Biclonal Gammopathy in a Dog with Myeloma and Cutaneous Lymphoma
Biclonal Gammopathy in a Dog with Myeloma and Cutaneous Lymphoma
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患有骨髓瘤和皮肤淋巴瘤的狗的双克隆丙种球蛋白病
DOI：
10.1177/030098588602300220
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发表时间：
1986
影响因子：
2.4
通讯作者：
M. Wellman
中科院分区：
文献类型：
--
作者：
R. Jacobs;C. Couto;M. Wellman
肾切片中，肾小球含有大的5至40 μ π ι透明结构，其在渗透组织中染色为黑色（图1A和1B）。1，2）（2小时，在2%OsO中，在0.1M磷酸盐缓冲液中，pH 7.4）。类似的结构，解释为脂质栓塞，很少出现在肾小动脉腔。PAS和Masson三色染色肾组织切片可见弥漫性、结节性肾小球硬化和肾小球毛细血管基底膜增厚。近端肾小管基底膜还含有PAS阳性物质的多灶性上皮下结节聚集体，被正常肾小管上皮细胞覆盖（图3）。透射电子显微镜检查Spurr树脂8包埋切片，OsO固定后，证实肾小球毛细血管腔内存在嗜中性粒细胞栓子（图4）。毛细血管基底膜增厚、真空。这些膜内的一些空泡含有与毛细血管栓子染色相似的嗜酸性物质。毛细血管基底膜经常折叠，足细胞足突增厚，多灶融合。肾小球系膜细胞常存在于增厚的基底膜和基底膜样物质的额外内皮下分支沉积物之间的外周毛细血管袢中。犬糖尿病肾病的光镜和超微结构病变以前已作过描述。并可能解释了弥漫性和结节性肾小球硬化、肾小球毛细血管基底膜增厚以及系膜细胞和基质增生。糖尿病犬的肾小球毛细血管和肝窦中有脂质栓塞的报道。肾脂质栓塞也可能是犬和人创伤后全身脂质栓塞的一个组成部分。在人类中，在肺、肾、心脏和脑的小动脉和毛细血管中发现栓子。在狗的自发性肾小球脂质沉积症中，肾小球脂质也可能出现在系膜细胞空泡中。9本病例中的脂质沉积是不寻常的，因为它们仅位于肾小动脉和肾小球毛细血管腔中。在脑、心脏、肝脏或肺的渗透切片中未检测到先前在患有糖尿病或创伤后栓塞的犬中观察到的栓塞。电子显微镜检查证实脂质位于毛细血管腔内，因此排除了自发性肾小球脂质沉积。本例中间歇性栓塞可能在肾小球毛细血管腔内产生脂滴，但可能不会导致此类管腔栓塞的选择性肾分布。其他可能的来源包括肾小动脉壁上的脂肪沉积，继发于手术创伤。在人类中，肾栓塞导致动脉粥样硬化血管壁的胆固醇晶体在手术后释放，而糖尿病患者发生这种情况的风险更高。
renal sections, glomeruli contained large 5 to 40 pm clear structures which stained black in osmicated tissues (Figs. 1, 2) (2 hours in 2% OsO, in 0.1 M phosphate buffer, pH 7.4). Similar structures, interpreted as lipid emboli, were present rarely in renal arteriolar lumens. In PAS and Masson's tri- chrome-stained renal sections, there were diffuse and nodular glomerulosclerosis and thickened glomerular capillary base- ment membranes. Proximal tubular basement membranes also contained multifocal subepithelial nodular aggregates of PAS-positive material covered by normal tubular epithelium (Fig. 3). Transmission electron microscopy of Spurr resin8 embed- ded sections post-fixed in OsO, confirmed the presence of osmophilic emboli within glomerular capillary lumens (Fig. 4). Capillary basement membranes were thickened and vac- uolated. Some vacuoles within these membranes contained an osmophilic substance similar in staining to the capillary emboli. Capillary basement membranes were frequently folded, and podocyte foot processes appeared thickened and multifocally fused. Mesangial cells were often present in pe- ripheral capillary loops between the thickened basement membrane and additional subendothelial branching deposits of basement membrane-like material. The light and ultrastructural lesions seen with canine di- abetic nephropathy have been previously de~cribed'.~ and may account for the diffuse and nodular glomerulosclerosis, thickened glomerular capillary basement membranes, and mesangial cell and matrix proliferations. Lipid emboli have been previously reported in glomerular capillaries and he- patic sinusoids of diabetic dogs. Renal lipid emboli may also be a component of post-traumatic systemic lipid emboliza- tion in dogs and h~mans.~.~ In humans, emboli are found in small arterioles and capillaries of the lung, kidneys, heart, and brain.' Glomerular lipid may also occur in mesangial cell vacuoles in spontaneous glomerular lipoidosis of dogs.9 The lipid deposits in the present case are unusual due to their localization only in renal arterioles and glomerular cap- illary lumens. No emboli were detected in osmicated sections of brain, heart, liver, or lung as previously noted in dogs with diabetes mellitus or post-traumatic embolization. Electron microscopy confirmed the lipid was within capillary lumens thus excluding spontaneous glomerular lipoidosis. The in- termittent lipidemia present in this case may have produced lipid droplets in glomerular capillary lumens but probably would not have resulted in selective renal distribution of such lumenal emboli. Other possible sources include the fatty de- posits on renal arteriolar walls with release secondary to sur- gical trauma. Post-surgical release of cholesterol crystals from atheromatous vessel walls with renal embolization occurs in humans, and diabetic humans are at higher risk for such