Amyloidosis is a protein folding disease that causes organ injuries and even death. In humans, 42 proteins are now known to cause amyloidosis. Some proteins become amyloidogenic as a result of a pathogenic variant as seen in hereditary amyloidoses. In acquired forms of amyloidosis, the proteins form amyloid in their wild-type state. Four types (serum amyloid A (AA), transthyretin (ATTR), apolipoprotein AIV (ApoAIV), and beta-2-macroglobulin (AB2m)) of amyloid can occur either as acquired or as a mutant. Iatrogenic amyloid from injected protein medications have also been reported and AIL1RAP (anakinra) has been recently found to involve the kidney. Finally, the mechanism of how leukocyte cell derived chemotaxin-2 (ALECT2) forms amyloid remains unknown. This paper will review amyloids that involve the kidney and how they are typed.

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2024 年肾淀粉样变性的分类、病因和分型更新

淀粉样变性是一种蛋白质折叠疾病，会导致器官损伤甚至死亡。目前已知有 42 种蛋白质会导致人类淀粉样变性。一些蛋白质由于致病性变异而产生淀粉样变，如遗传性淀粉样变性中所见。在获得性淀粉样变性中，蛋白质在野生型状态下形成淀粉样蛋白。淀粉样蛋白有四种类型（血清淀粉样蛋白 A (AA)、运甲状腺素蛋白 (ATTR)、载脂蛋白 AIV (ApoAIV) 和 β-2-巨球蛋白 (AB2m)），可以是获得性的，也可以是突变型的。注射蛋白质药物引起的医源性淀粉样蛋白也有报道，最近发现 AIL1RAP（阿那白滞素）涉及肾脏。最后，白细胞衍生的趋化因子-2 (ALECT2) 如何形成淀粉样蛋白的机制仍不清楚。本文将回顾涉及肾脏的淀粉样蛋白及其类型。