White Kathryn E, Bilous Rudolf W
School of Clinical Medical Studies, Medical School, University of Newcastle upon Tyne, NE2 4HH, UK.
Nephrol Dial Transplant. 2004 Jun;19(6):1437-40. doi: 10.1093/ndt/gfh129. Epub 2004 Feb 19.
The podocyte is believed to play a key role in maintaining the integrity of the glomerular filtration barrier, and damage or loss has been linked to the development of albuminuria.
Renal biopsies from 16 type 2 diabetic patients with nephropathy and 28 non-diabetic controls were analysed using light and electron microscopy.
Podocyte number per glomerulus was significantly lower in the type 2 patients compared with controls [mean (95% confidence interval) 464 (382-546) vs 589 (543-635), P = 0.004]. Mean glomerular volume was significantly increased in diabetic patients compared with controls [5.5 (4.9-6.1) vs 3.1 (2.7-3.5) x 10(6) microm(3), P<0.001], thus the diabetic patients demonstrated an even greater proportional reduction in podocyte density per glomerulus [88 (68-108) vs 201 (182-220)/10(6) microm(3), P<0.001]. Podocyte foot process width on both the filtration surface (FPWgbm) and mesangial surface (FPWmes) was significantly increased compared with controls [796 (708-884) vs 556 (460-908) nm, P = 0.001; 1108 (821-1394) vs 760 (555-1078) nm, P = 0.029, respectively]. There was a significant negative correlation between proteinuria and both podocyte number and podocyte density per glomerulus (r = -0.63, P = 0.009; r = -0.58, P = 0.018, respectively). There was a significant positive correlation between proteinuria and both FPWgbm and FPWmes (r = 0.64, P = 0.008, for both).
Podocyte loss occurs in type 2 diabetic nephropathy and is related to increasing proteinuria. Whether the accompanying glomerular enlargement and widening of foot processes are a cause of podocyte loss is uncertain. Longitudinal studies are required to determine the sequence of events leading to podocyte loss in diabetic nephropathy.
足细胞被认为在维持肾小球滤过屏障的完整性中起关键作用，其损伤或丢失与蛋白尿的发生有关。
对16例2型糖尿病肾病患者和28例非糖尿病对照者的肾活检组织进行光镜和电镜分析。
与对照组相比，2型糖尿病患者每个肾小球的足细胞数量显著减少[平均值（95%可信区间）464（382 - 546）对589（543 - 635），P = 0.004]。与对照组相比，糖尿病患者的平均肾小球体积显著增加[5.5（4.9 - 6.1）对3.1（2.7 - 3.5）×10⁶立方微米，P < 0.001]，因此糖尿病患者每个肾小球的足细胞密度成比例降低得更明显[88（68 - 108）对201（182 - 220）/10⁶立方微米，P < 0.001]。与对照组相比，滤过表面（FPWgbm）和系膜表面（FPWmes）的足细胞足突宽度均显著增加[796（708 - 884）对556（460 - 908）纳米，P = 0.001；1108（821 - 1394）对760（555 - 1078）纳米，P = 0.029]。蛋白尿与每个肾小球的足细胞数量和足细胞密度均呈显著负相关（r分别为 - 0.63，P = 0.009；r = - 0.58，P = 0.018）。蛋白尿与FPWgbm和FPWmes均呈显著正相关（两者r均为0.64，P = 0.008）。
2型糖尿病肾病中存在足细胞丢失，且与蛋白尿增加有关。伴随的肾小球增大和足突增宽是否是足细胞丢失的原因尚不确定。需要进行纵向研究以确定导致糖尿病肾病中足细胞丢失的事件顺序。
