Short-term responsiveness of membranous glomerulopathy to cyclosporine.
Short-term responsiveness of membranous glomerulopathy to cyclosporine.
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DOI：
10.1016/s0272-6386(12)70259-7
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发表时间：
1992-11
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影响因子：
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通讯作者：
A. Guasch;M. Suranyi;L. Newton;B. Hall;B. Myers
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作者：
A. Guasch;M. Suranyi;L. Newton;B. Hall;B. Myers
我们给膜性肾小球病（MG）肾病患者服用环孢素（CsA）（4 - 6 mg/kg/24 h），疗程12周。以伴有微小病变肾病（MCN）的肾病患者作为对照组。我们评估了CsA对蛋白尿、肾小球功能和培养的外周血单个核细胞释放细胞因子的影响。MCN患者蛋白尿在2 ~ 4周内恢复正常。14例MG患者中有10例的蛋白尿从肾病水平降至亚肾病水平（<3，500 mg/24 h），也是在治疗开始后2 - 4周内。四名无反应者表现出快速进展和可能不可逆的MG形式，最终导致肾衰竭。平均而言，MG患者的白蛋白和IgG清除率分别下降了59%和73%（P< 0.005）; MCN患者相应下降了99%（P <0.0001）。相应的肾小球滤过率在每个肾小球损伤保持不变。在这两种疾病中，CsA停药后蛋白尿复发的强烈趋势是明显的。在CsA治疗前后，培养的单个核细胞释放的肿瘤坏死因子（TNF）-α在每个肾小球损伤中均增加。我们的结论是，在大多数情况下，MG的蛋白尿表现出的反应，CsA是定性相似，但不完全比，在MCN。屏障功能改善的速度表明MG中细胞介导的免疫损伤可能起作用。
We administered a 12-week course of cyclosporine (CsA) (4 to 6 mg/kg/24 h) to nephrotic patients with membranous glomerulopathy (MG). Nephrotic patients with minimal change nephropathy (MCN) served as a comparison group. We evaluated the effects of CsA on proteinuria, glomerular function, and the release of cytokines by peripheral blood mononuclear cells in culture. Proteinuria was restored to normal levels within 2 to 4 weeks in MCN. Proteinuria declined from nephrotic to subnephrotic levels (<3,500 mg j24 h) in 10 of 14 patients with MG, also within 2 to 4 weeks of onset of therapy. The four nonresponders exhibited a rapidly progressive and presumably irreversible form of MG culminating in renal failure. On average, fractional clearances of albumin and IgG declined by 59% and 73% in MG (P< 0.005); corresponding declines in MCN were by 99% (P < .0001). Corresponding rates of glomerular filtration in each glomerular injury remained unchanged. A strong trend for proteinuria to relapse after CsA was withdrawn was evident in both disorders. The release of tumor necrosis factor (TNF)-α by mononuclear cells in culture was enhanced in each glomerular injury, both before and after the course of CsA. We conclude that the proteinuria in most cases of MG exhibits a responsiveness to CsA that is qualitatively similar to, but less complete than, that in MCN. The rapidity with which barrier function improves suggests a possible role for cell-mediated immune injury in MG.