[29-31] GalNAc exposure may induce the injury of podocyte and PTECs by mesangial-podocyte crosstalk and glomerulotubular crosstalk, respectively. Recently, Roberta et al. found that oxidative stress and galactose deficient IgA1 were markers of progression in IgA nephropathy.[32] Moldoveanu et al. using HAA to detect the GalNAc of serum IgA1, the sensitivity as a diagnostic test of IgAN was 76.5%, with specificity 94%.[12] Furthermore, cells secreting antibodies specific for Gal-deficient IgA1 can be easily detected and enumerated in peripheral blood from IgAN patients.[33] It was also shown

in our data that serum IgG concentration was higher in the GalNAc exposure more than the 40% group. Using a lectin-binding assay to detect GalNAc exposure of IgA1 in serum might have potential as a non-invasive predictive test for IgAN prognosis. However, whether the immunosuppressive treatment will change the GalNAc exposure Kinase Inhibitor Library mouse level needs to be confirmed in further

prospective therapeutic trials. Proteinuria has a particularly strong association with poor kidney prognosis in IgA nephropathy.[3, 34-36] Remission of proteinuria is an important predictor of renal survival. The correlation of proteinuria with GalNAc exposure is not well established yet. Recently, Hastings et al. found that GalNAc exposure was not associated with the proteinuria at presentation of paediatric IgAN.[37] However, in a research carried Sorafenib mouse out by Camilla et al., it was suggested that some weak correlations were indeed found between proteinuria and IgA galactose deficiency.[32] The proteinurias of both studies were detected once at the diagnosis of IgA nephropathy. Xie et al. demonstrated that proteinuria was strongly associated with the risk of end-stage renal disease in univariate analysis; however, it did not independently contribute to the risk in multivariate models.[35] Although

proteinuria at presentation is an important consideration, increasing evidence suggests that proteinuria overtime more closely correlates with disease outcome. Several studies suggest that regardless of the peak level of proteinuria, partial remission to protein Tryptophan synthase excretion <1/g will improve the renal progression.[38, 39] Repeated measurements of proteinuria averaged over time have been shown to predict GFR loss better than proteinuria at presentation in several studies. Expanded proteinuria evaluation beyond 1-time cross-sectional assessments at the time of diagnosis to include longitudinal measurements of proteinuria for improved quantification of disease activity and risks of progression are very important.[40, 41] The therapy of steroid and angiotensin converting enzyme inhibitor/ angiotensin receptor blocker (antagonist) (ACEI/ARB) could drastically improve the clinical parameters but could not affect the HAA-IgA levels.