The rapid growth in obesity worldwide contributes to an increase in metabolic syndrome and obesity-related kidney disease with an enhanced increased risk for chronic kidney disease, finally progressing to end-stage renal disease. Adipose tissue is a highly active endocrine organ secreting numerous factors that contribute to renal and cardiovascular complications. In renal damage, various adipokines are involved through mediating endothelial dysfunction, inducing oxidative stress and inflammation as well as stimulating renal sympathetic nervous activity, and it reduces cancellous bone but conversely increases cortical bone. Adipokines may also be involved in the development of renal anaemia. A balance exists between more protective adipokines (adiponectin) and factors mediating pathophysiological effects (angiotensin II, TNF alpha). Obesity may cause a disruption of this delicate balance, thereby inducing renal disease. Consequently, weight reduction and lifestyle changes affecting all components of the metabolic syndrome are essential to disrupt this vicious cycle.
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[1]
Amemiya Nobuyuki., 2012, Clinical and experimental nephrology, P1
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Univ Texas Hlth Sci Ctr San Antonio, Dept Med Renal Dis, San Antonio, TX 78229 USAUniv Texas Hlth Sci Ctr San Antonio, Dept Med Renal Dis, San Antonio, TX 78229 USA
Day, Robert T.
Cavaglieri, Rita C.
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Univ Texas Hlth Sci Ctr San Antonio, Dept Med Renal Dis, San Antonio, TX 78229 USAUniv Texas Hlth Sci Ctr San Antonio, Dept Med Renal Dis, San Antonio, TX 78229 USA
机构:
Univ Texas Hlth Sci Ctr San Antonio, Dept Med Renal Dis, San Antonio, TX 78229 USAUniv Texas Hlth Sci Ctr San Antonio, Dept Med Renal Dis, San Antonio, TX 78229 USA
Day, Robert T.
Cavaglieri, Rita C.
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Univ Texas Hlth Sci Ctr San Antonio, Dept Med Renal Dis, San Antonio, TX 78229 USAUniv Texas Hlth Sci Ctr San Antonio, Dept Med Renal Dis, San Antonio, TX 78229 USA