Klajman A, Avital A, Myers B D
Nephron. 1976;16(5):333-43. doi: 10.1159/000180620.
Complementuria is a common finding in patients with heavy proteinuria from a variety of causes, and was detected in 23 out of 34 nephrotic subjects. Mean excretion of C3 and C4 in these patients was 49 +/- 22 and 14 +/- 3 mg/24h, respectively. The renal handling of complement appears to be largely molecular weight (MW) dependent, an inverse relationship between the sieving coefficient and MW of transferrin, IgG, C3, and C4 obtaining, in nephrotic patients irrespective of the nature of their glomerulopathy or degree of renal function. Furthermore, glomerular sieving of C3 and C4 was not significantly different in patients with immune glomerular injury associated with extensive glomerular complement deposition, from that in patients with non-immune glomerulopathy, suggesting that no unique mechanism exists for the transglomerular passage of complement from serum into the urine of the former group. The finding of a large increase of sieving of C3 and C4 in nephrotic patients with end-stage renal failure may indicate a failure by atrophic tubules to reabsorb and catabolize filtered complement.
补体尿在各种原因导致的大量蛋白尿患者中很常见,在34例肾病患者中有23例检测到补体尿。这些患者中C3和C4的平均排泄量分别为49±22和14±3mg/24小时。补体的肾脏处理似乎很大程度上取决于分子量(MW),在肾病患者中,无论其肾小球病变的性质或肾功能程度如何,转铁蛋白、IgG、C3和C4的筛滤系数与MW之间都呈反比关系。此外,与广泛肾小球补体沉积相关的免疫性肾小球损伤患者的C3和C4肾小球筛滤与非免疫性肾小球病患者并无显著差异,这表明前一组患者中补体从血清经肾小球进入尿液不存在独特机制。终末期肾衰竭肾病患者中C3和C4筛滤大幅增加的发现可能表明萎缩的肾小管无法重吸收和分解代谢滤过的补体。