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The pathogenesis and diagnosis of acute kidney injury in multiple myeloma

机译:多发性骨髓瘤急性肾损伤的发病机制和诊断

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Renal failure remains a principal cause of morbidity for patients with multiple myeloma. Once reversible factors such as hypercalcemia have been corrected, the most common cause of severe renal failure in these patients is a tubulointerstitial pathology that results from the very high circulating concentrations of monoclonal immunoglobulin free light chains. These endogenous proteins can result in isolated proximal tubule cell cytotoxicity, tubulointerstitial nephritis and cast nephropathy (myeloma kidney). Less frequently, high levels of free light chains can lead to immunoglobulin light chain amyloidosis and light chain deposition disease, although these conditions are usually associated with insidious progression of renal failure rather than acute kidney injury. Unless there is rapid intervention, progressive and irreversible damage occurs, particularly interstitial fibrosis and tubular atrophy. Despite advances in our understanding of the pathogenesis of these processes there has been a gap in translating these achievements into improved patient outcomes. The International Kidney and Monoclonal Gammopathy Research Group was formed to address this need. In this Review, we discuss the mechanisms of disease and diagnostic approaches to patients with acute kidney injury complicating multiple myeloma.
机译:肾衰竭仍然是多发性骨髓瘤患者发病的主要原因。一旦纠正了可逆性因素,例如高钙血症,这些患者中严重肾衰竭的最常见原因是肾小管间质病变,这是由于单克隆免疫球蛋白游离轻链的循环浓度很高所致。这些内源性蛋白质可导致孤立的近端肾小管细胞毒性,肾小管间质性肾炎和铸型肾病(骨髓瘤肾)。较少的情况是,高水平的游离轻链可导致免疫球蛋白轻链淀粉样变性和轻链沉积病,尽管这些疾病通常与肾功能衰竭的隐性进展而不是急性肾损伤有关。除非进行快速干预,否则会发生进行性和不可逆转的损伤,尤其是间质纤维化和肾小管萎缩。尽管我们对这些过程的发病机理有了新的了解,但在将这些成就转化为改善的患者预后方面仍存在差距。为了解决这一需求,成立了国际肾脏和单克隆丙种球蛋白病研究小组。在这篇综述中,我们讨论了急性肾脏损伤并发多发性骨髓瘤的患者的疾病机制和诊断方法。

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