Kraft Steven W, Schwartz Melvin M, Korbet Stephen M, Lewis Edmund J
Section of Nephrology, Department of Medicine, Rush University Medical Center, 1426 W. Washington Boulevard, Chicago, IL 60607, USA.
J Am Soc Nephrol. 2005 Jan;16(1):175-9. doi: 10.1681/ASN.2004050350. Epub 2004 Nov 17.
A series of patients with systemic lupus erythematosus (SLE) and proteinuria were studied to determine whether nephrotic-range proteinuria was associated with diffuse epithelial cell foot process effacement in the absence of peripheral glomerular immune aggregate deposition. Biopsies from patients with known or suspected SLE and a histologic diagnosis of (1) normal by light microscopy, (2) mesangial proliferative glomerulonephritis, or (3) focal segmental glomerulosclerosis were studied. Biopsies were excluded when they demonstrated endocapillary proliferation or necrosis by light microscopy or electron-dense glomerular basement membrane deposits by electron microscopy. Patients were required to fulfill four of 11 American Rheumatologic Association criteria for the diagnosis of SLE, and proteinuria could not be associated with nonsteroidal anti-inflammatory drug use. Eighteen biopsies were studied, eight from patients with nephrotic-range proteinuria (>/=3 g/d) and 10 from patients with non-nephrotic proteinuria. The time from diagnosis of SLE to biopsy was shorter for nephrotic patients that for nonnephrotic patients. Seven of eight biopsies from nephrotic patients demonstrated at least 80% foot process effacement, whereas no biopsy from a nonnephrotic patient exhibited >20% effacement. There were no other significant pathologic differences between the nephrotic and nonnephrotic patients. The single common morphologic feature associated with nephrotic proteinuria was diffuse visceral epithelial cell foot process effacement. It is concluded that the development of nephrotic-range proteinuria in patients with SLE without peripheral immune aggregate deposition or endocapillary proliferation on renal biopsy is more likely a manifestation of SLE than the coexistence of idiopathic minimal-change glomerulopathy and SLE.
对一系列系统性红斑狼疮（SLE）伴蛋白尿患者进行了研究，以确定在无外周肾小球免疫复合物沉积的情况下，肾病范围蛋白尿是否与弥漫性上皮细胞足突消失相关。研究了已知或疑似SLE且组织学诊断为（1）光镜下正常、（2）系膜增生性肾小球肾炎或（3）局灶节段性肾小球硬化的患者的活检标本。若活检标本光镜下显示毛细血管内增生或坏死，或电镜下显示电子致密的肾小球基底膜沉积物，则予以排除。患者需符合美国风湿病学会11条SLE诊断标准中的4条，且蛋白尿不能与使用非甾体抗炎药相关。共研究了18份活检标本，其中8份来自肾病范围蛋白尿（≥3g/d）患者，10份来自非肾病性蛋白尿患者。肾病患者从SLE诊断到活检的时间比非肾病患者短。8份肾病患者的活检标本中有7份显示至少80%的足突消失，而非肾病患者的活检标本无一份显示超过20%的足突消失。肾病患者和非肾病患者之间无其他显著的病理差异。与肾病性蛋白尿相关的唯一共同形态学特征是弥漫性脏层上皮细胞足突消失。结论是，肾活检无外周免疫复合物沉积或毛细血管内增生的SLE患者出现肾病范围蛋白尿，更可能是SLE的一种表现，而非特发性微小病变性肾小球病与SLE并存。
