Mechanisms of Light Chain Injury along the Tubular Nephron
Mechanisms of Light Chain Injury along the Tubular Nephron
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DOI：
10.1681/asn.2012040388
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发表时间：
2012-11-01
影响因子：
13.6
通讯作者：
Sanders, Paul W.
中科院分区：
文献类型：
--
作者：
Sanders, Paul W.
肾小管肾单位负责包括IG游离轻链的过滤的低分子量蛋白质的重吸收和催化。在浆细胞恶液质的情况下，大量的游离轻链，现在是单克隆蛋白质，存在于肾小管肾单位中进行处置。结果可能是阿基、进行性CKD和终末期肾病形式的临床肾功能不全。在这里，我回顾了这些过程中的机制，导致肾小管损伤，包括近端小管病变和管型肾病。
The tubular nephron is responsible for reabsorption and catabolism of filtered low molecular weight proteins that include Ig free light chains. In the setting of a plasma cell dyscrasia, significant amounts of free light chains, now monoclonal proteins, present to the tubular nephron for disposal. The result may be clinical renal dysfunction in the form of AKI, progressive CKD, and end-stage kidney disease. Here, I review the mechanisms involved in these processes that result in tubular injury, including proximal tubulopathy and cast nephropathy.