Kidney oxygenation by telemetry

Kidney related diseases are a worldwide burden reaching epidemic proportions. Renal hypoxia is thought to be a crucial factor in the vicious circle of disease progression leading to kidney failure. The mechanisms underlying physiological regulation of kidney oxygenation is only partially known. The contribution of renal tissue hypoxia in the initiation and progression of renal disease remains rudimentary. Therefore, the main goal of this thesis was to continuously record dynamics in renal oxygenation during development of kidney injury. In 1998, Fine et al. proposed ‘the hypoxia hypothesis’. This hypothesis describes a vicious circle towards renal failure fueled by hypoxia. During the progression of chronic kidney disease (CKD), low oxygen levels within the kidney are almost always measured at some point. However, the temporal relationship between changes in oxygenation within the kidney during complex physiological and pathophysiological responses is still missing. All oxygenation measurements in the kidney described in this thesis were performed with a telemetry-based technique, that enables direct continuous renal tissue oxygenation measurements in conscious, unwired rats. This thesis adequately shows that oxygen measurements performed by telemetry reveal extra information about the course of renal oxygenation. Kidney oxygenation has circadian rhythmicity and hypoxia can occur transiently in Angiotensin II infused rats. In addition, we further substantiate the view that renal hypoxia is a causative factor in CKD and show the importance of NO availability in oxygenation. This thesis demonstrates the trajectory of oxygenation during altered renal hemodynamics, without confounding effects of anesthesia.