Obesity is an independent risk factor for
chronic kidney disease (CKD). The mechanisms linking
obesity and CKD include systemic changes such as
high blood pressure and
hyperglycemia, and intrarenal effects relating to
lipid accumulation. Normal lipid metabolism is integral to renal physiology and disturbances of renal
lipid and energy metabolism are increasingly being linked with
kidney disease.
AMP-activated protein kinase (AMPK) and
acetyl-CoA carboxylase (ACC) are important regulators of
fatty acid oxidation, which is frequently abnormal in the kidney with CKD. A high fat diet reduces renal AMPK activity, thereby contributing to reduced
fatty acid oxidation and energy imbalance, and treatments to activate AMPK are beneficial in animal models of
obesity-related CKD. Studies have found that the specific cell types affected by excessive
lipid accumulation are proximal tubular cells, podocytes, and mesangial cells. Targeting disturbances of renal energy metabolism is a promising approach to addressing the current epidemic of
obesity-related
kidney disease.