Recurrence of Membranoproliferative Glomerulonephritis Type II in Renal Allografts

Braun, Michael C.; Stablein, Don; Hamiwka, Lorraine; Bell, Lorraine; Bartosh, Sharon M.; Strife, C. Frederic

doi:10.1681/asn.2005020175

Cited by 121 publications

(69 citation statements)

References 31 publications

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“…11 DDD has a high rate of recurrence after kidney transplantation and results in graft failure in up to 50% of patients, with graft loss occurring within 2.5 years of transplantation. 10,12,13 With regards to C3GN, we noted a recurrence rate of 66.7%, with graft failure in 50% of rC3GN. Thus, the rates of recurrence and graft failure are comparable with DDD.…”

Section: Discussionmentioning

confidence: 78%

“…The median time to recurrence was 28 months, and the median time to graft failure of 77 months after transplantation seems to be longer than DDD. 12 Regarding pathology, native kidney biopsy of C3GN more often shows an MPGN (nine cases) and less commonly shows a diffuse proliferative/postinfectious GN (three cases) pattern of injury. 14 However, rC3GN often shows a mesangial proliferative (eight cases) or membranoproliferative pattern (six cases) of injury.…”

Section: Discussionmentioning

confidence: 99%

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Clinical Findings, Pathology, and Outcomes of C3GN after Kidney Transplantation

Zand

Lorenz

Cosio

et al. 2014

Journal of the American Society of Nephrology

139

109

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C3 glomerulonephritis (C3GN) results from abnormalities in the alternative pathway of complement, and it is characterized by deposition of C3 with absent or scant Ig deposition. In many patients, C3GN progresses to ESRD. The clinical features, pathology, and outcomes of patients with C3GN receiving kidney transplantation are unknown. Between 1996 and 2010, we identified 21 patients at our institution who received a kidney transplant because of ESRD from C3GN. The median age at the time of initial diagnosis of C3GN at kidney biopsy was 20.8 years. The median time from native kidney biopsy to dialysis or transplantation was 42.3 months. Of 21 patients, 14 (66.7%) patients developed recurrent C3GN in the allograft. The median time to recurrence of disease was 28 months. Graft failure occurred in 50% of patients with recurrent C3GN, with a median time of 77 months to graft failure post-transplantation. The remaining 50% of patients had functioning grafts, with a median follow-up of 73.9 months. The majority of patients had hematuria and proteinuria at time of recurrence. Three (21%) patients were positive for monoclonal gammopathy and had a faster rate of recurrence and graft loss. Kidney biopsy at the time of recurrence showed mesangial proliferative GN in eight patients and membranoproliferative GN in six patients. All allograft kidney biopsies showed bright C3 staining (2-3+), with six biopsies also showing trace/1+ staining for IgM and/or IgG. To summarize, C3GN recurs in 66.7% of patients, and one half of the patients experience graft failure caused by recurrence.

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Section: Discussionmentioning

confidence: 78%

Section: Discussionmentioning

confidence: 99%

Clinical Findings, Pathology, and Outcomes of C3GN after Kidney Transplantation

Zand

Lorenz

Cosio

et al. 2014

Journal of the American Society of Nephrology

139

109

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“…MPGN associated with monoclonal gammopathy seems to have an earlier recurrence with a more aggressive course. Interestingly, recurrence of MPGN in renal allografts is associated with the presence of crescents in the native kidneys as well as the allograft (34).…”

Section: Recurrence Post-transplantationmentioning

confidence: 99%

Update on Membranoproliferative GN

Masani

Jhaveri²,

Fishbane³

2014

Clinical Journal of the American Society of Nephrology

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Membranoproliferative GN represents a pattern of injury seen on light microscopy. Historically, findings on electron microscopy have been used to further subclassify this pathologic entity. Recent advances in understanding of the underlying pathobiology have led to a proposed classification scheme based on immunofluorescence findings. Dysregulation of the complement system has been shown to be a major risk factor for the development of a membranoproliferative GN pattern of injury on kidney biopsy. Evaluation and treatment of this complex disorder rest on defining the underlying mechanisms.

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“…Progression toward ESRD occurs in .50% of patients within 10 years of diagnosis, with younger patients more prone to development of ESRD than older patients (4). Finally, recurrence of DDD after kidney transplantation is common (5,6).…”

Section: Introductionmentioning

confidence: 99%

Eculizumab in Pediatric Dense Deposit Disease

Oosterveld¹,

Garrelfs²,

Höppe

et al. 2015

Clinical Journal of the American Society of Nephrology

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Background and objectives Dense deposit disease (DDD), a subtype of C3 glomerulopathy, is a rare disease affecting mostly children. Treatment options are limited. Debate exists whether eculizumab, a monoclonal antibody against complement factor C5, is effective in DDD. Reported data are scarce, especially in children.Design, setting, participants, & measurements The authors analyzed clinical and histologic data of five pediatric patients with a native kidney biopsy diagnosis of DDD. Patients received eculizumab as therapy of last resort for severe nephritic or nephrotic syndrome with alternative pathway complement activation; this therapy was given only when the patients had not or only marginally responded to immunosuppressive therapy. Outcome measures were kidney function, proteinuria, and urine analysis.Results In all, seven disease episodes were treated with eculizumab (six episodes of severe nephritic syndrome [two of which required dialysis] and one nephrotic syndrome episode). Median age at treatment start was 8.4 (range, 5.9-13) years. For three treatment episodes, eculizumab was the sole immunosuppressive treatment. In all patients, both proteinuria and renal function improved significantly within 12 weeks of treatment (median urinary protein-to-creatinine ratio of 8.5 [range, 2.2-17] versus 1.1 [range, 0.2-2.0] g/g, P,0.005, and eGFR of 58 [range, 17-114] versus 77 [range, 50-129] ml/min per 1.73 m 2 , P,0.01). A striking finding was the disappearance of leukocyturia within 1 week after the first eculizumab dose in all five episodes with leukocyturia at treatment initiation.Conclusions In this case series of pediatric patients with DDD, eculizumab treatment was associated with reduction in proteinuria and increase in eGFR. Leukocyturia resolved within 1 week of initiation of eculizumab treatment. These results underscore the need for a randomized trial of eculizumab in DDD.

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Recurrence of Membranoproliferative Glomerulonephritis Type II in Renal Allografts

Cited by 121 publications

References 31 publications

Clinical Findings, Pathology, and Outcomes of C3GN after Kidney Transplantation

Clinical Findings, Pathology, and Outcomes of C3GN after Kidney Transplantation

Update on Membranoproliferative GN

Eculizumab in Pediatric Dense Deposit Disease

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