Kaysen G A, Paukert T T, Menke D J, Couser W G, Humphreys M H
Am J Physiol. 1985 Feb;248(2 Pt 2):F247-53. doi: 10.1152/ajprenal.1985.248.2.F247.
Edema formation in nephrotic syndrome has been attributed to intravascular volume depletion resulting from leakage of plasma water into the interstitial space and activating secondary renal sodium retention. However, clinical studies indicate that edematous patients with nephrotic syndrome may have normal or expanded plasma volumes. We evaluated the relationship between plasma volume and edema formation in control rats and rats with chronic renal failure (CRF) produced by 7/8 nephrectomy. In each group, plasma volume and 22Na space were measured during the control period and after induction of hypoalbuminemia from passive Heymann nephritis. Rats with CRF had expanded plasma volume during the initial period (4.23 +/- 0.46 vs. 3.32 +/- 0.68 ml/100 g body wt) that became significantly more expanded (to 5.44 +/- 1.16 ml/100 g body wt) when they became nephrotic as 22Na space also increased. Plasma volume and 22Na space did not change in the sham-operated rats when nephrosis was produced. Plasma renin activity was lower in the CRF rats during the control period than in the sham-operated rats and fell significantly during the nephrotic period when edema developed. Nonnephrotic rats had a plasma colloid osmotic pressure (COP) of 17.8 +/- 4.3 mmHg compared with 8.5 +/- 2.9 mmHg when nephrotic. Despite this large difference in COP, both nephrotic and nonnephrotic rats exhibited the same relationship between plasma volume and extravascular sodium space, a measure of edema formation. Hypoproteinemia is not sufficient for edema formation in the rat with passive Heymann nephritis; concomitant plasma volume expansion resulting from CRF is a necessary additional component.
肾病综合征中的水肿形成归因于血浆水漏入间质间隙导致的血管内容量减少，并激活继发性肾钠潴留。然而，临床研究表明，患有肾病综合征的水肿患者可能具有正常或扩大的血浆容量。我们评估了对照组大鼠和通过7/8肾切除术产生慢性肾衰竭（CRF）的大鼠的血浆容量与水肿形成之间的关系。在每组中，在对照期以及被动海曼肾炎诱导低白蛋白血症后测量血浆容量和22Na空间。CRF大鼠在初始期血浆容量扩大（4.23±0.46对3.32±0.68 ml/100 g体重），当它们患肾病时血浆容量显著扩大（至5.44±1.16 ml/100 g体重），因为22Na空间也增加。当产生肾病时，假手术大鼠的血浆容量和22Na空间没有变化。CRF大鼠在对照期的血浆肾素活性低于假手术大鼠，在水肿发展的肾病期显著下降。非肾病大鼠的血浆胶体渗透压（COP）为17.8±4.3 mmHg，而肾病时为8.5±2.9 mmHg。尽管COP有如此大的差异，但肾病大鼠和非肾病大鼠在血浆容量与血管外钠空间（一种水肿形成的指标）之间表现出相同的关系。低蛋白血症不足以在被动海曼肾炎大鼠中形成水肿；CRF导致的伴随血浆容量扩张是必要的附加因素。
