ELEVATED LEVELS OF TUMOR-NECROSIS-FACTOR-ALPHA IN THE NEPHROTIC SYNDROME IN HUMANS
ELEVATED LEVELS OF TUMOR-NECROSIS-FACTOR-ALPHA IN THE NEPHROTIC SYNDROME IN HUMANS
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DOI：
10.1016/s0272-6386(12)80742-6
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发表时间：
1993-03-01
影响因子：
13.2
通讯作者：
MYERS, BD
中科院分区：
文献类型：
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作者：
SURANYI, MG;GUASCH, A;MYERS, BD
为探讨细胞因子在肾病综合征肾小球损伤中的作用，检测了原发性肾病综合征患者外周血中白细胞介素1β、白细胞介素2、干扰素α、干扰素γ、肿瘤坏死因子α的水平。这些患者在活检中有微小病变肾病(MCN)、局灶性和节段性肾小球硬化(FSGS)或膜性肾病(MN)。用免疫放射分析法检测细胞因子水平，标本包括血浆、尿液和丝裂原刺激的外周血单个核细胞(PBMC)培养上清液。只有肿瘤坏死因子-α在FSGS和MN患者的血浆和尿液中显著升高，高于健康对照组和MN患者。肿瘤坏死因子-a的升高与肾病综合征的长度或严重程度或体重减轻没有相关性。IL-1β、IL-2、干扰素-α、干扰素-γ水平未见升高。在培养中，来自三组肾病患者的丝裂原刺激的PBMC与对照组相比释放了过量的肿瘤坏死因子-α，这一反应在所测量的其他细胞因子中并不一致。这项对肾病患者细胞因子水平的调查结果支持这样一种可能性，即肿瘤坏死因子-α可能在人类肾小球屏障功能障碍的诱导或维持中发挥致病作用。
To investigate the possible role of cytokines in the mediation of glomerular injury in the nephrotic syndrome, the levels of interleukin (IL)-1β, IL-2, interferon (IFN)-α, IFN-γ, and tumor necrosis factor-α (TNF-α) were measured in patients with primary nephrotic syndrome. These patients had minimal change nephropathy (MCN), focal and segmental glomerulosclerosis (FSGS), or membranous nephropathy (MN) on biopsy. Cytokine levels were assessed by immunoradiometric assays, and specimens consisted of plasma, urine, and the culture supernate of mitogen-stimulated peripheral blood mononuclear cells (PBMC). Only TNF-α was found to be significantly elevated, in the plasma and urine of patients with FSGS and MN, above that found in healthy control subjects and patients with MCN. The elevation of TNF-a could not be shown to correlate with the length or severity of the nephrotic syndrome or with loss of body mass. IL-1β, IL-2, IFN-α, and IFN-γ levels were not elevated. In culture, mitogen-stimulated PBMC from all three groups of nephrotic subjects released an excess of TNF-α compared with controls, a response not consistently observed for the other cytokines measured. The findings of this survey of cytokine levels in nephrotic patients support the possibility that TNF-α may play a pathogenic role in the induction or maintenance of glomerular barrier dysfunction in humans.