Schrier R W, Shapiro J I, Chan L, Harris D C
Department of Medicine, University of Colorado School of Medicine, Denver 80262.
Am J Kidney Dis. 1994 Feb;23(2):176-82. doi: 10.1016/s0272-6386(12)80968-1.
We have previously reported that remnant kidneys demonstrate marked increases in oxygen consumption (QO2) when normalized for sodium transport as compared with normal kidneys. This increase in oxygen consumption could be attenuated by dietary maneuvers such as protein restriction and phosphate restriction and also by calcium channel blockers. The basis of this enhanced metabolic activity, however, has not been fully defined. Furthermore, circumstances of increased oxygen consumption are associated with enhanced oxygen radical generation. These oxygen radicals could lead to renal tissue lipid peroxidation if the remnant kidney contains insufficient oxygen radical scavengers. This review summarizes available evidence for increased nephron oxygen consumption as a cause of tubulointerstitial injury and its relationship to progression of chronic renal disease.
我们之前曾报道，与正常肾脏相比，残余肾单位在按钠转运进行标准化后，其氧耗量（QO2）显著增加。通过蛋白质限制和磷限制等饮食措施以及钙通道阻滞剂可减弱这种氧耗量的增加。然而，这种增强的代谢活性的基础尚未完全明确。此外，氧耗量增加的情况与氧自由基生成增加有关。如果残余肾中氧自由基清除剂不足，这些氧自由基可能导致肾组织脂质过氧化。本综述总结了有关肾单位氧耗量增加作为肾小管间质损伤原因及其与慢性肾病进展关系的现有证据。
