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IgA Nephropathy Studies

The GIGA-kids Study (Genomics of IgA-related disorders in kids Study) is a multicenter collaborative study based at Columbia University and sponsored by the Midwest Pediatric Nephrology Consortium (MWPNC). The study aims to recruit over 1,000 children with IgA nephropathy or Henoch-Schönlein purpura (with or without nephritis) for the purpose of genetic, genomic and biomarker studies.

IgA nephropathy represents the leading cause of kidney failure among young adults. Henoch-Schönlein purpura is a related disorder with skin manifestations that frequently leads to nephropathy in children. Our prior genetic studies suggest that patients carrying more risk alleles have an earlier onset of disease. Accordingly, GIGA-kids extends our genetic investigations to pediatric patients, aiming to validate the known disease markers and to discover new genetic and biochemical predictors of disease that may be specific to children.

Cure Glomerulonephropathy (CureGN) is a multicenter five-year cohort study of glomerular disease patients funded by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) at the National Institutes for Health (NIH) and NephCure Kidney International (NKI).

The CureGN project will study 2,400 children and adults with the following glomerular diseases: minimal change disease (MCD), focal segmental glomerulosclerosis (FSGS), membranous nephropathy (MN), and IgA nephropathy (IGAN).

Participants will be followed longitudinally to better understand the causes of disease, response to therapy, and disease progression, with the ultimate objective to cure glomerulonephropathy.

 
 

References

  • Hall, Y.N., Fuentes, E.F., Chertow, G.M. et al. Race/ethnicity and disease severity in IgA nephropathy. BMC Nephrol 5, 10 (2004). https://doi.org/10.1186/1471-2369-5-10
  • Kiryluk K, Li Y, Sanna-Cherchi S, Rohanizadegan M, Suzuki H, et al. (2012) Geographic Differences in Genetic Susceptibility to IgA Nephropathy: GWAS Replication Study and Geospatial Risk Analysis. PLoS Genet 8(6): e1002765. doi:10.1371/journal.pgen.1002765