传统观点认为,肾病综合征(NS)时的水肿是由于血浆自蛋白(ALB)降低致血浆胶体渗透压下降,血管内液体渗漏入组织间隙,使循环血容量减少,肾脏对钠水重吸收增加,同时激活肾素—血管紧张素—醛固酮系统,继发抗利尿激素分泌增多,致使水钠潴留,水肿加重。但近年来研究表明,大多数NS病人的血容量和血浆量并无降低,认为NS时的水钠潴留尚有其它机制参与。我们对近二年来收治的54例NS病人的水肿与 The traditional view is that nephrotic syndrome (NS) edema is due to plasma from the protein (ALB) decreased plasma colloid osmotic pressure decreased, intravascular fluid leakage into the tissue space, so that reduced circulating blood volume, renal reabsorption of sodium Increase, while activating the renin - angiotensin - aldosterone system, secondary to increased secretion of antidiuretic hormone, resulting in sodium and water retention, increased edema. In recent years, however, studies have shown that most patients with NS have no reduction in blood volume and plasma volume, suggesting that there are other mechanisms involved in the sodium and water retention during NS. In the past two years, we treated 54 NS patients with edema and