Table 3.
Biologics | Source | Rationale |
Galactose deficient IgA1 | Serum | Core antigen of the pathogenic IgA1 immune complex; leads to activation of mesangial cells and glomerulonephritis |
Glycan-specific IgG | Serum | Form glycan-dependent complex with galactose-deficient IgA1; alanine to serine substitution in complementary-determining region 3 of IgG heavy chain; able to differentiate IgA nephropathy patients from controls with 88% specificity and 95% sensitivity |
Activated complement C3 | Serum | Up-regulated level in 30% of patients; correlated with deteriorating renal function |
FGF 23 | Serum | FGF23 serum levels are significantly associated with IgAN progression |
Soluble CD89 | Serum | Low levels in patients with disease progression compared with those without disease progression |
Mannose-binding lectin | Urine | Significantly higher in patients than healthy controls; associated with histopathologic aggravations such as mesangial hypercellularity, tubular atrophy, interstitial fibrosis |
EGF and MCP-1 | Urine | An EGF/MCP-1 ratio greater than 366.66 extends renal survival to at least 84 mo in a cohort of 44 patients |
Proteomic pattern | Urine | High throughput characterization of 2000 polypeptide using capillary electrophoresis on-line coupled to a mass spectrometer |
microRNA profile | Urine | Sequencing identified microRNA profiling that is specific to IgA nephropathy |
IgA1: Immunoglobulin A1; IgG: Immunoglobulin G; FGF23: Fibroblast growth factor 23; IgAN: Immunoglobulin a nephritis; RNA: Ribonucleic acid; EGF: Epidermal growth factor; MCP-1: Monocyte chemotactic peptide-1.