Mycophenolate mofetil for systemic vasculitis and IgA nephropathy

Nowack, Rainer; Birck, Rainer; Woude, Fokko J. van der

doi:10.1016/s0140-6736(05)60198-5

Cited by 139 publications

(52 citation statements)

References 5 publications

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“…[7] However, some pilot data suggested that MMF could affect the clinical course of recurrent IgA nephropathy. [16] Our study found that of these patients who had been diagnosed as IgA nephropathy before 2000, the majority of them were administered the triple regimens of CsA+Azp+Pred, and only two cases received the regimen of CsA+MMF+Pred. Similar to Kowalewska's patients, [12] there was only one who received MMF therapy of eight recurrent IgA nephropathy patients with crescent formation.…”

Section: Discussionmentioning

confidence: 70%

Recurrent or De Novo IgA Nephropathy with Crescent Formation after Renal Transplantation

Tang

Chen

et al. 2008

Renal Failure

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Section: Discussionmentioning

confidence: 70%

Recurrent or De Novo IgA Nephropathy with Crescent Formation after Renal Transplantation

Tang

Chen

et al. 2008

Renal Failure

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“…6 Compared with azathioprine, MMF seems to be a more powerful immunosuppressive drug. 7 It has been used in the setting of kidney, 7 liver, 17 heart, 18 and lung 19 transplantation and in the treatment of autoimmune diseases, such as Wegener' s granulomatosis, microscopic polyangiitis, immunoglobulin A nephropathy, 20 and other glomerular diseases. 21 In the setting of OLT, the use of MMF seems to allow a reduction in cyclosporine or tacrolimus dose and therefore decreased toxicity.…”

Section: Discussionmentioning

confidence: 99%

Conversion of liver transplant recipients on cyclosporine with renal impairment to mycophenolate mofetil

et al. 1999

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The management of liver transplant recipients with renal function impairment remains controversial because cyclosporine withdrawal from triple immunosuppression regimens may be followed by graft rejection. A nonnephrotoxic and powerful immunosuppressant such as mycophenolate mofetil (MMF) could allow a reduction of cyclosporine dosage or its withdrawal and an improvement in renal function in these patients. Eleven patients with serum creatinine levels greater than 1.5 mg/dL, normal graft function, and a rejection-free period of at least 1 year started MMF at a dose of 2000 mg/d (reduced in case of adverse events) while cyclosporine dosage was slowly reduced. At last follow-up (63 ؎ 5 weeks), 7 patients remained free of cyclosporine (6 of those patients are also free of steroids), 2 patients reduced their cyclosporine dose, and 2 patients developed mild acute rejection that responded to a switch to tacrolimus therapy. Serum creatinine and urea levels in the 7 patients free of cyclosporine decreased from 2.22 ؎ 0.13 to 1.90 ؎ 0.19 mg/dL (P ‫؍‬ .05) and 0.95 ؎ 0.10 to 0.60 ؎ 0.10 g/L (P F .001), respectively. Creatinine clearance increased from 38.16 ؎ 5.60 to 47.01 ؎ 6.76 mL/min (P ‫؍‬ .005). Control of arterial hypertension also improved. Tolerance to MMF was good, but 6 patients required dose reductions, mainly because of asymptomatic anemia. In conclusion, in liver transplant recipients with stable graft function, MMF may allow cyclosporine dose reduction or discontinuation, thus improving renal function and the control of arterial hypertension. This change of treatment must be carefully monitored because of the frequent need for MMF dose reduction and the risk for rejection.

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“…In all patients, remission was achieved, with only one relapse after 14 mo. Successful MMF treatment of IgA nephritis and Goodpasture syndrome has also been reported in anecdotal form (26,58). In the study by Choi and co-workers (11), patients with membranoproliferative glomerulonephritis and IgA nephropathy also experienced improvement with MMF treatment.…”

Section: Beneficial Effects Of Mmf In Immunemediated Nephropathiesmentioning

confidence: 91%

Experimental and clinical rationale for use of MMF in nontransplant progressive nephropathies

Zatz

Noronha

Fujihara

2002

American Journal of Physiology-Renal Physiology

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The incidence of progressive nephropathies and, consequently, the population suffering from end-stage renal disease have increased steadily in recent years, posing an ever-growing cost, in both human and financial terms, to society. There is mounting evidence that, in both immune-mediated and nonimmune-mediated chronic nephropathies, renal inflammatory events are key to the propagation and perpetuation of renal injury. Mycophenolate mofetil (MMF) is an antilymphocyte agent recently introduced in clinical practice for the prevention of allograft rejection. The present review discusses clinical and experimental evidence that the anti-inflammatory action of MMF can be advantageously used to arrest immune- and nonimmune-mediated progressive injury of native kidneys as well.

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Mycophenolate mofetil for systemic vasculitis and IgA nephropathy

Cited by 139 publications

References 5 publications

Recurrent or De Novo IgA Nephropathy with Crescent Formation after Renal Transplantation

Recurrent or De Novo IgA Nephropathy with Crescent Formation after Renal Transplantation

Conversion of liver transplant recipients on cyclosporine with renal impairment to mycophenolate mofetil

Experimental and clinical rationale for use of MMF in nontransplant progressive nephropathies

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