Department of Clinical Chemistry, Medical University of Gdańsk, 80-210 Gdańsk, Poland.
Clinic & Chair of Nephrology, Transplantology and Internal Diseases, Medical University of Gdańsk, 80-210 Gdańsk, Poland.
Int J Mol Sci. 2019 Mar 9;20(5):1202. doi: 10.3390/ijms20051202.
In chronic kidney disease (CKD), the level of high-density lipoprotein (HDL) decreases markedly, but there is no strong inverse relationship between HDL-cholesterol (HDL-C) and cardiovascular diseases. This indicates that not only the HDL-C level, but also the other quantitative changes in the HDL particles can influence the protective functionality of these particles, and can play a key role in the increase of cardiovascular risk in CKD patients. The aim of the present study was the evaluation of the parameters that may give additional information about the HDL particles in the course of progressing CKD. For this purpose, we analyzed the concentrations of HDL containing apolipoprotein A-I without apolipoprotein A-II (LpA-I), preβ1-HDL, and myeloperoxidase (MPO), and the activity of paraoxonase-1 (PON-1) in 68 patients at various stages of CKD. The concentration of HDL cholesterol, MPO, PON-1, and lecithin-cholesterol acyltransferase (LCAT) activity were similar in all of the analyzed stages of CKD. We did not notice significant changes in the LpA-I concentrations in the following stages of CKD (3a CKD stage: 57 ± 19; 3b CKD stage: 54 ± 15; 4 CKD stage: 52 ± 14; = 0.49). We found, however, that the preβ1-HDL concentration and preβ1-HDL/LpA-I ratio increased along with the progress of CKD, and were inversely correlated with the estimated glomerular filtration rate (eGFR), even after adjusting for age, gender, triacylglycerols (TAG), HDL cholesterol, and statin therapy (β = -0.41, < 0.001; β = -0.33, = 0.001, respectively). Our results support the earlier hypothesis that kidney disease leads to the modification of HDL particles, and show that the preβ1-HDL concentration is significantly elevated in non-dialyzed patients with advanced stages of CKD.
在慢性肾病（CKD）中，高密度脂蛋白（HDL）水平显著降低，但 HDL-胆固醇（HDL-C）与心血管疾病之间没有很强的反向关系。这表明，不仅是 HDL-C 水平，HDL 颗粒的其他定量变化也可以影响这些颗粒的保护功能，并在 CKD 患者心血管风险的增加中发挥关键作用。本研究的目的是评估可能在 CKD 进展过程中提供有关 HDL 颗粒的附加信息的参数。为此，我们分析了载脂蛋白 A-I 而不含载脂蛋白 A-II（LpA-I）、前β1-HDL 和髓过氧化物酶（MPO）的 HDL 浓度，以及对氧磷酶-1（PON-1）在 68 名处于不同 CKD 阶段的患者中的活性。在所有分析的 CKD 阶段，HDL 胆固醇、MPO、PON-1 和卵磷脂胆固醇酰基转移酶（LCAT）活性均相似。我们没有注意到 LpA-I 浓度在以下 CKD 阶段有显著变化（3a CKD 期：57±19；3b CKD 期：54±15；4 CKD 期：52±14；=0.49）。然而，我们发现前β1-HDL 浓度和前β1-HDL/LpA-I 比值随着 CKD 的进展而增加，并且与估算的肾小球滤过率（eGFR）呈负相关，即使在调整年龄、性别、三酰甘油（TAG）、HDL 胆固醇和他汀类药物治疗后也是如此（β=-0.41，<0.001；β=-0.33，=0.001）。我们的结果支持早期的假设，即肾脏疾病导致 HDL 颗粒的修饰，并表明在未接受透析的晚期 CKD 患者中，前β1-HDL 浓度显著升高。
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