ormsby,

• Ortiz, Pablo A., Henry Ford Hospital, Detroit, Michigan, United States

Pablo A. Ortiz,

Background

Since the emergence of the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), most of the focus has been on the respiratory failure caused by the resulting disease, COVID-19. However, the effects of COVID-19 in the kidney are increasingly recognized. Acute kidney injury (AKI) has been identified with varying prevalence around the world with higher rates (37-46%) reported in the USA. It is debatable whether AKI is an indirect consequence of systemic inflammation or a consequence of viral renal cell infection and tropism. We hypothesize that SARS-CoV-2 directly infects kidney tissue and increases the risk of developing AKI, worsening prognosis of COVID-19 patients.

Methods

We studied 88 COVID-19 patients admitted to the Henry Ford Hospital, Detroit after April 15, 2020. Demographics were: mean age 60, 71% African American, 55% male. We quantified viral copies by RT-PCR (S and N genes) in urine sediments from 52 PCR-confirmed COVID-19 patients. We performed immunofluorescence for Membrane and Spike viral proteins in two COVID-19 biopsies.

Results

The prevalence of AKI was 72%, with 32% of patients admitted to the ICU. The overall mortality rate was 14%, with no deaths in non-AKI patients. Viral proteins M and S were detected in the glomerulus, parietal cells and tubules of COVID-19 patients. In some tubules, positive SARS-CoV-2 overlapped with ACE2, the receptor for viral entry. Virus was detected in 61% of urine sediments, with 6-fold greater viral load in AKI-patient urines (copies/ng RNA: AKI, 7422±1338 vs No-AKI: 1523 ± 404; p<0.05, n=52). The highest viral loads were detected three weeks post-AKI at 11,374±2248 copies/ng RNA (p<0.01). Among COVID-19 AKI-patients who died, the urine viral load exceeded 8000 copies/ng RNA. Above this threshold, the mortality rate was 55%.

Conclusion

Our data support that direct viral renal cell infection occurs in COVID-19 AKI patients with urinary viral genome detection. Greater urinary viral loads portend increased mortality. Urinary viral detection can facilitate management and treatment of COVID-19 and improve outcomes. Future research should focus on studying whether urine contains infective virus or sheds non-infective genomic fragments.

Funding

• NIDDK Support