Nephrology and Dialysis Unit, Humanitas Clinical and Research Center, via Manzoni 56, 20089, Rozzano (Mi), Italy.
Clin Rev Allergy Immunol. 2017 Feb;52(1):99-107. doi: 10.1007/s12016-015-8524-5.
Renal involvement in idiopathic inflammatory myopathies is not as uncommon as was previously thought, as it develops in about one fifth of patients. Clinical presentation includes either acute kidney injury or chronic glomerulonephritis. The former usually develops abruptly during acute phases of rhabdomyolysis: in this case, kidney injury is caused by the toxic effects that myoglobinuria has on the kidney tubules, including cast formation and iron-induced oxidative stress and the development of a third space into the injured muscles. The latter instead has an autoimmune nature, a pleomorphic histological picture, and a more indolent course, with the exception of crescentic glomerulonephritis. Accurate diagnosis and management is crucial for these patients, as timely evaluation and treatment can prevent most of the complications. In the setting of rhabdomyolysis-induced acute kidney injury, the necessity of dialysis can be avoided through aggressive hydration and alkalinization, in order to force diuresis and avoid acidosis and hyperkalemia. In immune-mediated glomerulonephritis, renal biopsy is of undoubtedly value in the diagnostic process and can add prognostic and therapeutic information. In these forms, the development of chronic kidney disease can be prevented or at least delayed by the institution or modification of immunosuppressive treatment. Moreover, the use of drugs that inhibit the renin-angiotensin-aldosterone system and some lifestyle modifications, such as smoking cessation, weight loss, and salt restriction have also value in reducing proteinuria and the progression of kidney damage. In this review, we have summarized the currently available evidence and the different case series in an attempt to provide the readers with the most complete and practical notions that are needed to handle these delicate patients.
特发性炎性肌病的肾脏受累并不像以前认为的那样罕见,大约五分之一的患者会出现这种情况。临床表现包括急性肾损伤或慢性肾小球肾炎。前者通常在横纹肌溶解症的急性发作期间突然发生:在这种情况下,肌红蛋白尿对肾小管的毒性作用导致肾损伤,包括铸型形成、铁诱导的氧化应激以及第三间隙进入受损肌肉。后者则具有自身免疫性质、多形性组织学表现和更惰性的病程,新月体性肾小球肾炎除外。准确的诊断和管理对这些患者至关重要,因为及时的评估和治疗可以预防大多数并发症。在横纹肌溶解症引起的急性肾损伤中,通过积极的水化和碱化可以避免透析的必要性,以强制利尿并避免酸中毒和高钾血症。在免疫介导的肾小球肾炎中,肾活检在诊断过程中具有无可置疑的价值,并可以提供预后和治疗信息。在这些形式中,通过实施或修改免疫抑制治疗,可以预防或至少延迟慢性肾脏病的发展。此外,使用肾素-血管紧张素-醛固酮系统抑制剂和一些生活方式改变,如戒烟、减肥和限制盐摄入,也有助于减少蛋白尿和肾脏损伤的进展。在这篇综述中,我们总结了目前可用的证据和不同的病例系列,试图为读者提供处理这些敏感患者所需的最完整和实用的概念。