In the human kidney, various patterns of lipid accumulation have been described in patients with genetic defects of lipid metabolism, including familial dysbetalipoproteinemia, lecithin-cholesterol acyltransferase deficiency, lipoprotein glomerulopathy and alpha-galactosidase A deficiency, as well as in patients with acquired conditions such as hypertensive nephrosclerosis, focal segmental glomerulosclerosis, minimal change disease with massive proteinuria and hepatorenal syndrome. However, whether lipid accumulation occurs with increasing BMI was not known prior to the present study. As the general definition of steatosis is ����any abnormal accumulation of Ramatroban triglycerides within parenchymal cells����, our data suggest that obesity may be associated with renal steatosis, although absolute triglyceride levels in the steatotic kidney are much lower than in the steatotic liver. A large number of animal Imazapic studies using genetic, pharmacologic or dietary manipulations have shown that renal lipid accumulation can occur both in glomeruli and in tubule cells, primarily in proximal tubules, with some variations between genetic strains and experimental models. Lipid accumulation in glomeruli as well as in tubule cells has been postulated to contribute to the pathogenesis of kidney disease in animal models of progressive renal injury. In addition, prior in vivo and in vitro studies from our group have proposed a causal relationship between lipid accumulation in the proximal tubule and altered renal acidification, which can increase uric acid stone risk. It is absolutely imperative to determine whether these studies are relevant for human pathophysiology. One sine qua non condition is detectability of lipid accumulation within the respective renal structures in at-risk individuals. Our findings that kidney cortex triglycerides are localized in both tubule cells and in glomeruli, and track with increasing BMI, suggest that renal lipid accumulation could play a role in obesity-related kidney disease and nephrolithiasis risk.Intracellular lipid droplets are not static fat depots, but dynamic and highly regulated organelles with important normal functions in cellular energy storage and metabolism.