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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

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)

Authors

  • Caceres, Paulo S., Henry Ford Hospital, Detroit, Michigan, United States
  • Savickas, Gina, Henry Ford Hospital, Detroit, Michigan, United States
  • Uduman, Junior, Henry Ford Hospital, Detroit, Michigan, United States
  • Umanath, Kausik, Henry Ford Hospital, Detroit, Michigan, United States
  • Sharma, Yuvraj, Henry Ford Hospital, Detroit, Michigan, United States
  • Yee, Jerry, Henry Ford Hospital, Detroit, Michigan, United States
  • Murray, Shannon, Henry Ford Hospital, Detroit, Michigan, United States
  • Sarkar, Sarah, Henry Ford Hospital, Detroit, Michigan, United States
  • Fitzgerald, Jamie, Henry Ford Hospital, Detroit, Michigan, United States
  • Maskey, Dipak, Henry Ford Hospital, Detroit, Michigan, United States
  • Ormsby, Adrian, Henry Ford Hospital, Detroit, Michigan, United States
  • Ortiz, Pablo A., Henry Ford Hospital, Detroit, Michigan, United States
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