The emerging biology of adipose tissue in chronic kidney disease: from fat to facts

“No diet will remove all the fat from your body because the brain is entirely fat. Without a brain, you might look good, but all you could do is run for public office.” George Bernard Shaw Regardless of the implications, the incidence of obesity is increasing worldwide [ 1 ] and along with it the proportion of the population subject to hypertension [ 1 ] or type-2 diabetes mellitus [ 1 ]. Furthermore, the metabolic syndrome is an important risk factor for proteinuria and chronic kidney disease (CKD) independently of diabetes and hypertension [ 2 ]. For the nephrologist, this has resulted in both an increased influx of patients with CKD [ 2 ] and a larger and more obese end-stage renal disease (ESRD) population [ 3 ]. However, despite the generally reduced lifespan of obese patients not suffering from CKD [ 4 ], epidemiological studies of the impact of obesity on outcome in CKD remain conflicting, with several well-designed studies even suggesting a survival advantage for obese ESRD patients [ 5,6 ]. These studies were recently addressed in an excellent review in these pages by Mafra et al. [ 7 ] and will not be discussed in detail here. Instead, the present review aims to address the current lack of understanding of the biological basis for any effects attributed to obesity in the context of uraemia. Specifically, in order to better treat the obese CKD patient, we should ask ourselves what mechanisms may link fat to uraemic complications, and how the putative beneficial effects of obesity could be harnessed to benefit our patients.