Moreover, respiratory motion compensation techniques to assess these lipid pools have been used in 1H-MRS previously, including the heart and pancreas. The mean percentage of renal TG content in the present study content is in line with previous, Dixon-based techniques. The ratio of TG and water show values which are comparable to the quantified amounts of TG found in the human heart. However, one subject showed a consistently higher percentage, which could not be attributed to technical failure, physical activity or nutritional status. Moreover, this volunteer was not different from other subjects in terms of age. In contrast, deliberate planning of the voxel in the region of the renal sinus in a subset of volunteers showed clear overestimation, with TG values ranging from 8 to 25 percent. We can therefore not exclude a relatively wide range in physiological TG content in humans. Future studies on the effects of age, gender differences and the relation of renal cortical TG content with parameters of renal function or proteinuria should address this variability in TG content. A recent study indeed showed an age related increase in renal lipid content in mice, associated with increased glomerulosclerosis, as well as an increase after a high-fat diet. Moreover, high-fat diet induced renal steatosis is reversed with the use of a peroxisome proliferator-activated alpha agonist in mice, with associated improvements in albuminuria and fibrosis. In addition to the PPAR-gamma pathway, the reninangiotensin aldosteron system activation has also been linked to renal adipogenesis. Lisinopril, an ACE-inhibitor, caused normalization of renal adipogenesis and diminished lipid accumulation in uninephrectomized rats. Moreover, it was shown in pigs with the metabolic syndrome that renal adiposity was associated with glomerular hyperfiltration and microvascular proliferation. These animal studies suggest that renal adipogenesis is linked to necessity develop precise controlled national systems permit identify critical pathways in obesity-associated renal disease with possibilities for intervention. However, data in humans is scarce. In humans renal sinus fat is associated with intra-abdominal and retroperitoneal fat content and with control of hypertension. During respiration, movement of the diaphragm causes a displacement of the kidney relative to the spectroscopic voxel. Respiration may thereby influence spectral accuracy and reproducibility by influencing shimming, water suppression as well as varying partial volume changes in fat fraction. To overcome these problems, respiratory motion compensation has been used before to improve 1H-MRS spectral quality. For example by using triggering on exhalation, or with breath-hold acquisition. Both studies were not primarily designed for detection and reproducibility of renal TG content. However, one study reports variations in lipid content as a consequence of contamination with lipids from outside the region of interest during free breathing. The present results are in line with these findings, as spectral quality and reproducibility of renal TG stores improved with respiratory motion compensation. Moreover, all spectra obtained with respiratory motion compensation could be accurately fitted, whereas 4 of the spectra obtained without respiratory motion compensation were of insufficient quality, due to poor water suppression or ghosting signals. The improvements in spectral quality in terms of linewidth are in line with previous reported values for cardiac and skeletal muscle spectroscopy. Moreover, the use of the respiratory navigator improved the coefficient of variation and showed narrower limits of agreement in Bland-Altman analyses. However, the resulting coefficient of variation of 27% remains relatively high. We hypothesize this may be due to local inhomogeneities in renal parenchymal TG content, or variations in cortical and medullar TG content 
contribution within the voxel.