Inflammatory stress in SARS-COV-2 associated Acute Kidney Injury

Int J Biol Sci. 2021 Apr 10;17(6):1497-1506. doi: 10.7150/ijbs.58791. eCollection 2021.


Increasing clinical evidence shows that acute kidney injury (AKI) is a common and severe complication in critically ill COVID-19 patients. The older age, the severity of COVID-19 infection, the ethnicity, and the history of smoking, diabetes, hypertension, and cardiovascular disease are the risk factor for AKI in COVID-19 patients. Of them, inflammation may be a key player in the pathogenesis of AKI in patients with COVID-19. It is highly possible that SARS-COV-2 infection may trigger the activation of multiple inflammatory pathways including angiotensin II, cytokine storm such as interleukin-6 (IL-6), C-reactive protein (CRP), TGF-β signaling, complement activation, and lung-kidney crosstalk to cause AKI. Thus, treatments by targeting these inflammatory molecules and pathways with a monoclonal antibody against IL-6 (Tocilizumab), C3 inhibitor AMY-101, anti-C5 antibody, anti-TGF-β OT-101, and the use of CRRT in critically ill patients may represent as novel and specific therapies for AKI in COVID-19 patients.

Keywords: AKI; COVID-19; cytokines; inflammation; mechanisms.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Acute Kidney Injury / epidemiology
  • Acute Kidney Injury / etiology*
  • Acute Kidney Injury / therapy
  • COVID-19 / complications*
  • COVID-19 / virology
  • Complement Activation
  • Cytokine Release Syndrome
  • Diabetes Complications / metabolism
  • Humans
  • Inflammation / etiology*
  • Renal Replacement Therapy
  • SARS-CoV-2 / isolation & purification*
  • Stress, Physiological*