Khamaisi Mogher, Heyman Samuel N
Institute of Endocrinology, Department of Internal Medicine C, Rambam Medical Center, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Harefuah. 2009 Oct;148(10):721-6, 732.
Renal parenchymal hypoxia has recently been documented in a host of clinical and experimental conditions characterized by tubulointerstitial changes and progressive chronic kidney disease (CKD). The nature of renal hypoxia under these settings, its causes and modes of detection are outlined in this review. Cellular hypoxia response, mediated in part by hypoxia-inducible factors (HIF), includes protective components, such as erythropoietin and heme-oxygenase-1, as well as the induction of harmful mediators. Prevention of the progression of CKD include strategies that attenuate renal parenchymal hypoxia, perhaps with selective intensification or inhibition of protective and harmful components, respectively of the hypoxia adaptive response.
最近在一系列以肾小管间质改变和进行性慢性肾脏病(CKD)为特征的临床和实验条件下,均已证实存在肾实质缺氧。本综述概述了在这些情况下肾缺氧的本质、其原因及检测方式。细胞缺氧反应部分由缺氧诱导因子(HIF)介导,包括促红细胞生成素和血红素加氧酶-1等保护性成分,以及有害介质的诱导。预防CKD进展的策略包括减轻肾实质缺氧的措施,或许分别通过选择性增强或抑制缺氧适应性反应中的保护性和有害性成分来实现。