Remission of membranoproliferative glomerulonephritis type I with the use of tacrolimus

Haddad, Maha; Lau, Keith K.; Butani, Lavjay

doi:10.1007/s00467-007-0523-1

Cited by 20 publications

(6 citation statements)

References 17 publications

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“…On the contrary the rate of complete remission after 10 months was 79% in an (uncontrolled) observational study of 19 patients by Faedda et al [24]. Only limited data from small case series are available for mycophenolate mofetil [25], cyclosporine A [26], and tacrolimus [27] for treatment of immunoglobulin-associated MPGN. Both C3GN and DDD are extremely rare diseases and data on treatment are even more limited than for immunoglobulin-associated or idiopathic MPGN.…”

Section: Clinicopathological Features and Treatment Of Mpgnmentioning

confidence: 99%

Rituximab for Treatment of Membranoproliferative Glomerulonephritis and C3 Glomerulopathies

Rudnicki

2017

BioMed Research International

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Membranoproliferative glomerulonephritis (MPGN) is a histological pattern of injury resulting from predominantly subendothelial and mesangial deposition of immunoglobulins or complement factors with subsequent inflammation and proliferation particularly of the glomerular basement membrane. Recent classification of MPGN is based on pathogenesis dividing MPGN into immunoglobulin-associated MPGN and complement-mediated C3 glomerulonephritis (C3GN) and dense deposit disease (DDD). Current guidelines suggest treatment with steroids, cytotoxic agents with or without plasmapheresis only for subjects with progressive disease, that is, nephrotic range proteinuria and decline of renal function. Rituximab, a chimeric B-cell depleting anti-CD20 antibody, has emerged in the last decade as a treatment option for patients with primary glomerular diseases such as minimal change disease, focal-segmental glomerulosclerosis, or idiopathic membranous nephropathy. However, data on the use of rituximab in MPGN, C3GN, and DDD are limited to case reports and retrospective case series. Patients with immunoglobulin-associated and idiopathic MPGN who were treated with rituximab showed partial and complete responses in the majorities of cases. However, rituximab was not effective in few cases of C3GN and DDD. Despite promising results in immunoglobulin-associated and idiopathic MPGN, current evidence on this treatment remains weak, and controlled and prospective data are urgently needed.

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Section: Clinicopathological Features and Treatment Of Mpgnmentioning

confidence: 99%

Rituximab for Treatment of Membranoproliferative Glomerulonephritis and C3 Glomerulopathies

Rudnicki

2017

BioMed Research International

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“…Both children achieved rapid and complete remission; however, the second child had a relapse 24 months later [8].…”

Section: Discussionmentioning

confidence: 97%

Remission of resistant MPGN type I with mycophenolate mofetil and steroids

Al-Nabhani

Thorner

et al. 2009

Pediatr Nephrol

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Very few studies have been published on how to treat children with membranoproliferative glomerulonephritis type I (MPGN I), and as yet there is only one report on the use of mycophenolate mofetil (MMF) in children with MPGN I. We report a 12-year-old boy who presented with edema, hypertension, nephrotic range proteinuria, and microscopic hematuria following an upper respiratory tract infection. Laboratory tests revealed a serum creatinine of 90 micromol/l, albumin of 20 g/l, and a C3 of 0.11 g/l (normal range: 0.7-1.4). Renal biopsy showed the presence of MPGN I. Upon failure to induce remission with prednisone, we started the patient on MMF at 500 mg/day (300 mg/m(2)), increasing up to a final dose of 2 g/day (1200 mg/m(2)), with a MMF metabolite mycophenolic acid (MPA) target range of 2-5 mg/l. Prednisone was subsequently reduced to alternate day therapy and gradually weaned to 7.5 mg on alternate days over 9 months. Within 4 months of starting MMF therapy, there was significant improvement in serum creatinine (decrease from 156 to 64 micromol/l), serum albumin (increase from 23 to 40 g/l), and proteinuria (decrease from 13 g/day to 40 mg/day). Twelve months following the introduction of MMF into his therapeutic regimen, he remains in remission with no further relapses. In summary, this case suggests that there may be potential benefit for use of MMF in children with refractory MPGN I, which supports the rationale for prospectively evaluating MMF treatment in a treatment trial of refractory MPGN I.

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“…There is no evidence-based guideline on how we should treat patients with DDD/ MPGN II who fail to respond to corticosteroids. Based on our recent success in treating two other patients with MPGN type I with tacrolimus, we anecdotally treated our patient using the same approach [18].…”

Section: Discussionmentioning

confidence: 98%

Dense deposit disease and the factor H H402 allele

Lau

Smith

Kolbeck³

et al. 2008

Clin Exp Nephrol

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Herein, we describe the case of an 8-year-old boy who presented with a nephritic nephrotic syndrome. His laboratory investigation was significant for a persistently low serum complement 3 level. A renal biopsy was performed, based on which, he was diagnosed with dense deposit disease/membranoproliferative glomerulonephritis type II (DDD/MPGN II). He was treated with alternate-day oral corticosteroids, angiotensin-converting enzyme (ACE) inhibitors and tacrolimus. Factor H mutational analysis showed the Y402H and I62V allele polymorphisms. The purpose of our report is to discuss the association of the H402 allele variant of factor H with the DDD/MPGN II phenotype and its possible therapeutic implications.

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Remission of membranoproliferative glomerulonephritis type I with the use of tacrolimus

Cited by 20 publications

References 17 publications

Rituximab for Treatment of Membranoproliferative Glomerulonephritis and C3 Glomerulopathies

Rituximab for Treatment of Membranoproliferative Glomerulonephritis and C3 Glomerulopathies

Remission of resistant MPGN type I with mycophenolate mofetil and steroids

Dense deposit disease and the factor H H402 allele

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