Cañas Laura, Iglesias Eva, Pastor María Cruz, Barallat Jaume, Juega Javier, Bancu Ioana, Lauzurica Ricardo
Department of Nephrology, Germans Trias i Pujol University Hospital, Autonomous University of Barcelona, Red de Investigacion Renal (RedinRen), CTRA. Canyet s/n, 08916, Badalona, Barcelona, Spain.
Department of Clinical Biochemistry, Germans Trias i Pujol University Hospital, Autonomous University of Barcelona, Barcelona, Spain.
Int Urol Nephrol. 2017 Mar;49(3):533-540. doi: 10.1007/s11255-016-1435-4. Epub 2016 Dec 24.
Patients with chronic kidney disease (CKD) are characterized by a state of inflammation and oxidative stress that seems to improve after kidney transplantation (KT). Nevertheless, there is controversy regarding what is the best marker that better define inflammation and specially oxidative stress.
To evaluate the biomarkers which are associated with improvements in inflammation and lipid peroxidation in patients who have undergone KT. To evaluate the relationship between inflammation, lipid peroxidation and mortality in KT.
196 KT (between 2003 and 2008). 67.9% men; median age: 51.9 years. Inflammation markers analyzed previous KT and 3 months after KT: c-reactive protein(CRP), interleukin 6(IL-6), tumor necrosis factor alpha(TNFα), soluble tumor necrosis factor receptor alpha(sTNFRα), soluble interleukin-2 receptor (sIL-2R). Lipid peroxidation markers analyzed: oxidized low-density lipoprotein (oxLDL) and anti-oxLDL antibodies. Calculation of glomerular filtration rate after KT: MDRD equation.
Following KT, there is a significant decrease in CRP (p = 0.006), IL-6 (p = 0.0037), TNFα (p < 0.0001), sTNFRα (p < 0.0001) and sIL-2R (p < 0.0001), while levels of oxLDL increase after KT (p < 0.0001) and there is not a significantly difference in anti-oxLDL. 12.8% of the patients had died in 2012. These patients had higher levels of IL-6 (p = 0.011) and sTNFRα (p < 0.006) after KT and a lower MDRD (p < 0.0001), hemoglobin (p = 0.012) and albumin (p = 0.007). We observed no statistically differences in the levels of markers previous KT. Of the patients who died, the 43.5% of them had anti-oxLDL antibody levels greater than 75th percentile (P: 3781 UI/ml, p = 0.028). In the multivariate analysis, age (OR:1.12; p = 0.0129), MDRD (OR:0.92; p = 0.013) and P of anti-oxLDL(OR: 5.19; p = 0.026) were independent risk factors for mortality. Independent risk factors for survival were: P of IL-6 (HR: 2.45; p = 0.027), oxLDL (HR:19.85; p = 0.002) and anti-oxLDL (HR: 9.55; p = 0.003).
KT improved inflammation but not lipid oxidative state. KT patients who died had a higher inflammatory state (with higher levels of IL-6 and sTNFRα), a worse lipid oxidative state and a worse renal function 3 months after KT. Age, anti-oxLDL and renal function at 3 months after KT were independent risk factors for mortality.
慢性肾脏病（CKD）患者的特征是存在炎症和氧化应激状态，肾移植（KT）后这种状态似乎有所改善。然而，关于哪种标志物能更好地定义炎症尤其是氧化应激，仍存在争议。
评估与KT患者炎症改善和脂质过氧化相关的生物标志物。评估KT患者炎症、脂质过氧化与死亡率之间的关系。
196例KT患者（2003年至2008年期间）。男性占67.9%；中位年龄：51.9岁。分析KT前及KT后3个月的炎症标志物：C反应蛋白（CRP）、白细胞介素6（IL-6）、肿瘤坏死因子α（TNFα）、可溶性肿瘤坏死因子受体α（sTNFRα）、可溶性白细胞介素-2受体（sIL-2R）。分析脂质过氧化标志物：氧化型低密度脂蛋白（oxLDL）和抗氧化型低密度脂蛋白抗体。KT后计算肾小球滤过率：采用MDRD方程。
KT后，CRP（p = 0.006）、IL-6（p = 0.0037）、TNFα（p < 0.0001）、sTNFRα（p < 0.0001）和sIL-2R（p < 0.0001）显著降低，而KT后oxLDL水平升高（p < 0.0001），抗氧化型低密度脂蛋白无显著差异。2012年12.8%的患者死亡。这些患者KT后IL-6（p = 0.011）和sTNFRα（ p < .006）水平较高，MDRD（p < 0.0001）、血红蛋白（p = 0.012）和白蛋白（p = 0.007）较低。我们观察到KT前标志物水平无统计学差异。在死亡患者中，43.5%的患者抗氧化型低密度脂蛋白抗体水平高于第75百分位数（P：3781 UI/ml，p = 0.028）。多因素分析中，年龄（OR：1.12；p = 0.0129）、MDRD（OR：0.92；p = 0.013）和抗氧化型低密度脂蛋白的P值（OR：5.19；p = 0.026）是死亡的独立危险因素。生存的独立危险因素为：IL-6的P值（HR：2.45；p = 0.027）、oxLDL（HR：19.85；p = 0.002）和抗氧化型低密度脂蛋白（HR：9.55；p = 0.003）。
KT改善了炎症，但未改善脂质氧化状态。死亡的KT患者炎症状态较高（IL-6和sTNFRα水平较高），脂质氧化状态较差，KT后3个月肾功能较差。年龄、抗氧化型低密度脂蛋白和KT后3个月的肾功能是死亡的独立危险因素。
