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发热性疾病患者十种血浆蛋白的尿排泄情况。

Urinary excretion of ten plasma proteins in patients with febrile diseases.

作者信息

Hemmingsen L, Skaarup P

出版信息

Acta Med Scand. 1977;201(4):359-64. doi: 10.1111/j.0954-6820.1977.tb15712.x.

Abstract

The 24-hour urinary excretion of albumin, transferrin, haptoglobin, IgG, IgA, IgM, free lambda and kappa light chains from immunoglobulin, lysozyme, and beta2-microglobulin has been investigated in 22 patients with febrile diseases, using an automated immunoprecipitin reaction. The average excretion of the 10 proteins was significantly increased in the patients compared with a control group. In patients with body temperature is greater than or equal to 38.5 degrees C the tubular type of proteinuria was significantly increased compared with those with body temperature is less than 38.5 degrees C. Sequential studies in 10 patients showed that the tubular type of proteinuria occurred in all, whereas the glomerular type was demonstrated in 8. when the fever had subsided, the tubular proteinuria disappeared rapidly i in all patients, while the glomerular proteinuria disappeared in only 4 out of 8. It was shown that tubular proteinuria was caused by fever per se, and it is suggested that glomerular prteinuria might be due to an immue response to antigens, derived from the infectious agents, producing a transient or permanent glomerular injury.

摘要

利用自动免疫沉淀反应,对22例发热性疾病患者的24小时尿白蛋白、转铁蛋白、触珠蛋白、IgG、IgA、IgM、免疫球蛋白游离λ和κ轻链、溶菌酶及β2 -微球蛋白排泄情况进行了研究。与对照组相比,患者这10种蛋白质的平均排泄量显著增加。体温≥38.5℃的患者,肾小管性蛋白尿较体温<38.5℃的患者显著增多。对10例患者的连续研究表明,所有患者均出现肾小管性蛋白尿,8例出现肾小球性蛋白尿。发热消退后,所有患者的肾小管性蛋白尿迅速消失,而8例中的4例肾小球性蛋白尿消失。结果表明,肾小管性蛋白尿由发热本身引起,提示肾小球性蛋白尿可能是由于对来源于感染因子的抗原产生免疫反应,导致肾小球一过性或永久性损伤。

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