Department of Nephrology, Aristotle University of Thessaloniki, Hippokration Hospital, Thessaloniki, Greece.
Fourth Department of Internal Medicine, Aristotle University of Thessaloniki, Hippokration Hospital, Thessaloniki, Greece.
Hypertens Res. 2021 Feb;44(2):179-187. doi: 10.1038/s41440-020-0525-y. Epub 2020 Jul 29.
Cardiovascular disease is the main cause of mortality in chronic kidney disease (CKD). Endothelial dysfunction and capillary rarefaction are established cardiovascular risk factors. Nailfold video capillaroscopy provides a thorough assessment of capillary density and functional reserve. This study aimed to examine possible differences in structural and functional capillary density in CKD stages 2-4 with nailfold video capillaroscopy. Ninety-six CKD patients, divided into four equally sized groups according to CKD stage (2, 3a, 3b, 4), underwent nailfold video capillaroscopy, during which capillary density was measured at baseline, after 4-min arterial occlusion and after 2-min venous occlusion. Arterial stiffness and wave parameters were measured with applanation tonometry and common carotid intima-media thickness (ccIMT) with ultrasound. Baseline capillary density showed a progressive reduction with advancing CKD stages (stage 2: 32.6 ± 2.8, stage 3a: 31.2 ± 3.8, stage 3b: 32.5 ± 3.3, stage 4: 28.5 ± 3.1, p = 0.011). Similar reductions were observed during postocclusive hyperemia (39.4 ± 3.0, 37.6 ± 4.2, 38.4 ± 3.8, and 33.8 ± 3.3, respectively; p = 0.021) and after venous congestion (41.1 ± 3.1, 39.0 ± 4.4, 39.9 ± 3.5, and 35.2 ± 3.4; p = 0.032). Office PWV and ccIMT showed nonsignificant increasing trends with advancing CKD. In multivariate analysis, eGFR showed a positive association (per ml/min increase; β: 0.053, 95% CI: 0.004-0.101), whereas diabetes (β: -1.706, 95% CI: -3.176 to -0.236) and parathyroid hormone (PTH) (per pg/ml increase; β: -0.022, 95% CI: -0.036 to -0.008) had negative associations with postocclusive capillary density. Both structural and functional capillary density progressively decrease with advancing CKD stages. Apart from reduced eGFR, diabetes and increased PTH levels are independently associated with this reduction. This capillary rarefaction may largely contribute to the increased cardiovascular risk of CKD patients.
心血管疾病是慢性肾脏病（CKD）患者死亡的主要原因。内皮功能障碍和毛细血管稀疏是已确立的心血管危险因素。甲襞微血管检查提供了毛细血管密度和功能储备的全面评估。本研究旨在通过甲襞微血管检查检查 CKD 2-4 期患者的结构和功能毛细血管密度的可能差异。96 名 CKD 患者根据 CKD 分期（2 期、3a 期、3b 期、4 期）分为四组进行甲襞微血管检查，在基线、动脉闭塞 4 分钟后和静脉闭塞 2 分钟后测量毛细血管密度。使用平板张力计测量动脉僵硬度和波参数，使用超声测量颈总动脉内膜-中层厚度（ccIMT）。随着 CKD 分期的进展，基线毛细血管密度逐渐降低（2 期：32.6±2.8，3a 期：31.2±3.8，3b 期：32.5±3.3，4 期：28.5±3.1，p=0.011）。在闭塞后充血期间也观察到类似的减少（分别为 39.4±3.0、37.6±4.2、38.4±3.8 和 33.8±3.3，p=0.021），静脉充血后也有减少（分别为 41.1±3.1、39.0±4.4、39.9±3.5 和 35.2±3.4，p=0.032）。办公室 PWV 和 ccIMT 显示随着 CKD 的进展呈非显著增加趋势。在多变量分析中，eGFR 呈正相关（每毫升/分钟增加；β：0.053，95%CI：0.004-0.101），而糖尿病（β：-1.706，95%CI：-3.176 至-0.236）和甲状旁腺激素（PTH）（每 pg/ml 增加；β：-0.022，95%CI：-0.036 至-0.008）呈负相关。随着 CKD 分期的进展，结构和功能毛细血管密度逐渐降低。除了 eGFR 降低外，糖尿病和升高的 PTH 水平与这种降低独立相关。这种毛细血管稀疏可能在很大程度上导致 CKD 患者心血管风险增加。
