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非甾体抗炎药可引起多种肾中毒征群,最常见者是阻滞前列腺素(PG)合成而引起血流动力学介导性肾功能障碍。肾皮质和髓质皆能合成PG。皮质中PG主要是PGI_2(前列环素),对肾小球滤过率有重要影响,髓质中PG则主要是PGE_2,它抑制肾小管钠和氯化物再吸收而促进排钠,抑制肾小管对加压素(抗利尿激素)的反应而促进游离水的排泄。因而,非甾体抗炎药通过阻滞PG(特别是PGE_2)的作用,可能导致钠潴留(水肿),甚至增强加压素的作用(低钠血症)。
Non-steroidal anti-inflammatory drugs can cause a wide range of kidney toxicity syndromes, the most common being blockade of prostaglandin (PG) synthesis leading to hemodynamic-mediated renal dysfunction. Renal cortex and medulla can synthesize PG. PG is mainly PGI2 (prostacyclin) in the cortex, has an important effect on the glomerular filtration rate, medulla pGG is mainly PGE2, which inhibits renal tubular reabsorption of sodium and chloride to promote sodium discharge, inhibition of renal tubules Vasopressin (vasopressin) response to promote the release of free water. Thus, NSAIDs can cause sodium retention (edema) and even vasopressin (hyponatremia) by blocking the action of PGs, especially PGE_2.