Cause of Death in Patients With Diabetic CKD Enrolled in the Trial to Reduce Cardiovascular Events With Aranesp Therapy (TREAT).
Cause of Death in Patients With Diabetic CKD Enrolled in the Trial to Reduce Cardiovascular Events With Aranesp Therapy (TREAT).
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DOI：
10.1053/j.ajkd.2015.02.324
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发表时间：
2015-09
期刊：
影响因子：
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通讯作者：
Solomon SD
中科院分区：
文献类型：
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作者：
Charytan DM;Lewis EF;Desai AS;Weinrauch LA;Ivanovich P;Toto RD;Claggett B;Liu J;Hartley LH;Finn P;Singh AK;Levey AS;Pfeffer MA;McMurray JJ;Solomon SD
慢性肾脏病(CKD)患者的死亡原因随CKD严重程度的不同而不同，但差异尚未量化。前瞻性随机临床试验的回顾分析。我们分析了来自Treat的4038名贫血和糖尿病CKD患者，这是一项比较达贝泊丁阿尔法和安慰剂的随机试验。基线估计肾小球滤过率(EGFR)和蛋白-肌酐比(PCR)。死因由一个盲目的委员会裁决。第一四分位(Q1)的EGFR和PCR值的中位数分别为20.6mL/min/1.73m2和4.1g/g，Q4的中位数为47.0mL/min/1.73m2和0.1g/g(P<；0.01)。在806例死亡中，441例死于心血管疾病，298例死于非心血管疾病，67例死于不明原因。较低的EGFR(Q1，15.5%；Q2，11.1%；Q3，11.2%；Q4，10.3%；P<；0.001)或较高的PCR值(Q1，15.2%；Q2，12.3%；Q3，11.7%；Q4，9.0%；P<；0.001)的累积循环病死率较高。同样，非心血管病死率越低(第一季度，12.7%；第二季度，8.4%；第三季度，6.7%；第四季度，6.1%；P<；0.001)或PCR值较高(第一季度，10.3%；第二季度，7.9%；第三季度，9.4%；第四季度，6.4%；P<；0.01)。猝死是EGFR低的患者的1.7倍(P<；0.04)和高PCR值的2.1倍(P<；0.001)。与感染相关的死亡率在表皮生长因子受体最低四分位数(P<；0.001)中高3.3倍，在聚合酶链式反应最高四分位数(P<；0.02)中高2.8倍。在EGFR或PCR四分位数中，心血管死亡和非心血管死亡的总体比例没有显著差异。结果可能不能推广到非糖尿病CKD或无贫血的糖尿病CKD。测量的GFR不可用。在糖尿病CKD中，较低的基线GFR和较高的PCR值都与较高的心血管死亡率和非心血管死亡率相关，尤其是猝死和感染。改善预后的努力应集中在心血管疾病和感染的早期诊断和治疗上。
The cause of death in patients with chronic kidney disease (CKD) varies with CKD severity, but variation has not been quantified. Retrospective analysis of prospective randomized clinical trial. We analyzed 4,038 individuals with anemia and diabetic CKD from TREAT, a randomized trial comparing darbepoetin alfa and placebo. Baseline estimated glomerular filtration rate (eGFR) and protein-creatinine ratio (PCR). Cause of death as adjudicated by a blinded committee. Median eGFR and PCR ranged from 20.6 mL/min/1.73 m2 and 4.1 g/g in quartile 1 (Q1) to 47.0 mL/min/1.73 m2 and 0.1 g/g in Q4 (P < 0.01). Of 806 deaths, 441, 298, and 67 were due to cardiovascular (CV), non-CV, and unknown causes, respectively. Cumulative CV mortality at 3 years was higher with lower eGFR (Q1, 15.5%; Q2, 11.1%; Q3, 11.2%; Q4, 10.3%; P < 0.001) or higher PCR (Q1, 15.2%; Q2, 12.3%; Q3, 11.7%; Q4, 9.0%; P < 0.001). Similarly, non-CV mortality was higher with lower eGFR (Q1, 12.7%; Q2, 8.4%; Q3, 6.7%; Q4, 6.1%; P < 0.001) or higher PCR (Q1, 10.3%; Q2, 7.9%; Q3, 9.4%; Q4, 6.4%; P < 0.01). Sudden death was 1.7-fold higher with lower eGFR (P < 0.04) and 2.1-fold higher with higher PCR (P < 0.001). Infection-related mortality was 3.3-fold higher in the lowest eGFR quartile (P < 0.001) and 2.8-fold higher in the highest PCR quartile (P < 0.02). The overall proportion of CV and non-CV deaths was not significantly different across eGFR or PCR quartiles. Results may not be generalizable to nondiabetic CKD or diabetic CKD in the absence of anemia. Measured GFR was not available. In diabetic CKD, both lower baseline GFR and higher PCR are associated with higher CV and non-CV mortality rates, particularly from sudden death and infection. Efforts to improve outcomes should focus on CV disease and early diagnosis and treatment of infection.