Wickens Olivia, Rengarajan Sharmilee, Chinnadurai Rajkumar, Ford Ian, Macdougall Iain C, Kalra Philip A, Sinha Smeeta
Salford Royal Hospital, Northern Care Alliance NHS Foundation Trust, Salford M6 8HD, UK.
Faculty of Biology, Medicine and Health, University of Manchester, Manchester M13 9PL, UK.
J Clin Med. 2022 Sep 29;11(19):5779. doi: 10.3390/jcm11195779.
Calcific uraemic arteriolopathy (CUA), also known as calciphylaxis, is a rare and often fatal condition, frequently diagnosed in end-stage renal disease (ESRD) patients. Although exact pathogenesis remains unclear, iron supplementation is suggested as a potential risk factor. Iron and erythropoietin are the main stay of treatment for anaemia in ESRD patients. Few observational studies support the role of iron in the pathogenesis of calciphylaxis although data from the pivotal trial was not strongly supportive of this argument, i.e., no difference in incidence of calciphylaxis between the low-dose and high-dose iron treatment arms. Elevated levels of vascular cell adhesion molecules in association with iron excess were postulated to the pathogenesis of CUA by causing inflammation and calcification within the microvasculature. In-addition, oxidative stress generated because of iron deposition in cases of systemic inflammation, such as those seen in ESRD, may play a role in vascular calcification. Despite these arguments, a direct correlation between cumulative iron exposure with CUA incidence is not clearly demonstrated in the literature. Consequently, we do not have evidence to recommend iron reduction or cessation in ESRD patients that develop CUA.
钙化性尿毒症小动脉病（CUA），也称为钙化防御，是一种罕见且往往致命的疾病，常见于终末期肾病（ESRD）患者。尽管确切发病机制尚不清楚，但补铁被认为是一个潜在危险因素。铁和促红细胞生成素是ESRD患者贫血治疗的主要手段。虽然关键试验的数据并不强烈支持这一观点，但很少有观察性研究支持铁在钙化防御发病机制中的作用，即低剂量和高剂量铁治疗组之间钙化防御的发生率没有差异。血管细胞粘附分子水平升高与铁过量有关，被认为通过引起微血管内的炎症和钙化而导致CUA的发病机制。此外，在系统性炎症（如ESRD患者所见）中，由于铁沉积产生的氧化应激可能在血管钙化中起作用。尽管有这些观点，但文献中并未明确证明累积铁暴露与CUA发病率之间存在直接关联。因此，对于发生CUA的ESRD患者，我们没有证据建议减少或停止补铁。
