The metabolic burden of diabetes and dyslipidaemia in chronic kidney disease.
Hyperglycaemia induces mitochondrial superoxide production, increases oxidative stress, and leads to activation of the acute-phase response. Hyperglycaemia, impaired renal function, and uraemia cause inflammatory and oxidative processes. Advanced oxidation protein products and advanced glycation end products are formed, leading to subsequent cytokine release. This promotes alterations in lipoprotein metabolism, composition, and function. These changes result in a highly atherogenic environment, perpetuating the vicious cycle of accelerated atherogenesis. The terminal pathway is an elevation of C-reactive protein, a biomarker of both overall and cardiovascular outcome.
Krane
Vera
V
Department of Medicine, Division of Nephrology, University of Würzburg, Würzburg, Germany.
Wanner
Christoph
C
D003920:Diabetes Mellitus / Q000378:metabolism* / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000503:physiopathology*; D006801:Humans; D006949:Hyperlipidemias / Q000378:metabolism* / Q000503:physiopathology*; D007249:Inflammation; D007676:Kidney Failure, Chronic / Q000378:metabolism; D018384:Oxidative Stress; D014511:Uremia / Q000503:physiopathology