As well as in patients with essential hypertension and a normal renal function and in control subjects. Moreover, we analyzed the potential determinants of renal cortical and medullary tissue oxygenation in these patient groups. The second finding of our study is that renal cortical and medullary oxygenation as measured by BOLD-MRI appears to be extremely well maintained in patients with CKD. Indeed, in contrast to what has been observed experimentally we did not find any decrease in cortical or medullary oxygenation even in advanced CKD; the nature of the underlying renal disease does not appear to play a major role. In this respect, our data are in accordance with the study by Michaely et al, although the latter study could be criticized for some methodological issues. Despite the fact that our study has been performed under very standardized hydration conditions, and detailed information was available on possible confounders such as medication, sodium intake and the type of underlying kidney disease we were not able to demonstrate a reduction of tissue oxygenation as renal disease progressed. The discrepancy between animal studies and BOLD-studies in humans regarding oxygenation can be interpreted in different ways. First of all, it might be that BOLD-MRI is not sensitive enough or simply not as good a tool to assess renal tissue oxygenation in CKD-patients as is direct invasive measurements using microelectrodes. Nonetheless, early animal studies performed to validate the BOLD-MRI technique have reported linear relationships between directly measured renal pO2 values and the BOLD signal. Alternatively, the ROI-technique used to analyze BOLD-images might be less applicable in CKD patients, where loss of cortico-medullary differentiation hampers manual placement of ROIs. Besides, the majority of subjects in the present study had less advanced stage I–III kidney disease, and largely maintained cortico-medullary differentiation; in patients with preserved differentiation, BOLD-MRI is a reliable, reproducible method. Nevertheless, it remains an open question if studies using different methods of analysis such as the recently described compartmental model would obtain similar results. Assuming that BOLDMRI is able to correctly estimate tissue oxygenation in humans, our findings together with those of Michaely et al put into question whether ‘chronic renal hypoxia’ truly exists in humans. In conditions of acute hypoxia, hypoxia-inducible factors are stabilized, which stimulates erythropoietin production, angiogenesis and metabolic reprogramming, offering protection and increasing survival of renal tubular cells under hypoxic conditions. In contrast, chronic HIF stabilization stimulates interstitial fibrosis, a process that is generally believed to compress peritubular capillaries, which further decreases local tissue oxygenation and leads to a vicious circle of HIF-stabilization.