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Abstract: PO0663

Acute Tubular Injury in Patients with Severe COVID-19 Infection

Session Information

Category: Coronavirus (COVID-19)

  • 000 Coronavirus (COVID-19)

Authors

  • Fukao, Yusuke, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Nagasawa, Hajime, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Nihei, Yoshihito, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Ueda, Seiji, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Kihara, Masao, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Gohda, Tomohito, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
  • Suzuki, Yusuke, Department of Nephrology, Juntendo University Faculty of Medicine, Tokyo, Japan
Background

Novel coronavirus, severe acute syndrome coronavirus 2 (SARS-CoV-2), has rapidly spread all over the world. SARS-CoV-2 enters host target via angiotensin-converting enzyme-2 which are ubiquitously expressed in many organs including proximal tubules in kidney. Indeed, autopsy cases with coronavirus disease-2019 (COVID-19) revealed the existence of coronavirus particles in the renal tubular epithelium. Several reports have shown COVID-19-associated acute kidney injury (AKI), however involvements of SARS-CoV2 in tubular injury has not been fully understood. Here, we evaluated tubular injury in patients with severe and non-severe COVID19.

Methods

We investigated the relationship between urinary levels of tubule markers (NAG, β2-MG, α1MG, and L-FABP) and laboratory markers in 17 COVID-19 patients without chronic kidney disease on admission. We also analyzed the relationship between the laboratory markers and respiratory status in severe (n=7) or non-severe (n=10) COVID-19 patients which were defined by requirements of supplemental oxygen.

Results

Although only 2 patients developed AKI in severe cases, serum Interleukin-6 (IL-6) level significantly increased in all of severe patients and correlated with levels of proteinuria (R2=0.37, p=0.01), NAG (R2=0.41, p=0.006), α1MG (R2=0.47, p=0.007), L-FABP (R2=0.57, p=0.001) on admission. In addition, severe patients had significantly higher levels of proteinuria (severe: 0.67 vs non-severe: 0.14g/gCr), NAG (33.3 vs 10.1U/L), β2MG (17134.4 vs 1168.5μg/L), α1MG (63.6 vs 12.4mg/L), L-FABP (57.9 vs 7.5μg/gCr) as compared to non-severe cases. Proteinuria and elevated tubular markers were observed only in 2 and 6 cases respectively in non-severe patients, despite those were found in all severe cases.

Conclusion

We found that acute tubular injury was associated with the severity of COVID-19 infection. Since the pathophysiological hallmark of COVID-19 is severe systemic inflammation, it remains obscure whether progressive damage of tubules in SARS-CoV-2 is the result of direct viral infection, ischemic injury, or exposure of any humoral factors. Further large scaled studies focusing on tubular damage should be needed to elucidate underlying mechanisms of renal complication in COVID-19 infection.