Proliferative Glomerulonephritis With Monoclonal IgG Deposits Recurs or May Develop De Novo in Kidney Allografts

Albawardi, Alia; Satoskar, Anjali A.; Visger, Jon Von; Brodsky, Sergey V.; Nadasdy, Gyongyi; Nádasdy, Tibor

doi:10.1053/j.ajkd.2011.05.003

Cited by 37 publications

(51 citation statements)

References 7 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Our previous demonstration that all three constant domains of the IgG molecule are present suggests that there is glomerular deposition of a circulating nondeleted monoclonal IgG molecule followed by fixation of complement and activation of downstream inflammatory mediators that promote glomerular leukocyte infiltration and proliferation (5,16). In all four patients with PGNMID reported here, the IgG subtype deposited in glomeruli was IgG3, which is the isoform identified in most native kidney biopsies of PGNMID (6,13). This subtype, which comprises only 8% of IgG in the serum of normal individuals, has the unique physicochemical property of self-aggregability via Fc-Fc interactions (18,19).…”

Section: Discussionmentioning

confidence: 51%

“…On follow-up available in 32 of our 37 previously reported patients, 37.5% recovered renal function, 37.5% developed persistent renal dysfunction, and 22% progressed to ESRD (6). Over 40 additional patients with PGNMID in the native kidney have been reported by other groups (7)(8)(9)(10)(11)(12)(13)(14)(15)(16). Except for a single case reported in abstract form (13), recurrent PGNMID in the renal allograft has not been described in the literature.…”

Section: Introductionmentioning

confidence: 81%

“…Albawardi et al recently described in abstract form 16 cases of PGNMID, two of which occurred in the renal transplant, one as de novo disease, and one as recurrent disease (13). The de novo disease was diagnosed 13 years posttransplant in a patient with ESRD secondary to polycystic kidney disease.…”

Section: Discussionmentioning

confidence: 99%

“…Over 40 additional patients with PGNMID in the native kidney have been reported by other groups (7)(8)(9)(10)(11)(12)(13)(14)(15)(16). Except for a single case reported in abstract form (13), recurrent PGNMID in the renal allograft has not been described in the literature. Here we present the clinical-pathologic features and outcome of four patients with recurrent PGNMID in the renal allograft.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Proliferative Glomerulonephritis with Monoclonal IgG Deposits Recurs in the Allograft

Nasr

Sethi²,

Cornell³

et al. 2011

Clinical Journal of the American Society of Nephrology

124

118

View full text Add to dashboard Cite

SummaryBackground and objectives Proliferative GN with monoclonal IgG deposits (PGNMID) is a newly described entity resembling immune complex GN. Its potential to recur in the allograft is undefined.Design, setting, participants, & measurements The first cases of recurrent PGNMID in the allograft are reported. ResultsThe cohort includes four Caucasians (3 women, 1 man) with a mean age 58.5 years. No patient had M spike or hematologic malignancy. Recurrence was first documented by biopsy at a mean of 3.8 months posttransplant for indications of renal insufficiency in four patients, proteinuria in three patients, and microhematuria in three patients. Monoclonal IgG deposits (3 IgG3 and 1 IgG3) in the transplants had identical heavy-and light-chain isotypes as in the native kidneys. In two patients, a pattern of endocapillary GN was identified in the native and transplant biopsies, whereas two patients with membranoproliferative GN in the native kidney developed endocapillary or mesangial GN in the transplant. Recurrence was treated with combined high-dose prednisone plus rituximab (n ϭ 3) or plus cyclophosphamide (n ϭ 1). After a mean posttransplant follow-up of 43 months, all four patients achieved reduction in proteinuria and three had reduction in creatinine. Repeat biopsies showed reduced histologic activity after treatment.Conclusions PGNMID can recur in the transplant despite the absence of a serum M spike. Recurrence is heralded by proteinuria, hematuria, and allograft dysfunction and manifests diverse histologic patterns. Although the pathogenesis remains unknown, early immunosuppressive therapy appears to stabilize the course.

show abstract

Section: Discussionmentioning

confidence: 51%

Section: Introductionmentioning

confidence: 81%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Proliferative Glomerulonephritis with Monoclonal IgG Deposits Recurs in the Allograft

Nasr

Sethi²,

Cornell³

et al. 2011

Clinical Journal of the American Society of Nephrology

124

118

View full text Add to dashboard Cite

show abstract

“…Thus, PGNMID in kidney allografts can recur frequently [4][5][6], although its recurrence rate is uncertain due to its rarity. The recurrence of PGN-MID is usually detected at 3-5 months after transplantation using episode biopsies [4][5][6], whereas the timing of recurrence of MPGN varies from 1 week to several years after transplantation [7][8][9]. The renal prognosis is usually favorable, with the exception of cases with concurrent infection [5].…”

mentioning

confidence: 99%

Recurrent proliferative glomerulonephritis with monoclonal immunoglobulin G deposits leads to rapid graft loss after kidney transplantation: a case report

et al. 2013

View full text Add to dashboard Cite

We present a case of recurrent proliferative glomerulonephritis with monoclonal immunoglobulin G (IgG) deposits (PGNMID) that progressed rapidly to allograft failure. A 56-year-old man had progressed to end-stage renal failure within 1 year after the diagnosis of membranoproliferative glomerulonephritis (MPGN) by kidney biopsy. He underwent living donor kidney transplantation from his brother 6 months later. Serial allograft biopsies revealed early glomerular deposition of IgG, C1q, and C3 at post-operative day 26, and gradual progression of the glomerular deposition and histology of glomerulonephritis. Several immunosuppressive therapies did not prevent proteinuria, microhematuria, and graft dysfunction, and the patient returned to hemodialysis at 7 months after transplantation. Retrospectively, we demonstrated monoclonal IgG3κ deposition in the native and allograft kidney, and the patient was diagnosed with recurrent PGNMID. The serial graft biopsies revealed the pathological details of the progression of PGNMID. This is a rare case of PGNMID that recurred and progressed rapidly to graft failure after kidney transplantation.

show abstract

Non-Randall Glomerulonephritis with Non-Organized Monoclonal Ig Deposits

Ronco¹,

Karras²,

Plaisier³

2015

Current Clinical Pathology

View full text Add to dashboard Cite

Proliferative Glomerulonephritis With Monoclonal IgG Deposits Recurs or May Develop De Novo in Kidney Allografts

Cited by 37 publications

References 7 publications

Proliferative Glomerulonephritis with Monoclonal IgG Deposits Recurs in the Allograft

Proliferative Glomerulonephritis with Monoclonal IgG Deposits Recurs in the Allograft

Recurrent proliferative glomerulonephritis with monoclonal immunoglobulin G deposits leads to rapid graft loss after kidney transplantation: a case report

Non-Randall Glomerulonephritis with Non-Organized Monoclonal Ig Deposits

Contact Info

Product

Resources

About