Adipokines as a link between obesity and chronic kidney disease

Abstract

Adipocytes secrete a number of bioactive adipokines that activate a variety of cell signaling pathways in central and peripheral tissues. Obesity is associated with the altered production of many adipokines and is linked to a number of pathologies. As an increase in body weight is directly associated with an increased risk for developing chronic kidney disease (CKD), there is significant interest in the link between obesity and renal dysfunction. Altered levels of the adipokines leptin, adiponectin, resistin, and visfatin can decrease the glomerular filtration rate and increase albuminuria, which are pathophysiological changes typical of CKD. Specifically, exposure of the glomerulus to altered adipokine levels can increase its permeability, fuse the podocytes, and cause mesangial cell hypertrophy, all of which alter the glomerular filtration rate. In addition, the adipokines leptin and adiponectin can act on tubular networks. Thus, adipokines can act on multiple cell types in the development of renal pathophysiology. Importantly, most studies have been performed using in vitro models, with future studies in vivo required to further elucidate the specific roles that adipokines play in the development and progression of CKD.

Visfatin levels are decreased in advanced stages of diabetic nephropathy

“…7 CKD is associated with an abnormal high adipokines level that may be caused by increased fat tissue production and/or reduced renal clearance of them. 8 Recent studies showed that visfatin levels are changed in CKD (DN or not) in parallel to the glomerular dysfunction, severity of proteinuria and endothelial dysfunction. [9][10][11][12] We investigated the association between visfatin levels and stages of CKD in T2DM patients with DN and the correlations with anthropometric and laboratory parameters.…”

Estimación de la tasa de filtración glomerular en personas con y sin síndrome metabólico

“…La exposición del glomérulo a niveles elevados de adipoquinas aumenta su permeabilidad generando hipertrofia celular con la consecuente hiperflitración (10,12,35,36). Así mismo, los adipocitos viscerales secretan angiotensinógeno, estimulando el eje renina-angiotensinaaldosterona, provocando HTA, HF y posterior ERC (36) En esta investigación se encontraron 28 (46,7%) y 24 (40%) casos de pacientes con y sin SM respectivamente con HF.…”

“…Ello es debido a que el tejido adiposo, y en especial el abdominal es considerado un órgano endocrino altamente activo que contribuye a las complicaciones renales mediante la disfunción endotelial, el estrés oxidativo y cambios en la respuesta inmune e inflamación (11), las elevaciones en los niveles de leptina, adiponectina, resistina y visfatin pueden disminuir la filtración glomerular e incremetar la albuminuria con los consecuentes cambios típicos de la enfermedad renal crónica (12).…”

New Insight on Adipose Tissue Function in Advanced Renal Failure

“…Although the exact mechanism of adipokines' action is still unclear, they may play their role by affecting various types of cells in kidney nephrons. 6 Previous studies have shown that increased levels of leptin could lead to hypertrophy in glomerular mesangial cells that could activate fibrotic and inflammatory pathways, and also thickening of the basement membrane and consequently glomerulosclerosis. 6 Moreover, it has been demonstrated that hyperleptinemia could alter the metabolic function of proximal tubular cells and lead to tubular apoptosis.…”

“…6 Previous studies have shown that increased levels of leptin could lead to hypertrophy in glomerular mesangial cells that could activate fibrotic and inflammatory pathways, and also thickening of the basement membrane and consequently glomerulosclerosis. 6 Moreover, it has been demonstrated that hyperleptinemia could alter the metabolic function of proximal tubular cells and lead to tubular apoptosis. 7 These structural changes in the nephrons could result in increased proteinuria, albuminuria and fibrotic pathways in tubular cells through altering the permeability of the cells.…”