Hara M, Yanagihara T, Kihara I
Department of Pediatrics, Yoshida Hospital, Niigata, Japan.
Nephron. 2001 Nov;89(3):342-7. doi: 10.1159/000046097.
BACKGROUND/AIM: Focal segmental glomerulosclerosis (FSGS) is a common cause of nephrotic syndrome. Although the pathogenesis is not known, recent studies suggest that FSGS may be a podocyte disease. The aim of this study was to look for podocyte injury in this disease, using measurements of urinary podocytes.
We examined the first morning urine of the day collected from 71 patients (45 men and 26 women, median age and range 11.2 and 3-29 years) diagnosed as having nephrotic syndrome. Freshly voided urine samples were examined by immunofluorescence labeling using monoclonal antibodies against human podocalyxin. Renal histological examinations were performed in 58 of the 71 patients: 28 had minimal-change disease, 20 had FSGS, and 10 had membranous nephropathy.
Median and range of urinary podocytes measured were 0.2 and 0-40.8 cells/ml for 71 patients with nephrotic syndrome and 0 and 0-0.8 cells/ml for normal healthy control subjects (n = 200). Patients with FSGS had significantly higher levels of urinary podocytes (median and range 1.3 and 0-40.8 cells/ml) than those with minimal-change disease (median and range 0 and 0-6.9 cells/m; p = 0.003) or membranous nephropathy (median and range 0 and 0-1.4 cells/ml; p = 0.02).
The urinary excretion of podocytes is significantly higher in patients with FSGS as compared with those having membranous nephropathy or minimal-change disease. These findings suggest that podocyte injury and loss in the urine may have an important role in the pathogenesis of FSGS.
背景/目的:局灶节段性肾小球硬化(FSGS)是肾病综合征的常见病因。尽管其发病机制尚不清楚,但最近的研究表明FSGS可能是一种足细胞疾病。本研究的目的是通过检测尿足细胞来寻找该疾病中的足细胞损伤。
我们检查了71例诊断为肾病综合征的患者(45例男性和26例女性,中位年龄及范围为11.2岁和3 - 29岁)当日晨尿。使用抗人足细胞标记蛋白的单克隆抗体通过免疫荧光标记检测新鲜排出的尿液样本。71例患者中的58例进行了肾脏组织学检查:28例为微小病变病,20例为FSGS,10例为膜性肾病。
71例肾病综合征患者尿足细胞的中位值及范围为0.2和0 - 40.8个细胞/毫升,正常健康对照者(n = 200)为0和0 - 0.8个细胞/毫升。FSGS患者的尿足细胞水平(中位值及范围为1.3和0 - 40.8个细胞/毫升)显著高于微小病变病患者(中位值及范围为0和0 - 6.9个细胞/毫升;p = 0.003)或膜性肾病患者(中位值及范围为0和0 - 1.4个细胞/毫升;p = 0.02)。
与膜性肾病或微小病变病患者相比,FSGS患者尿足细胞排泄显著更高。这些发现表明尿中足细胞损伤和丢失可能在FSGS发病机制中起重要作用。