Couser W G, Stilmant M M
J Gerontol. 1976 Jan;31(1):13-22. doi: 10.1093/geronj/31.1.13.
Immunofluorescence studies of rat kidneys from 3-24 mo. of age demonstrated deposition of immunoglobulins, predominately IgM, within the glomerular mesangium by age 3 mo. Immunoglobulins eluted in acid buffer, did not fix complement, were not associated with inflammatory changes, and increased markedly with the onset of proteinuria at about 12 mo. Rats 24 mo. old also had mesangial deposits of IgG and fibrin. No basement membrane deposits were seen, and autoantibodies to antigens in normal kidney, liver, spleen, and skeletal muscle were not demonstrable in serum or eluates of kidneys from aged animals. The focal and segmental glomerular sclerosis which develops in aged rats does not appear to be mediated by glomerular deposition of auto-antibody or immune complexes. Mesangial accumulation of macro-molecular material, perhaps as a consequency of the age-associated increase in glomerular permeability, may contribute to the development of the glomerular sclerosis of aging in the rat by impairing mesangial phagocytic or clearing mechanisms rather than through immunologically mediated tissue injury.
对3至24月龄大鼠肾脏进行的免疫荧光研究表明,3月龄时免疫球蛋白在肾小球系膜内沉积,主要为IgM。免疫球蛋白在酸性缓冲液中洗脱,不固定补体,与炎症变化无关,并在约12月龄蛋白尿开始时显著增加。24月龄的大鼠肾小球系膜中也有IgG和纤维蛋白沉积。未观察到基底膜沉积,老年动物血清或肾脏洗脱液中未检测到针对正常肾脏、肝脏、脾脏和骨骼肌抗原的自身抗体。老年大鼠发生的局灶节段性肾小球硬化似乎不是由自身抗体或免疫复合物在肾小球沉积介导的。大分子物质在系膜中的积聚,可能是肾小球通透性随年龄增长而增加的结果,可能通过损害系膜吞噬或清除机制,而非通过免疫介导的组织损伤,导致大鼠衰老性肾小球硬化的发展。