Treatment with cyclosporin of patients with idiopathic nephrotic syndrome

Meyrier, Alain

doi:10.1007/bf00197220

Cited by 15 publications

(9 citation statements)

References 37 publications

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“…It is beyond the scope of this study to analyze in detail the arguments in favor of an immunological origin of nephrosis. Despite the absence of definitive demonstration, much clinical, experimental and biochemical evidence has been adduced to support the role of secretion of a lymphokine by the patient's lymphocytes [3,11,[24][25][26][27][28][29][30]. This lymphokine would be the humoral factor which modifies the electronegativity of the glomerular basement membrane, thereby inducing massive albuminuria.…”

Section: Commentsmentioning

confidence: 99%

Ciclosporin in the Treatment of Nephrosis

Meyrier

1989

Am J Nephrol

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Section: Commentsmentioning

confidence: 99%

Ciclosporin in the Treatment of Nephrosis

Meyrier

1989

Am J Nephrol

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“…From our experiences in the treatment of children with idiopathic nephrotic syndrome and those of other preliminary reports [4,7,12,13,15], we conclude that:…”

Section: Discussionmentioning

confidence: 77%

Ciclosporin in Idiopathic Nephrotic Syndrome of Children

Brodehl¹,

Hoyer²

1989

Am J Nephrol

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“…CsA and tacrolimus have been used extensively to treat steroid-resistant nephrotic syndrome (13,24). Gregory et al (13) treated 22 children who had steroid-resistant nephrotic syndrome with CsA for 8 wk and was able to induce a complete remission in Ͼ87% of patients.…”

Section: Discussionmentioning

confidence: 99%

“…The high rates of recurrent glomerulonephritis have led many clinicians to extend the duration of CsA treatment, thus contributing to the development of calcineurin nephrotoxicity (13,14,24). To determine the time course of CsA nephrotoxicity, Meyrier et al (24) performed serial renal biopsies in patients with FSGS and noted that after 2 yr of therapy, glomerulosclerosis and interstitial fibrosis were detectable in up to 20% of patients.…”

Section: Discussionmentioning

confidence: 99%

A Prospective, Open-Label Trial of Sirolimus in the Treatment of Focal Segmental Glomerulosclerosis

Tumlin

Miller²,

Near³

et al. 2006

Clinical Journal of the American Society of Nephrology

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Calcineurin inhibitors are effective therapy for steroid-resistant focal segmental glomerulosclerosis (FSGS) but are associated with significant morbidity and nephrotoxicity. Sirolimus is a novel immunosuppressive agent that is structurally related to tacrolimus but demonstrates no long-term nephrotoxicity. For determination of the efficacy of sirolimus in reducing proteinuria, a prospective, open-label trial was conducted of 21 patients with idiopathic, steroid-resistant FSGS. A complete response was defined as <300 mg protein/24 h after 6 mo, whereas a partial response was defined as a 50% reduction in baseline proteinuria. After 6 mo of therapy, sirolimus induced complete remission in four (19%) of 21 patients and partial remissions in eight (38%). Among sirolimus-responsive patients, 6 mo of therapy decreased proteinuria from a mean of 8.8 ؎ 1.7 to 2.1 ؎ 0.5 g/24 h (P ‫؍‬ 0.0003). In responsive patients, GFR was maintained (45 ؎ 6 versus 47 ؎ 7 ml/min per 1.73 m 2 at 6 mo) throughout the study, whereas nonresponders tended to decrease (31 ؎ 4 versus 28 ؎ 5 ml/min per 1.73 m 2 ). Using dextran sieving analysis, complete or partial response was associated with an increase in the glomerular ultrafiltration coefficient (K f , 7 ؎ 1. versus 8 ؎ 0.9 units at 6 mo; P < 0.05). Glomerular permselectivity and K f tended to decrease in nonresponders (8.2 ؎ 1.9 versus 6.2 ؎ 1.3 units at 6 mo; P ‫؍‬ 0.07). Patients with complete remission had a higher GFR (45 ؎ 6 versus 31 ؎ 4 ml/min per 1.73 m 2 ) at the end of 6 mo compared with nonresponders. In patients with steroid-resistant FSGS, sirolimus reduced proteinuria and glomerular pore size and increased K f in patients with steroid-resistant FSGS.Clin J Am Soc Nephrol 1: 109 -116, 2006. doi: 10.2215/CJN.00120605 P rimary focal segmental glomerulosclerosis (FSGS) is a significant cause of the nephrotic syndrome within adult and pediatric populations (1). Recent epidemiologic studies demonstrated that the incidence of FSGS has increased significantly over the past 2 decades and now accounts for Ͼ35% of all cases of adult-onset nephrotic syndrome (1,2). Black individuals are two-to four-fold more likely to develop FSGS compared with age-matched white individuals and are at increased risk for progression to ESRD (2,3).The pathogenesis of FSGS is unknown, but numerous human and animal model studies suggest that alteration in podocyte structure and function is central to the development of the disorder (4). The de-differentiation and proliferation of podocytes leads to effacement of footplate processes, detachment of podocytes from glomerular basement membranes, and expansion of the mesangial matrix (4 -7). The resulting loss of glomerular barrier function allows for massive proteinuria, sclerosis, and adhesions of the glomerular tuft to Bowman's capsule (8). Other data suggest that cytokines such as TGF-␤ or the presence of circulating vascular permeability factors contribute to footplate effacement and glomerular sclerosis (9,10).Oral steroids remain the primary therapy for ...

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Treatment with cyclosporin of patients with idiopathic nephrotic syndrome

Cited by 15 publications

References 37 publications

Ciclosporin in the Treatment of Nephrosis

Ciclosporin in the Treatment of Nephrosis

Ciclosporin in Idiopathic Nephrotic Syndrome of Children

A Prospective, Open-Label Trial of Sirolimus in the Treatment of Focal Segmental Glomerulosclerosis

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