Giles R D, Sturgill B C, Suratt P M, Bolton W K
Am J Med. 1978 Feb;64(2):336-42. doi: 10.1016/0002-9343(78)90063-3.
Acute pulmonary silicoproteinosis, massive proteinuria and fatal renal failure developed in a 23 year old male sandblaster. Examination of the kidney by immunofluorescence revealed granular deposits of immunoglobulin M (IgM) and the third component of complement (C3) along the glomerular basement membrane. Light microscopy disclosed mild proliferative glomerulonephritis with loss of colloidal iron staining for sialoprotein, and electron microscopy disclosed an increased density of epithelial cytoplasm, altered lysosomes and endothelial cell microtubular structures. The silicon content of the kidney was 264 parts per million (ppm), but particles of silicon were not demonstrated by electron microscopy. No primary or systemic causes of renal diseases were elucidated. The renal dysfunction apparently resulted from acute renal silicon toxicity, a new complication of acute pulmonary silicoproteinosis.
一名23岁的男性喷砂工出现了急性肺硅蛋白沉着症、大量蛋白尿和致命性肾衰竭。通过免疫荧光检查肾脏发现免疫球蛋白M(IgM)和补体第三成分(C3)沿肾小球基底膜呈颗粒状沉积。光镜检查显示轻度增生性肾小球肾炎,涎蛋白胶体铁染色缺失,电镜检查显示上皮细胞质密度增加、溶酶体改变和内皮细胞微管结构改变。肾脏的硅含量为百万分之264(ppm),但电镜未发现硅颗粒。未阐明肾脏疾病的原发性或全身性病因。肾功能障碍显然是由急性肾硅中毒引起的,这是急性肺硅蛋白沉着症的一种新并发症。