Conger J D, Falk S A, Guggenheim S J
J Clin Invest. 1981 May;67(5):1334-46. doi: 10.1172/jci110162.
The roles of glomerular functional and morphologic changes were examined in the acute renal failure associated with generalized Shwartzman reaction in postpartum Munich Wistar rats. The susceptibility of postpartum rats to acute deterioration in renal function after a 2-h endotoxin infusion was found to be greater than in virgin litter mates: glomerular filtration rate fell by 93% in the former vs. 24% in the latter group (P less than 0.001). In postpartum rats there were marked changes in platelet count and fibrinogen level (P less than 0.025) compatible with consumption coagulopathy. Renal blood flow and glomerular filtration rate fell from 5.5 +/- 0.9 and 0.74 +/- 0.12 to 2.0 +/- 0.7 and 0.12 +/- 0.01 ml/min, respectively (both P less than 0.001). Blood pressure did not change. Results of glomerular dynamics studies showed decreases in single nephron filtration rate from 28 +/- 7 to 6 +/- 4 nl/min and in glomerular plasma flow rate from 77 +/- 26 to 23 +/- 12 nl/min (both P less than 0.001). Afferent net ultrafiltration pressure fell from 20 +/- 3 to 5 +/- 4 mm Hg due to a fall in glomerular capillary hydraulic pressure from 47 +/- 1 to 29 +/- 5 mm Hg (P less than 0.001). There were four- and twofold increases in afferent and efferent arteriolar resistances, respectively. Less than 20% of glomeruli had evidence of fibrin deposition after 2 h of endotoxin infusion, a time when glomerular filtration rate was reduced by greater than 90%. [1-Sar, 5-Ile, 8-Gly] angiotensin II infusion before endotoxin significantly protected glomerular filtration rate, 62 vs. 7% of control in rats with no preinfusion (P less than 0.01) despite consumption coagulopathy and glomerular fibrin deposition similar to rats without pretreatment. These data suggest that the early deterioration in renal function in the generalized Shwartzman reaction in the postpartum rat is due to major changes in glomerular dynamics induced by neurohumoral agents and that glomerular fibrin deposition plays a lesser pathogenetic role at this time in this disorder. The study does not address the pathogenesis of renal failure in pregnancy nor peripartum renal failure in another species.
在产后慕尼黑Wistar大鼠的与全身性施瓦茨曼反应相关的急性肾衰竭中，研究了肾小球功能和形态学变化的作用。发现产后大鼠在内毒素输注2小时后肾功能急性恶化的易感性高于未生育的同窝仔鼠：前者的肾小球滤过率下降了93%，而后者组下降了24%（P<0.001）。产后大鼠的血小板计数和纤维蛋白原水平有明显变化（P<0.025），符合消耗性凝血病。肾血流量和肾小球滤过率分别从5.5±0.9和0.74±0.12降至2.0±0.7和0.12±0.01 ml/min（均P<0.001）。血压未改变。肾小球动力学研究结果显示，单个肾单位滤过率从28±7降至6±4 nl/min，肾小球血浆流速从77±26降至23±12 nl/min（均P<0.001）。由于肾小球毛细血管液压从47±1降至29±5 mmHg，入球净超滤压从20±3降至5±4 mmHg（P<0.001）。入球和出球小动脉阻力分别增加了四倍和两倍。内毒素输注2小时后，不到20%的肾小球有纤维蛋白沉积迹象，此时肾小球滤过率降低超过90%。在内毒素注射前输注[1- Sar，5-Ile，8-Gly]血管紧张素II可显著保护肾小球滤过率，在未预先输注的大鼠中为62%，而对照组为7%（P<0.01），尽管存在消耗性凝血病和与未预处理大鼠相似的肾小球纤维蛋白沉积。这些数据表明，产后大鼠全身性施瓦茨曼反应中肾功能的早期恶化是由于神经体液因子引起的肾小球动力学的主要变化，并且此时肾小球纤维蛋白沉积在这种疾病中的致病作用较小。该研究未涉及妊娠肾衰竭或其他物种围产期肾衰竭的发病机制。
