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长期以来肾病综合征患者的低γ球蛋白血症推测是由于它从尿中丢失所致。目前,许多学者认为这种获得性免疫缺陷是复杂的机制造成,但尚缺乏 IgG 合成受损的直接证据。为此,作者研究了肾功能正常的62例肾病综合征患者的淋巴细胞在美洲商陆(PWM)刺激下合成 IgG 的能力。62例成人肾病综合征患者,经肾活检证实,属微小病变肾病21刨(其中8例经激素治疗后长期缓解,停药1年以上;其余13例为活动期),膜性肾病30例,膜增殖性肾炎11例。设正常对照组18例。
The hypothesis that hypogammaglobulinemia has long been a cause of nephrotic syndrome is due to its loss from the urine. At present, many scholars believe that this acquired immune deficiency is a complex mechanism, but there is no direct evidence of impairment of IgG synthesis. To do this, we investigated the ability of lymphocytes from 62 patients with nephrotic syndrome with normal renal function to synthesize IgG stimulated by Pokeweed. 62 patients with adult nephrotic syndrome, confirmed by renal biopsy, is a minor lesion nephropathy 21 planing (including 8 cases of long-term relief after hormone therapy, withdrawal of more than 1 year; the remaining 13 cases of active), membranous nephropathy in 30 cases, Membrane proliferative nephritis in 11 cases. 18 cases of normal control group.