Increased nephron oxygen consumption: potential role in progression of chronic renal disease

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.