Baylis C
Baillieres Clin Obstet Gynaecol. 1987 Dec;1(4):789-813. doi: 10.1016/s0950-3552(87)80035-4.
The gestational increase in glomerular filtration rate (GFR) that occurs in the normal rat is the result exclusively of an increase in plasma flow rate, and there is no sustained increase in glomerular capillary blood pressure during a normal pregnancy. The factor or factors that initiate the gestational renal vasodilatation (and plasma volume expansion) are maternal, not fetoplacental in origin. Apart from ruling out prostaglandins as an initiating agent, animal studies have not yet defined the precise nature of the initiating factors; it is unlikely that the gestational plasma volume expansion can be the sole cause of the increased GFR seen in pregnancy. The normal kidney in pregnancy exhibits substantial renal reserve to amino acid infusion, despite being already vasodilated by the gestational stimulus. The renal volume-sensing and control system of tubuloglomerular feedback is fully operative in pregnancy, and appears to be 'reset' to perceive the expanded plasma volume of pregnancy as normal. This observation agrees with many other indications that the sensors perceiving and controlling intravascular volume are reset during a normal pregnancy to enable the mother to accommodate the increased plasma volume without provoking a natriuretic response. Multiple pregnancies do not have any cumulative, long-term deleterious effects on renal function, either when the underlying function is normal or when it has been compromised by removal of renal mass plus high-protein feeding. In the short-term, pregnancy does not worsen kidney function when underlying glomerulonephritis is present. Therefore, the hyperfiltration of pregnancy does not appear to be a damaging entity, unlike other hyperfiltration states studied in the male rat. Still unknown is the mechanism by which pregnancy does worsen underlying glomerular disease in some women. The preliminary data in the rat, presented above, suggest that the exacerbating influence may be something other than the glomerular haemodynamic changes of pregnancy.
正常大鼠孕期肾小球滤过率(GFR)的增加完全是血浆流速增加的结果,正常妊娠期间肾小球毛细血管血压并无持续升高。启动孕期肾血管舒张(及血浆量增加)的因素源自母体,而非胎儿胎盘。除了排除前列腺素作为启动因素外,动物研究尚未明确启动因素的确切性质;孕期血浆量增加不太可能是孕期GFR增加的唯一原因。尽管孕期刺激已使肾脏血管舒张,但孕期正常肾脏对氨基酸输注仍表现出大量的肾储备。肾小管-肾小球反馈的肾容积感应和控制系统在孕期完全起作用,并且似乎被“重置”,将孕期增加的血浆量视为正常。这一观察结果与许多其他迹象一致,即感知和控制血管内容量的传感器在正常妊娠期间会重置,以使母亲能够适应增加的血浆量而不引发利钠反应。无论是基础功能正常还是因切除肾组织加高蛋白喂养而受损,多胎妊娠对肾功能均无任何累积的长期有害影响。短期内,存在基础肾小球肾炎时,妊娠不会使肾功能恶化。因此,与在雄性大鼠中研究的其他超滤状态不同,孕期的超滤似乎并非有害情况。妊娠究竟通过何种机制使某些女性的基础肾小球疾病恶化仍不清楚。上述大鼠的初步数据表明,加重影响可能并非孕期肾小球血液动力学变化。