Abstract: TH-PO0345
Potential IgAN Biomarkers from the Glycine, Serine, and Threonine Metabolism Pathway
Session Information
- Glomerular Diseases: Omics
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology
Author
- Ji, Catherine, miRcore, Ann Arbor, Michigan, United States
Background
IgA Nephropathy (IgAN) is a chronic autoimmune disease caused by the buildup of immunoglobulin A in the glomeruli. Symptoms however are often not felt until late into the disease progression and can ultimately lead to kidney failure. There is no cure to the disease, though medicine can slow down inflammation or reduce organ stress by treating hypertension. Due to the complexity of the kidney, researchers and medical professionals struggle with pre-diagnosis and are still searching for biomarkers for disease predisposition.
Methods
The dataset GSE93798 from Gene Expression Omnibus (GEO) was analyzed using GEO2R. The dataset compared 20 samples of IgAN and 22 samples of normal patient gene expression data from the glomeruli of kidney biopsies. The 741 genes with a LogFC above 0.5 were inputted in string-db, and it was shown that the glycine, serine, and threonine metabolism pathway (FDR: 8.38E-07) had 13 of the 38 genes upregulated in IgAN patients. The pathway was further analyzed in the KEGG pathway and genes BHMT and CTH were examined.
Results
Pathway analysis of the glycine, serine, and threonine metabolism showed common genes BHMT and CTH that were upregulated in the IgAN cohort compared to the control cohort in the dataset. BHMT was significantly upregulated, having a 1.38 LogFC and an adjusted p-value of 7.89E-09. It encodes for a cytosolic enzyme that catalyzes betaine and homocysteine into methionine and dimethylglycine. CTH was upregulated with a 1.01 LogFC and adjusted p-value of 4.24E-11. It encodes for a cytoplasmic enzyme that converts cystathione into methionine and cysteine.
Conclusion
Elevated methionine levels have been linked to oxidative stress and metabolic burden for the renal system. It is also implicated in the overproduction of sulfuric acid and cysteine, which also contribute to increased renal stress. The upregulation of BHMT in IgAN patients increases methionine concentration while CTH's upregulation raises the rate of production for both methionine and cysteine, both of which may contribute to kidney damage. CTH and BHMT are potential biomarkers worthy of further exploration in the diagnosis and tracking of the onset of IgAN.