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蛋白尿通常为肾小球毛细血管壁对大分子通透性增加的征象。在大多数肾小球疾患,组织学和功能性肾小球损害的起始均涉及到体液免疫机制和炎症。这种概念促使皮质类固醇和非类固醇抗炎药(NSATD)自50年代早期以来被推广到用于治疗肾变病患者。大多数NSAID是抗蛋白尿药,特别在病人缺钠时。这些药物引起的尿蛋白减少总是明显超过肾小球滤过率之降低,而且剩余的蛋白尿显得选择性较好,这些发现提示NSAID蛋白尿作用由血液动力学介导。NSAID减少肾前列腺素E_2和蛋白尿的排泄,仅苏灵
Proteinuria is usually an indication of increased permeability of macromolecules in the glomerular capillary wall. In most glomerular disorders, the initiation of histological and functional glomerular lesions involves both humoral immune mechanisms and inflammation. This notion has led to the promotion of corticosteroids and non-steroidal anti-inflammatory drugs (NSATDs) since the early 1950s to be used to treat patients with nephropathy. Most NSAIDs are anti-proteinuria, especially when the patient is naïve. These drugs cause a decrease in urinary protein is always significantly lower than the glomerular filtration rate, and the remaining proteinuria appears to be better selectivity, these findings suggest that the role of NSAID proteinuria hemodynamics mediated. NSAID reduces renal prostaglandin E_2 and proteinuria excretion, only Suling