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Complement activation and increased expression of Syk, mucin-1 and CaMK4 in kidneys of patients with COVID-19

Simin Jamaly1, Maria G Tsokos2, Rhea Bhargava2

  • 1Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, United States; Department of Medical Biology, Faculty of Health Science, UiT Arctic University of Norway, N-9037 Tromsø, Norway.

Clinical Immunology (Orlando, Fla.)
|July 12, 2021
PubMed

Insights

COVID-19 kidney injury involves complement activation and increased expression of spleen tyrosine kinase (Syk), mucin-1 (MUC1), and CaMK4. Targeting these molecules may offer new COVID-19 treatments.

Area of Science:

  • Nephrology
  • Immunology
  • Virology

Background:

  • Acute and chronic kidney failure are frequent complications in COVID-19 patients.
  • The precise mechanisms driving COVID-19-associated kidney injury and associated risk factors are not fully understood.

Observation:

  • Kidney tissues from deceased COVID-19 patients were analyzed for complement components (C1q, C3, FH, C5b-9) and immunoglobulin deposition.
  • Expression levels of injury-associated molecules, including spleen tyrosine kinase (Syk), mucin-1 (MUC1), and calcium/calmodulin-dependent protein kinase IV (CaMK4), were assessed.

Findings:

  • Elevated deposition of complement components (C1q, C3, C5b-9) and total immunoglobulin was observed in COVID-19 patient kidneys.
  • Significantly increased expression of Syk, MUC1, and CaMK4 was detected in the kidneys of individuals who died from COVID-19.

Implications:

  • These findings suggest a critical role for complement activation and specific molecular pathways in COVID-19 kidney pathology.
  • The study supports further clinical trials investigating inhibitors of C1q, C3, Syk, MUC1, and CaMK4 for treating COVID-19 patients with kidney complications.

Keywords:
COVID-19CaMK4Complement activationImmune complexesKidney injuryMUC1SARS-CoV-2Syk

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