René van der Bel

| Chapter 7 | 120 disease cannot yet be determined based on the studies so far, upcoming prospective data will provide the opportunity to make the distinction. Kidney BOLD MRI associates most with the kidneys’ filtration fraction, not with GFR According to the conceptual framework the two determinants of tubular oxygen demand, kidney perfusion and thus oxygenation are sympathetic nerve and renin/angiotensin activity. However, the effect of sympathetic activity on kidney oxygenation has only been investigated in animal models  13 . Non-invasive assessment of kidney oxygenation in humans using blood oxygen level dependent (BOLD) MRI has rapidly developed over the past years. By compar- ing the effects of angiotensin II on kidney perfusion and oxygenation to gold standard GFR and effective renal plasma flow we were able to gather that kidney BOLD MRI associates most with the kidneys’ filtration fraction and not with GFR. As the FF is the product of both the GFR and renal plasma flow, we therefore conclude that simultaneous renal blood flow measurements are indispensable for the correct interpretation of renal BOLD ( Chapter 4 ). In the meantime, another group has substantiated this in CKD patients  14,15 . Sympathetic activation decreases kidney perfusion without a reduction in oxygenation With these insights we moved on to investigate the effects of sympathetic activation on kid- ney hemodynamics and oxygenation using lower body negative pressure (LBNP), in Chapter 5 . Using LBNP as a selective sympathetic stimulant we found that it substantially increased renal vascular resistance and reduced kidney perfusion, similar to that achieved by angioten- sin II infusion. However, this was not accompanied by a reduction in kidney oxygenation, not in the cortex nor in the medulla. These exploratory data question the physiological concept that sympathetic hyperactivity per se decreases kidney oxygenation. In contrast to the conceptual framework, this implies that systemic sympathetic activation decreases kidney perfusion without a parallel reduction in oxygenation, at least in healthy humans. Conversely in patients, pre-existent metabolic dysregulation in the kidneys may cause hypoxia during increased sympathetic activity. This has yet to be investigated. Improving MRI based functional assessment of the kidneys Current functional MRI of the kidneys is not yet capable to fully evaluate the complex rheo- logical attributes of the kidneys. On the one hand this can be overcome using innovative post processing techniques, and the implementation of new advanced MRI modalities on the other. Innovative post processing can for instance be used to visualize and quantify the oxygenation gradient within the kidneys, as shown in Chapter 4 16,17 . Adoption of other MRI modalities to quantify and map kidney perfusion could prove valuable in the future as the currently used phase contrast method only provides global kidney perfusion quantification