Deranged lipid metabolism is a common complication of chronic kidney disease (CKD). Uremia, and metabolic and endocrinological disturbances associated with uremia, as well as the high prevalence of comorbidities, wasting and inflammation in CKD patients, all play their role in promoting and modifying CKD-associated dyslipidemia. However, the exact pathomechanisms leading to lipid disorders are still poorly understood. Similarly, the impact of lipid disturbances on patient outcome is unclear. Many studies in dialysis patients have documented the, so called, ‘reverse epidemiology’, with low plasma cholesterol being an apparent risk factor for mortality. Potential explanations for this phenomenon include confounding by wasting and comorbidities, reverse causation, and also causal relationships with hypocholesterolemia having a direct impact on poor outcome. To elucidate the question of ‘reverse epidemiology’ some novel approaches have been introduced, for example, Mendelian randomization and time-dependent conditional survival analysis. This review aims to outline the major mechanisms responsible for the uremic dyslipidemia, and will attempt to shed light on the issue of CKD-associated reverse association between lipid risk factors and mortality.
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Bengt Lindholm (2009) studied this question.
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