摘要
作者探讨了NIDDM肾病尿PGs的来源,变化的机理及意义。结果提示它们主要来自肾脏;肾病早期尿TXB2、PGE2以及PXB2/PGE2比值即显著升高,6-酮-PGF1a无明显变化;TXB2升高与肾病恶化有关,可提示肾脏早期受损;PGE2升高则属肾病的自身保护反应。这些变化可能与肾小球病损及肾脏血流动力学异常有关。
The source of urinary PGs, the mechanism and significance of urinary PGs changes in NIDDM patients with diabetic nephropathy (DN ) were explored. The results indicated that the urinary PGs were primarily produced by kidneys. For incipient DN, urinary excretion of TXB2 and PGE2,and TXB,IPGE, ratios were significantly augmented,but urinary 6-keto-PGF1a excretion was not different from that of controls. The high production of renal TXB2 was involved in deteriorating of DN,and might reveal the presence of early renal damage. However,the increasedrenal PGE2 synthesis might be a beneficial self-regulation resisting against renal damage.These biochemical alterations are associated with changes in pathomorphism and hemodynamics of glomerulers.
出处
《西安医科大学学报》
CSCD
1994年第1期62-65,共4页
Journal of Xi'an Medical University(Chinese)
关键词
糖尿病
肾病
前列腺素
蛋白尿
diabetic nephropathy
prostaglandins
proteinuria
glomerular filtration rate