Idiopathic minimal lesion nephrotic syndrome (IMLNS) was proposed to be a disorder of T-cell dysfunction by Shalhoub in 1974. The mechanisms by which T-cells increase glomerular permeability have remained elusive (and unproven). There is evidence that IMLNS may be due to a circulating factor released from activated T-cells. In recent years, efforts have been made to identify this pathogenetic cytokine as well as to understand the mechanism(s) for the increased release of this factor. This review attempts to critically analyze the available published data. Using different methodologies, investigators have focused on the production of cytokines in patients with IMLNS during relapse and remission. This has resulted in a plethora of data without definitive conclusions. The pathogenetic cytokine has not been identified, and it is questionable whether there is a Th2 dominance in IMLNS. The review of the available data illustrates the difficulties encountered when one is studying the cytokine secretory pattern in patients with IMLNS. Differences in patient population, type of cells studies, sample preservation, and methodology used to measure cytokines are some of the factors that could account for the disparity of observed results.

中文翻译：

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期望未实现的情况。特发性小病变肾病综合征的细胞因子。

1974年，Shalhoub提出特发性小病灶性肾病综合征（IMLNS）是T细胞功能障碍的一种疾病。T细胞增加肾小球通透性的机制仍不清楚（尚未证实）。有证据表明IMLNS可能是由于活化T细胞释放的循环因子引起的。近年来，已努力鉴定该病原性细胞因子以及了解增加该因子释放的机制。本文试图对可用的公开数据进行严格分析。研究人员使用不同的方法，专注于IMLNS患者复发和缓解期间细胞因子的产生。这导致了大量的数据，没有确定的结论。尚未确定致病细胞因子，令人怀疑的是，IMLINS中是否存在Th2优势。对可用数据的回顾说明了在研究IMLNS患者的细胞因子分泌模式时遇到的困难。患者人群，细胞研究类型，样品保存以及用于测量细胞因子的方法的差异是造成观察结果差异的一些因素。