Yoshikawa Y, Truong L D, Mattioli C A, Ordonez N G, Balsaver A M
Department of Pathology, Baylor College of Medicine, Methodist Hospital, University of Texas M.D. Anderson Hospital and Tumor Institute, Houston.
Mod Pathol. 1990 Jan;3(1):36-42.
Glomerular diseases other than diabetic glomerulosclerosis (DGS) occurring in diabetic patients may pose a diagnostic challenge to both clinicians and pathologists. We studied 15 cases of membranous glomerulonephritis (MG) in patients with diabetes mellitus focusing on the morphologic changes of the kidney. Light microscopic observation revealed nodular and/or diffuse DGS in 12 cases and no DGS in three. Periodic acid-silver methenamine stain showed spikes or chain-like structures in the glomerular capillary wall in 13 cases, indicating the presence of MG. Ultrastructurally, MG was classified into Stage I (N = 2), II (N = 8), III (N = 4), or IV (N = 1). Six out of nine cases with Stages I and II MG showed a thickened lamina densa of the glomerular basement membrane (GBM), suggesting diabetic influence on the GBM. Moreover, MG in some of the cases suggested atypical ultrastructural features including (a) the presence of large immune type deposits separated by tall spikes (N = 4), (b) high electron density of deposits in spite of their intramembranous location (N = 4), and (c) the presence of immune type deposits of mesangial (N = 3) and subendothelial (N = 2) locations. It is postulated that these atypical features are caused by altered turnover of the GBM, impaired glomerular clearance of immune complexes, changes of the glomerular capillary wall as the result of hemodynamic alterations, and/or nonenzymatic glycosylation in diabetic milieu.
糖尿病患者中发生的除糖尿病肾小球硬化症(DGS)以外的肾小球疾病,可能会给临床医生和病理学家带来诊断挑战。我们研究了15例糖尿病患者的膜性肾小球肾炎(MG),重点关注肾脏的形态学变化。光镜观察显示,12例有结节性和/或弥漫性DGS,3例无DGS。高碘酸-银甲胺染色显示13例肾小球毛细血管壁有钉突或链状结构,提示存在MG。超微结构上,MG分为I期(N = 2)、II期(N = 8)、III期(N = 4)或IV期(N = 1)。I期和II期MG的9例患者中有6例显示肾小球基底膜(GBM)的致密层增厚,提示糖尿病对GBM有影响。此外,部分病例的MG显示出非典型超微结构特征,包括:(a)存在被高钉突分隔的大免疫型沉积物(N = 4);(b)尽管沉积物位于膜内,但电子密度高(N = 4);(c)存在系膜(N = 3)和内皮下(N = 2)位置的免疫型沉积物。据推测,这些非典型特征是由GBM更新改变、免疫复合物肾小球清除受损、血流动力学改变导致的肾小球毛细血管壁变化和/或糖尿病环境中的非酶糖基化引起的。