Iorember Franca, Aviles Diego
Division of Pediatric Nephrology, Department of Pediatrics, Louisiana State University Health Sciences Center, 200 Henry Clay Avenue, Rm 4241, Now Orleans, LA, 70118, USA.
Pediatr Nephrol. 2017 Aug;32(8):1323-1330. doi: 10.1007/s00467-016-3555-6. Epub 2016 Dec 21.
Nephrotic syndrome is one of the most common glomerular diseases that affect in children. Complications may occur in nephrotic syndrome as a result of the disease itself as well as its treatment. Most of these complications result from excessive urinary protein losses, and control of proteinuria is the most effective treatment strategy. Anemia is one of the many complications seen in patients with persistent nephrotic syndrome and may occur as a result of excessive urinary losses of iron, transferrin, erythropoietin, transcobalamin and/or metals. This leads to a deficiency of substrates necessary for effective erythropoiesis, requiring supplementation in order to correct the anemia. Supplementation of iron and erythropoietin alone often does not lead to correction of the anemia, suggesting other possible mechanisms which need further investigation. A clear understanding of the pathophysiologic mechanisms of anemia in nephrotic syndrome is necessary to guide appropriate therapy, but only limited evidence is currently available on the precise etiologic mechanisms of anemia in nephrotic syndrome. In this review we focus on the current state of knowledge on the pathogenesis of anemia in nephrotic syndrome.
肾病综合征是儿童中最常见的肾小球疾病之一。肾病综合征可能因其疾病本身及其治疗而出现并发症。这些并发症大多源于尿蛋白过度流失,控制蛋白尿是最有效的治疗策略。贫血是持续性肾病综合征患者中出现的众多并发症之一,可能是由于铁、转铁蛋白、促红细胞生成素、钴胺素和/或金属的尿中过度流失所致。这导致有效红细胞生成所需的底物缺乏,需要补充以纠正贫血。仅补充铁和促红细胞生成素往往无法纠正贫血,这表明还存在其他可能的机制,需要进一步研究。清楚了解肾病综合征贫血的病理生理机制对于指导恰当治疗很有必要,但目前关于肾病综合征贫血的确切病因机制仅有有限的证据。在本综述中,我们重点关注肾病综合征贫血发病机制的当前知识状况。