The Causes and Potential Injurious Effects of Elevated Serum Leptin Levels in Chronic Kidney Disease Patients

Abstract

Leptin is an adipokine that regulates appetite and body mass and has many other pleiotropic functions, including regulating kidney function. Increased evidence shows that chronic kidney disease (CKD) is associated with hyperleptinemia, but the reasons for this phenomenon are not fully understood. In this review, we focused on potential causes of hyperleptinemia in patients with CKD and the effects of elevated serum leptin levels on patient kidney function and cardiovascular risk. The available data indicate that the increased concentration of leptin in the blood of CKD patients may result from both decreased leptin elimination from the circulation by the kidneys (due to renal dysfunction) and increased leptin production by the adipose tissue. The overproduction of leptin by the adipose tissue could result from: (a) hyperinsulinemia; (b) chronic inflammation; and (c) significant lipid disturbances in CKD patients. Elevated leptin in CKD patients may further deteriorate kidney function and lead to increased cardiovascular risk.

Keywords: adipose tissue; cardiovascular risk; chronic kidney disease; leptin.

Figure 1

The potential mechanisms leading to hyperleptinemia in patients with CKD. SFA—saturated fatty acids, MUFA—monounsaturated fatty acids, PUFA—polyunsaturated fatty acids, CRP—C Reactive Protein, IL—interleukin, TNF-α—tumor necrosis factor α. The bold arrow symbolizes the increased secretion of leptin.

Figure 2

The potential mechanisms of the harmful effect of hyperleptinemia on kidney function in CKD patients. CVD—cardiovascular disease, ECM—extracellular matrix, RAA—renin–angiotensin–aldosterone system, ROS—reactive oxygen species, SNS—sympathetic nervous system.