When net delivery of fatty acids to non-adipose cells exceeds cellular energy needs or beta-oxidative capacity, one key mechanism of defense against lipotoxicity is the storage of excess fatty acids as triglycerides in lipid droplets. It is thus important to note that triglyceride accumulation is not considered harmful per se, but is instead a quantifiable marker of a disturbed balance between fatty acid supply and utilization. Excess fatty acids that are not betaoxidized or incorporated in triglycerides enter alternative metabolic pathways, resulting in increased cellular content of potentially lipotoxic metabolites, with ceramides as a much touted candidate. This model is compatible with the negative correlation between renal triglyceride and ceramide levels in a subset of samples from our study, suggesting that effective incorporation of excess fatty acids into triglycerides may protect against ceramide-induced renal lipotoxicity. Importantly, there was no detectable relationship between ceramide levels and BMI in our dataset. We postulate that our data on triglycerides reflect a general state of obesity-associated renal fatty acid oversupply, while our data on ceramides reflect inter-individual differences in the metabolic fates of excess fatty acids in the Lactulose kidney due to factors unrelated to BMI. These differences could potentially contribute to clinical variability, with obesity-related kidney disease and nephrolithiasis risk not Prochlorperazine dimaleate salt uniformly manifested in the general population. However, while ceramides have been implicated in lipotoxicity in other organs, little is known about their role in the kidney, and the potential contribution of other lipid metabolites to renal lipotoxicity is also unclear. To further explore the potential role of ceramides in renal pathophysiology, while controlling for the genetic and environmental heterogeneity inherent in human subject research, we studied a rodent model in which renal triglyceride accumulation has been linked with surrogate functional markers of uric acid stone risk, including data showing that reduction of triglyceride accumulation with a PPARc agonist reversed the functional defects.