Futrakul Prasit, Siriviriyakul Prasong, Patumraj Suthiluk, Bunnag Srichitra, Kulaputana Ornanong, Futrakul Narisa
Department of Pediatrics, King Chulalongkorn Memorial Hospital, Bangkok 10330, Thailand.
Clin Hemorheol Microcirc. 2003;29(3-4):183-7.
Glomerular endothelial cell (GEC) dysfunction due to oxidative stress and enhanced proinflammatory cytokines plays an important role in inducing proteinuria and procoagulant activity, namely blood hypercoagulability, hyperviscosity and local intravascular coagulation and altered hemorheology in NS. A dysfunctioning GEC releases fewer endothelium-dependent vasodilators but produces more vasoconstrictors. Severe intrarenal hemodynamic alteration associated with hemodynamic maladjustment with preferential constriction at the efferent arteriole has been uniquely implicated in severe GN and NS-FSGS. Such a constriction exerts three significant hemodynamic impacts. Proximal to the efferent arteriolar constriction, it induces (i) an overestimated GFR due to hyperfiltration and (ii) an elevated intraglomerular hydrostatic pressure. Distal to the efferent arteriolar constriction, it (iii) exaggeratedly reduces PTCF which correlates with the TIF.
由于氧化应激和促炎细胞因子增强导致的肾小球内皮细胞（GEC）功能障碍在诱导蛋白尿和促凝活性（即血液高凝性、高黏滞性和局部血管内凝血）以及改变NS中的血液流变学方面起着重要作用。功能失调的GEC释放的内皮依赖性血管舒张剂较少，但产生的血管收缩剂较多。与肾内血流动力学失调相关的严重肾内血流动力学改变，其特征是出球小动脉优先收缩，这与严重的肾小球肾炎和NS - FSGS独特相关。这种收缩产生三个显著的血流动力学影响。在出球小动脉收缩近端，它会导致（i）由于超滤导致肾小球滤过率（GFR）高估，以及（ii）肾小球内静水压力升高。在出球小动脉收缩远端，它会（iii）过度降低与肾小管间质纤维化（TIF）相关的肾血浆流量（PTCF）。
