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Abstract: SA-PO0831

Population-Level Associations Between C3 Glomerulopathy (C3GN), COVID-19 Disease (C19D), and Vaccination (C19V)

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics

Authors

  • Liu, Song, The University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States
  • Garcia, Pablo, The University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States
  • Singh, Namita, The University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States
  • de Leoz, Josephine B., The University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States
  • Iftikhar, Nimra, The University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States
  • Mir, Hamza, The University of New Mexico Health Sciences Center, Albuquerque, New Mexico, United States
  • Argyropoulos, Christos, University of New Mexico Clinical and Translational Science Center, Albuquerque, New Mexico, United States
Background

C3GN is caused by dysregulation of the alternative complement pathway (ACP), while SARS-CoV-2 infection is recognized to activate all three complement pathways. Several case reports have described relapsing C3GN following C19D and de-novo C3GN after C19V, but the association between C3GN, C19D,and C19V remains poorly defined at the population level.

Methods

We included all patients who had a C19 test and the C3GN ICD10 codes (N0*.A) between 3/1/20-3/31/24 in any US institute in the TrinetX federated database . C19V, & C19D were assessed by +ve results in respiratory panel testing (RPT) and the vaccination records. We used a Self Controlled Case Series (BMJ 2016;354:i4515) to analyze the temporal risk of repeat C19D and C19V on the appearance of N0*.A.

Results

Out of 14M patients with RPT, 115 met the inclusion criteria (figure). Age was 36.8 ± 24, 48.7 % of patients were female and 63% were white. There was no temporal association between C19 vaccination and the incidence of a new N0*.A code (RR of 0.94 per 6 months of follow up, 95% CI 0.69 - 1.27, p = 0.69). However, there was an increased risk of a new N0*.A following a C19D episode (RR 1.87 / 6 months of follow up, 95% CI 1.24 - 2.81, p =0.003)..

Conclusion

In this exploratory analysis C19D, but not C19V was associated with a higher temporal risk of C3GN, suggesting the possibility of viral persistence underlying this association. Whether this will translate to a higher burden of disease is unknown. Future studies should explore the mechanism of this association, including investigation of the complement pathway in those with kidney laboratory abnormalities after C19D. Limitations include undercoding of C3GN, small sample size and lack of the biopsy reports to corroborate the ICD10 code.

Funding

  • Other NIH Support – DCI, Inc

Digital Object Identifier (DOI)