الفهرس 
Association of dyslipidaemia with LDLreceptor (rs5925) polymorphism in lupus nephritis patients
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Abstract
Systemic lupus erythromatosus (SLE) is the prototypic autoimmune disease characterized by multisystem involvement and accelerated atherosclerosis and its consequences are recognized as one of the most frequent causes of morbidity and mortality. Lupus nephritis patients especially those with active disease and proteinuria is associated with pre-mature atherosclerosis owing to lipid abnormalities. Most of studies reveal that relative risk of myocardial infarction exceeds 5 to 8 times compared to general population (Mirghani HO et al., 2020).
Thus, renal impairment is a strong predictor of future cerebrovascular and cardiovascular events. Furthermore, risk factors that promote atherogenesis also contribute to deteriorating renal function, producing a vicious cycle of renal failure and vascular events. Although lipids alterations are a major risk factor for CVD especially with renal impairment and are routinely measured for CVD risk stratification, the association between dyslipidaemia and lupus nephritis patients remains unclear (Ronda N et al., 2014).
Low density lipoprotein receptor (LDLR) plays an important role in the lipoprotein metabolism, since low density lipoprotein (LDL‐C) is removed from blood vessels through LDLR endocytosis. LDLR gene mutations represent the main genetic cause of familial hypercholesterolemia. Early detection of the affected gene can reduce the risk of dyslipidaemia and its CVD consequences via usage of suitable curative methods (Riehan A et al., 2018). So, it was of interest to study the prevalence of LDLR rs5925 genetic variants among lupus nephritis patients and the effect of these genetic variants on plasma lipid phenotypes, kidney functions and disease activity.