Proximal tubular dysfunction in patients with COVID-19: what have we learnt so far?

Abstract

Recent studies have reported a variety of urine abnormalities in patients hospitalized due to severe acute respiratory syndrome coronavirus 2 infection. In a single-center study from Belgium, Werion et al. present a concise investigation of tubular dysfunction in patients with coronavirus disease 2019, identifying potential risk factors for increased disease severity. These data complement current evidence regarding severe acute respiratory syndrome coronavirus 2 presence and potential infection in the kidney.

Figure 1

Potential pathophysiological mechanisms driving coronavirus disease 2019 (COVID-19)–related proximal tubular dysfunction. To date, 3 pathomechanisms, including viral entry and infection, cytokine-mediated injury, and hemodynamic factors and ischemia, appear to be most plausible to cause proximal tubular dysfunction in patients with COVID-19. While each of them can explain tubular dysfunction, it is also possible that these factors coexist and interact with each other during the complex clinical course of COVID-19. In the cohort investigated by Werion et al., these functional alterations included low molecular weight (LMW) proteinuria, inadequate handling of uric acid or phosphate, and the loss of neutral amino acids into the urine.