Glomerulopathy with mesangial IgM deposits: Long‐term follow up of 64 children

Zeis, Petros M.; Kavazarakis, Emmanuel; Nakopoulou, Lydia; Moustaki, Maria; Messaritaki, A.; Zeis, M. P.; Nicolaidou, Polyxeni

doi:10.1046/j.1442-200x.2001.01396.x

Cited by 46 publications

(42 citation statements)

References 23 publications

(66 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This pattern was also noted in one third of the cases in our study (Mubarak et al, 2011). Still other investigators have reported progression of IgMN cases with minor changes or mesangial proliferation into FSGS on repeat biopsies (Myllimaki et al, 2003;Zeis et al, 2001). We have observed one case each of florid crescentic GN and a case of collapsing FSGS as a morphologic expression of IgMN (unpublished data).…”

Section: Light Microscopysupporting

confidence: 83%

Update on IgM Nephropathy

Kazi¹,

Mubarak²

2012

Topics in Renal Biopsy and Pathology

View full text Add to dashboard Cite

Section: Light Microscopysupporting

confidence: 83%

Update on IgM Nephropathy

Kazi¹,

Mubarak²

2012

Topics in Renal Biopsy and Pathology

View full text Add to dashboard Cite

“…Some series, however, have shown that the presence of IgM is of prognostic significance. 9,10 Furthermore, recent reports suggest that rituximab, a mAb to CD20 that depletes mature B cells, may be beneficial in some patients with the nephrotic syndrome. [11][12][13][14][15][16] However, the mechanisms by which rituximab alleviates the nephrotic syndrome are not yet known.…”

mentioning

confidence: 99%

IgM Contributes to Glomerular Injury in FSGS

Strassheim

Renner

Panzer

et al. 2013

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Glomerular IgM and C3 deposits frequently accompany idiopathic FSGS and secondary glomerulosclerosis, but it is unknown whether IgM activates complement, possibly contributing to the pathogenesis of these diseases. We hypothesized that IgM natural antibody binds to neoepitopes exposed in the glomerulus after nonimmune insults, triggering activation of the complement system and further injury. We examined the effects of depleting B cells, using three different strategies, on adriamycin-induced glomerulosclerosis. First, we treated wild-type mice with an anti-murine CD20 antibody, which depletes B cells, before disease induction. Second, we evaluated adriamycin-induced glomerulosclerosis in Jh mice, a strain that lacks mature B cells. Third, we locally depleted peritoneal B cells via hypotonic shock before disease induction. All three strategies reduced deposition of IgM in the glomerulus after administration of adriamycin and attenuated the development of albuminuria. Furthermore, we found that glomerular IgM and C3 were detectable in a subset of patients with FSGS; C3 was present as an activation fragment and colocalized with glomerular IgM, suggesting that glomerular IgM may have bound a cognate ligand. Taken together, these results suggest that IgM activates the complement system within the glomerulus in an animal model of glomerulosclerosis. Strategies that reduce IgM natural antibody or that prevent complement activation may slow the progression of glomerulosclerosis.

show abstract

“…The disease, like IgA nephropathy (IgAN), is defined by its immunohistologic features: the presence of IgM as the sole or dominant immunoglobulin in the mesangial regions of the glomeruli in a diffuse (all glomeruli) and global (the entire glomerulus) distribution [4][5][6][7] . Its incidence varies, in accordance with different series, between 4.8% and 8.6% of all renal biopsies, affecting all ages and without predilection for gender [6,8,9,10] . Some authors report a higher frequency of glucocorticoidresistance or glucocorticoid-dependence with relatively few cases of complete remission [2,11,12] .…”

Section: Introductionmentioning

confidence: 57%