Viero R M, Cavallo T
Department of Pathology and Laboratory Medicine, University of Cincinnati College of Medicine, OH 45267-0529, USA.
Hum Pathol. 1995 Dec;26(12):1347-53. doi: 10.1016/0046-8177(95)90300-3.
Granulomatous interstitial nephritis is a rare condition whose pathogenesis is poorly understood. Of 203 renal biopsies performed between 1974 to 1994 in which interstitial nephritis was the predominant change, granulomata occurred in 12. The authors reviewed the records of these patients and performed immunopathologic and immunohistochemical studies in their biopsies to characterize the phenotype of infiltrating cells. The authors used markers for T cells, B cells, and macrophages, and determined whether they were activated through assessment of upregulation of HLA-DR molecules. Additionally, the authors attempted to delineate whether or not tubules contributed to giant cell formation through assessment of intermediate filament for keratins and macrophage markers in epithelioid cells. Drug (aspirin, gentamycin, or combination of drugs), infection (Echerichia coli or various organisms), and sarcoidosis accounted for granulomatous inflammation in three patients each, Wegener's granulomatosis and oxalosis resulting from intestinal bypass in one patient each, and in one patient the possible cause could not be determined. Except for biopsies of granulomatous inflammation resulting from infection, in which neutrophils predominated, in all other biopsies, T cells and macrophages made up most of the inflammatory cell infiltrate. HLA-DR was upregulated in mononuclear cells infiltrating the interstitium and was expressed in proximal tubular cells and endothelial cells in all but biopsies of patients with sarcoidosis. In no instance was there evidence that tubules contributed epithelial cells to giant cell formation. These findings are consistent with the notion that granulomatous interstitial nephritis is a cell-mediated form of tissue injury in which T cell-macrophage seem to play a major role.
肉芽肿性间质性肾炎是一种罕见疾病，其发病机制尚不清楚。在1974年至1994年间进行的203例肾活检中，以间质性肾炎为主要病变，其中12例出现肉芽肿。作者回顾了这些患者的病历，并对其活检组织进行了免疫病理学和免疫组织化学研究，以确定浸润细胞的表型。作者使用了T细胞、B细胞和巨噬细胞的标志物，并通过评估HLA-DR分子的上调来确定它们是否被激活。此外，作者试图通过评估上皮样细胞中角蛋白中间丝和巨噬细胞标志物来确定肾小管是否参与巨细胞形成。药物（阿司匹林、庆大霉素或药物组合）、感染（大肠杆菌或各种生物体）和结节病各导致3例患者出现肉芽肿性炎症，韦格纳肉芽肿和肠道旁路术后草酸中毒各导致1例患者出现肉芽肿性炎症，1例患者的可能病因无法确定。除了感染引起的肉芽肿性炎症活检组织中以中性粒细胞为主外，在所有其他活检组织中，T细胞和巨噬细胞构成了大部分炎性细胞浸润。在间质性浸润的单核细胞中HLA-DR上调，除结节病患者的活检组织外，在所有近端肾小管细胞和内皮细胞中均有表达。在任何情况下都没有证据表明肾小管上皮细胞参与巨细胞形成。这些发现与肉芽肿性间质性肾炎是一种细胞介导的组织损伤形式的观点一致，其中T细胞-巨噬细胞似乎起主要作用。
