Few interesting points.
1. The presence of aberrantly glycosylated IgA1 in patients with this nephropathy was again confirmed. This usually happens at the GalNac site on the molecule of IgA.
2. This alteration alters the molecule and possibly could affect the binding to intrinsic mesangial glycoproteins and plasma proteins.
3. Using immortalized B cells from subjects with IgA nephropathy, and normal controls, investigators showed that the aberrant galactosylation in patients is nonrandomly distributed among the glycan residues and that the premature sialylation of the GalNac residues may interfere with the galactosylation of GalNac. These led to autoantibodies to GalNac. So, it seems that molecular mimicry from environmental agents maybe involved in the autoantibody response to the neo antigenic GalNac sites on the aberrant IgA.
4. RISK factors to predict IgA post transplant:- prior recurrence of disease and loss of graft from recurrence; rapidly progressive initial disease; use of zero mismatched donors; using a living related donor; lack of treatment with antilymphocyte or anti thymocyte as induction agents; and the presence of IgA deposits on transplant biopsy by zero hour of the transplant.
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