Baylis C, Deng A, Couser W G
Department of Physiology, Robert C Byrd Health Sciences Center of West Virginia University, Morgantown, USA.
J Am Soc Nephrol. 1995 Oct;6(4):1197-201. doi: 10.1681/ASN.V641197.
In these studies, the Fx1A model of accelerated, passive Heymann nephritis was used to produce membranous glomerulonephropathy. Female rats were studied at 7 wk after the administration of the Fx1A antibody either in the virgin state or in late pregnancy. The goals of these experiments were to determine whether preexisting membranous glomerulonephropathy compromises the pregnancy and whether the pregnancy acutely worsens the renal function. Virgin rats with membranous glomerulonephropathy developed massive proteinuria and exhibited glomerular capillary hypertension but without declines in GFR. In late pregnancy, there was no worsening of the proteinuria and glomerular blood pressure fell to normal values. Both afferent and efferent arteriolar resistances increased in pregnant rats with membranous glomerulonephropathy compared with virgins, leading to falls in glomerular plasma flow and single-nephron GFR. There were no histologic abnormalities in the glomeruli of either virgin or late pregnant rats with membranous glomerulonephropathy, and both groups exhibited similar immunoglobulin G and complement deposits. Up to Day 19 (term is 22 days), the pregnancy in rats with membranous glomerulonephropathy appeared uneventful. Thus, this study indicates that the Fx1A model of membranous glomerulonephropathy does not compromise the course of the pregnancy, at least until close to term. Pregnancy lowers glomerular blood pressure in rats with membranous glomerulonephropathy because of both a fall in systemic blood pressure and the atypical renal vasoconstriction, which leads to declines in single-nephron GFR.
在这些研究中,采用加速型被动海曼肾炎的Fx1A模型来诱发膜性肾小球肾炎。对处于未孕状态或妊娠晚期的雌性大鼠在给予Fx1A抗体7周后进行研究。这些实验的目的是确定预先存在的膜性肾小球肾炎是否会影响妊娠,以及妊娠是否会急性加重肾功能。患有膜性肾小球肾炎的未孕大鼠出现大量蛋白尿,并表现出肾小球毛细血管高压,但肾小球滤过率(GFR)没有下降。在妊娠晚期,蛋白尿没有加重,肾小球血压降至正常水平。与未孕大鼠相比,患有膜性肾小球肾炎的妊娠大鼠入球小动脉和出球小动脉阻力均增加,导致肾小球血浆流量和单肾单位GFR下降。患有膜性肾小球肾炎的未孕或妊娠晚期大鼠的肾小球均无组织学异常,两组均表现出相似的免疫球蛋白G和补体沉积。直到第19天(孕期为22天),患有膜性肾小球肾炎的大鼠的妊娠似乎进展顺利。因此,这项研究表明,膜性肾小球肾炎的Fx1A模型至少在接近足月前不会影响妊娠进程。妊娠会降低患有膜性肾小球肾炎大鼠的肾小球血压,这是由于全身血压下降和非典型肾血管收缩,导致单肾单位GFR下降。