Distribution pattern of mesangial C4d deposits as predictor of kidney failure in IgA nephropathy

IgA1 Protease Treatment Reverses Mesangial Deposits and Hematuria in a Model of IgA Nephropathy.

IgA nephropathy (IgAN), characterized by mesangial IgA1 deposits, is a leading cause of renal failure worldwide. IgAN pathogenesis involves circulating hypogalactosylated IgA1 complexed with soluble IgA Fc receptor I (sCD89) and/or anti-hypogalactosylated-IgA1 autoantibodies, but no specific treatment is available for IgAN. The absence of IgA1 and CD89 homologs in the mouse has precluded in viv...

Association of C4d deposition with clinical outcomes in IgA nephropathy.

BACKGROUND AND OBJECTIVES Several studies have suggested that activation of the complement system is a contributing pathogenic mechanism in IgA nephropathy (IgAN). C4d staining is an inexpensive and easy-to-perform method for the analysis of renal biopsies. This study aimed to assess the clinical and prognostic implications of C4d staining in IgAN. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENT...

Mesangial Proliferation in Murine Experimental IgA Nephropathy

The therapeutic effects of saccharolytic and proteolytic enzymes were investigated in models of IgA nephropathy. Mesangial glomerulonephritis was induced in mice by intravenous injection of preformed soluble immune complexes of dextran sulfate and either IgA (J 558) or IgM (MOPC 104 E) antidextran MAb (passive model) or by immunization with DEAE dextran (active model). In the passive model, onl...

C4d in IgA nephropathy: a marker sans boundaries

I gA nephropathy (IgAN) is the most common glomerulopathy worldwide (1). In the long-term, the disease is characterized by the development of end-stage renal disease (ESRD) in around 40% of cases at 20-year of follow-up (2,3). The rate of development of this complication varies, and in the majority of cases, the disease slowly progresses to this stage. In a minority of cases, the disease presen...

Silicosis associated with crescentic IgA mesangial nephropathy.