Bourgoignie J J
University of Miami School of Medicine, Division of Nephrology, Florida.
Kidney Int Suppl. 1992 May;36:S61-5.
The pathogenesis of progressive renal disease includes systemic hypertension and intrarenal factors that may be hemodynamic or metabolic in origin and involve mediators of inflammation. Most current information derives from experiments in rodents. In other species (rabbit, dog, baboon) subjected to renal mass reduction, a greater variety of pathologic changes is apparent than in rats. Clinical trials at controlling progression of renal disease are compounded by numerous factors; and it is not evident that extrapolation can safely be made from results of animal studies to human disease. The mechanism(s) of renal disease progression in humans, therefore, remain largely unknown. Current therapeutic recommendations in patients with chronic renal disease include limitation of phosphorus absorption, correction of lipid abnormalities and control of systemic blood pressure. The latter can be achieved with a variety of agents some of which, like angiotensin converting enzyme inhibitors and calcium antagonists, may be preferred because of specific intrarenal effects.
进行性肾病的发病机制包括系统性高血压和肾内因素，这些因素可能起源于血流动力学或代谢方面，并涉及炎症介质。目前的大多数信息来自于对啮齿动物的实验。在其他进行了肾质量减少的物种（兔子、狗、狒狒）中，与大鼠相比，明显出现了更多种类的病理变化。控制肾病进展的临床试验受到众多因素的影响；而且，从动物研究结果安全外推至人类疾病并不明显。因此，人类肾病进展的机制在很大程度上仍然未知。目前对慢性肾病患者的治疗建议包括限制磷的吸收、纠正脂质异常和控制系统性血压。后者可以通过多种药物来实现，其中一些药物，如血管紧张素转换酶抑制剂和钙拮抗剂，可能因其特定的肾内作用而更受青睐。
