Futrakul Narisa, Kittikowit Wipawee, Yenrudi Saowanee
Physiology Department, King Chulalongkorn Memorial Hospital, Bangkok, Thailand.
Ren Fail. 2003 Sep;25(5):759-64. doi: 10.1081/jdi-120024291.
Endothelial factor VIII staining in renal microcirculation was performed in eight nephrotic patients associated with mesangial proliferation (MesP) and six nephrotic patients associated with focal segmental glomerulosclerosis (FSGS). The result in MesP revealed a greater staining for glomerular endothelial factor VIII (35 +/- 15%) and for postglomerular capillary endothelial factor VIII (65 +/- 21%) than that observed in FSGS, which revealed a 11 +/- 8% staining for glomerular endothelial factor VIII and 19 +/- 15% staining for postglomerular capillary endothelial factor VIII. This finding implies that there is a greater loss of endothelial cell in renal microcirculation in FSGS. Such a finding correlates with the intrarenal hemodynamics which illustrated (Futrakul, P.; Sitprija, V.; Yenrusi, S. Glomerular endothelial dysfunction determines disease progression: a hypothesis. Am. J. Nephrol. 1997, 17, 533-540.) a mild reduction in renal plasma flow (535 +/- 106 mL/min/1.73 m2, normal 600 mL/min/1.73 m2) and in peritubular capillary flow (422 +/- 80 mL/min/1.73 m2, normal 480 mL/min/1.73 m2) in MesP and (Futrakul, P. Coagulation in glomerulonephritis and nephrotic symdrome: Its therapeutic intervention. In Asian Manual of Nephrology, Takeuchi, T.; Sugino, N.; Ota, K., Eds.; SEAMIC Publication, Tokyo, 1981; pp. 89-95.) a greater reduction in renal plasma flow (108 +/- 50 mL/min/1.73 m2) and in peritubular capillary flow (87 +/- 42 mL/min/1.78 m2) in FSGS. Therefore the study has emphasized both the structural and functional defects of endothelium in renal microcirculation in particular in FSGS.
对8例伴有系膜增生（MesP）的肾病患者和6例伴有局灶节段性肾小球硬化（FSGS）的肾病患者进行了肾微循环中内皮因子VIII染色。MesP组的结果显示，肾小球内皮因子VIII染色（35±15%）和肾小球后毛细血管内皮因子VIII染色（65±21%）高于FSGS组，FSGS组肾小球内皮因子VIII染色为11±8%，肾小球后毛细血管内皮因子VIII染色为19±15%。这一发现表明FSGS患者肾微循环中内皮细胞的丢失更多。这一发现与肾内血流动力学相关，肾内血流动力学表明（Futrakul, P.; Sitprija, V.; Yenrusi, S. 肾小球内皮功能障碍决定疾病进展：一种假说。《美国肾脏病杂志》1997年，17卷，533 - 540页）MesP组肾血浆流量（535±106 mL/min/1.73 m2，正常为600 mL/min/1.73 m2）和肾小管周围毛细血管流量（422±80 mL/min/1.73 m2，正常为480 mL/min/1.73 m2）轻度降低，以及（Futrakul, P. 肾小球肾炎和肾病综合征中的凝血：其治疗干预。《亚洲肾脏病手册》，Takeuchi, T.; Sugino, N.; Ota, K.编；SEAMIC出版社，东京，1981年；第89 - 95页）FSGS组肾血浆流量（108±50 mL/min/1.73 m2）和肾小管周围毛细血管流量（87±42 mL/min/1.78 m2）降低幅度更大。因此，该研究强调了肾微循环中内皮细胞的结构和功能缺陷，尤其是在FSGS中。
