Long-term immunosuppressive therapy of idiopathic membranoproliferative glomerulonephritis

Orłowski, T; Rancewicz, Z; M, Lao; Juskowa, J; Klepacka, Joanna; Gradowska, L; Morzycka-Michalik, W.; Glyda, J

doi:10.1007/bf01733447

Cited by 9 publications

(3 citation statements)

References 10 publications

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“…Evidence-based recommendations for the treatment of idiopathic MCGN [12] attributed grade A evidence (based on overview of randomized controlled trials with no heterogeneity) [17] to the use of high-dose alternate-day steroids for children presenting with nephrotic range proteinuria (>3 g/day) or impaired renal function. The evidence for this recommendation is predominantly based on the International Study of Kidney Disease in Children (ISKDC) [5] as well as other smaller studies that have corroborated the use of steroids [9,[18][19][20]. The ISKDC study [5] is the largest randomized controlled trial and recruited 80 children with MCGN, a creatinine clearance >70 ml/min/1.73 m 2 and proteinuria !40 mg/h/m 2 .…”

Section: Discussionmentioning

confidence: 99%

Prognosis, treatment and outcome of childhood mesangiocapillary (membranoproliferative) glomerulonephritis

Cansick¹

2004

Nephrology Dialysis Transplantation

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Section: Discussionmentioning

confidence: 99%

Prognosis, treatment and outcome of childhood mesangiocapillary (membranoproliferative) glomerulonephritis

Cansick¹

2004

Nephrology Dialysis Transplantation

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“…Such cases are treated with the classic scheme of methyl‐prednizolone (1 g intravenously for three consecutive days), followed by oral prednisone (1 mg/kg/day body weight) and cyclophosphamide . The use of cyclophosphamide in the treatment of MPGN is not clearly documented, although it is the most widely used, as the use of other agents is very limited . There is only one randomized trial, in which, 59 patients with MPGN were assigned to cyclophosphamide, warfarin, and dipyridamole or to no therapy .…”

Section: Treatment Of Glomerular Diseasementioning

confidence: 99%

Understanding the complement‐mediated glomerular diseases: focus on membranoproliferative glomerulonephritis and C3 glomerulopathies

Lionaki

Gakiopoulou

Boletis

2016

APMIS

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An enhanced understanding of the role of complement in the pathogenesis of membranoproliferative glomerulonephritis has led to reclassification of the latter into immunoglobulin-mediated and non-immunoglobulin-mediated disease. The new classification schema resulted in improved diagnostic clinical algorithms, while it brought into light again the diseases, which are characterized by the presence of glomerular deposits, composed predominantly by C3, in the absence of significant amounts of immunoglobulins in renal biopsy, namely, C3 glomerulopathies (dense deposit disease and C3 glomerulonephritis). Despite the lack of randomized controlled trials following the advances in the understanding of the pathogenetic pathways involved in membranoproliferative glomerulonephritis, it is important that the new mechanistic approach has opened new roads for the exploration and discovery of targeted therapies.

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“…Available studies using combined immunosuppressive regimens including steroids, cyclophosphamide and chlorambucil as well as dipyridamole and warfarin in adult idiopathic MPGN has, to date, not shown a convincing benefit, and side effects have outweighed clinical improvement [5][6][7].…”

Section: Discussionmentioning

confidence: 98%

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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Long-term immunosuppressive therapy of idiopathic membranoproliferative glomerulonephritis

Cited by 9 publications

References 10 publications

Prognosis, treatment and outcome of childhood mesangiocapillary (membranoproliferative) glomerulonephritis

Prognosis, treatment and outcome of childhood mesangiocapillary (membranoproliferative) glomerulonephritis

Understanding the complement‐mediated glomerular diseases: focus on membranoproliferative glomerulonephritis and C3 glomerulopathies

Remission of resistant MPGN type I with mycophenolate mofetil and steroids

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