Management of Anemia and other Hematologic Derangements in Patients with Chronic Kidney Disease.

Iqra Ansari, Asfandyar Sheikh, Syed Salman Ahmed, Qamar Jabbar, Sajid Ali
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Abstract

Introduction: Chronic Kidney Disease (CKD) has adverse consequences on almost all body systems. The kidney does not function merely as an excretory organ, but participates in normal erythropoiesis, normal bone mineral deposition and blood pressure regulation.

Review: Anemia is prevalent in CKD with known deleterious effects on the car diovascular system. It is mostly due to erythropoietin deficiency, inhibition of erythropoiesis by uremic solutes, and reduction in red blood cell life span. Other possible causes include iron, B12 or folic acid deficiency or blood loss. Dysfunction of the endogenous erythropoietin is usually clinically evident once the glomerular filtration rate (GFR) falls below 20-25 ml/min. Treating anemia of CKD is based on correction of iron deficiency and replacement of decreased erythropoietin production by erythropoietin stimulating agents (ESA). Guidelines recommend targeting hemoglobin levels of no more than 10-12 g/dl since there is evidence of increased mortality and morbidity in patients with higher levels. Increased level of pro-coagulant biomarkers cause enhanced thrombotic activity in CKD patients which promotes ischemic cardiac events while platelet dysfunction leads to bleeding diathesis. If anticoagulation is indicated, low molecular weight heparins (LMWHs) offer certain advantage sbut the dosage needs to be adjusted with increasing grade of renal insufficiency. Antiplatelet agents are effective in averting shunt and catheter thrombosis, but not for avoiding the thrombosis of arteriovenous grafts.

Conclusion: Health related quality of life in CKD patients can be improved by treating anemia. Newly available ESAs and the entry into the market of epoetinbiosimilars are expected to lead to improvements in the management of CKD and its complications.

慢性肾病患者贫血和其他血液学紊乱的处理。
慢性肾脏疾病(CKD)对几乎所有身体系统都有不良影响。肾脏不仅仅是一个排泄器官,它还参与正常的红细胞生成、正常的骨矿物质沉积和血压调节。回顾:贫血在慢性肾病中很普遍,已知对心血管系统有有害影响。这主要是由于促红细胞生成素缺乏、尿毒症溶质抑制红细胞生成和红细胞寿命缩短。其他可能的原因包括铁、B12或叶酸缺乏或失血。当肾小球滤过率(GFR)低于20- 25ml /min时,内源性促红细胞生成素功能障碍通常在临床表现明显。治疗慢性肾病贫血的基础是纠正缺铁和用促红细胞生成素刺激剂(ESA)替代减少的促红细胞生成素产生。指南建议靶向血红蛋白水平不超过10-12克/分升,因为有证据表明,较高水平的患者死亡率和发病率会增加。促凝生物标志物水平升高导致CKD患者血栓活动增强,从而促进缺血性心脏事件,而血小板功能障碍导致出血。如果需要抗凝治疗,低分子肝素(LMWHs)具有一定的优势,但剂量需要随着肾功能不全程度的增加而调整。抗血小板药物对避免分流和导管血栓形成有效,但对避免动静脉移植物血栓形成无效。结论:治疗贫血可改善慢性肾病患者的健康相关生活质量。新获得的esa和环氧生物仿制药市场的进入有望改善CKD及其并发症的管理。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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