The emerging pleiotrophic role of adipokines in the uremic phenotype

The obesity epidemic is undoubtedly increasing the total end-stage renal disease population, which has a larger proportion of obese individuals on reaching the dialysis stage. This review discusses recent advances in the pathophysiology of adipose tissue and adipokines that may contribute to increased risk of progression towards end-stage renal disease and cardiovascular damage.

Although leptin effects on blood pressure may negatively affect kidney function, leptin may also induce vascular damage through central and direct effects on both vessels and heart. The contradictory results of adiponectin in uremia are possibly confounded by the disease circumstances. Visfatin may have previously unrecognized roles in angiogenesis and nutrient homeostasis. As visfatin is a ubiquitously expressed enzyme, it may be inaccurate to refer to it as an adipokine.

We still face many unknowns when understanding the putative pleiotrophic effects that adipokines exert in the uremic milieu. Mechanistic and interventional studies are needed to move forward in this area. Conflicting results in patients with ESRD, in whom both beneficial and detrimental effects in uremia outcome are found, are perhaps the consequence of different timing or context-sensitive effects. Specifically, the presence of protein energy wasting and the changing pattern of disease risk may hinder or even reverse the natural action of these molecules.