An Updated Review and Meta Analysis of Lipoprotein Glomerulopathy

Abstract

More than 200 cases of lipoprotein glomerulopathy (LPG) have been reported since it was first discovered 30 years ago. Although relatively rare, LPG is clinically an important cause of nephrotic syndrome and end-stage renal disease. Mutations in the APOE gene are the leading cause of LPG. APOE mutations are an important determinant of lipid profiles and cardiovascular health in the population and can precipitate dysbetalipoproteinemia and glomerulopathy. Apolipoprotein E-related glomerular disorders include APOE2 homozygote glomerulopathy and LPG with heterozygous APOE mutations. In recent years, there has been a rapid increase in the number of LPG case reports and some progress in research into the mechanism and animal models of LPG. We consequently need to update recent epidemiological studies and the molecular mechanisms of LPG. This endeavor may help us not only to diagnose and treat LPG in a more personized manner but also to better understand the potential relationship between lipids and the kidney.

Lipoprotein glomerulopathy with markedly increased arterial stiffness successfully treated with a combination of fenofibrate and losartan: a case report

“…3 ). The mechanisms responsible for the marked reduction in proteinuria in patients with LPG are currently unknown; however, the reduction in blood very-low-density lipoprotein levels by acting on the peroxisomal proliferator-activated receptor and activating lipoprotein lipase by fenofibrate [ 5 ], resulting in the reduction in renal lipid accumulation can be contemplated to be the primary mechanism. Furthermore, once the lipoprotein thrombi are reduced with fenofibrate, the antiproteinuric effect of losartan can be more effective.…”

“…Among the known causative genetic mutations for LPG, ApoE Sendai is the most common in Japan [ 4 ]. The elucidated pathogenic mechanism of LPG has been summarized here [ 5 ]. First, the property of the mutant ApoE protein leads to easy self-aggregation, loss of its ability to bind to low-density lipoprotein (LDL) receptor, and retention of its binding ability to heparan sulfate proteoglycan.…”

“…Accumulating evidence suggests an association of dyslipidemia with the risk of CKD progression and cardiovascular outcomes in patients with CKD [ 8 ]. However, few studies have highlighted the clinical course of cardiovascular diseases (CVDs) associated with LPG [ 5 ].…”

The role of exercise in improving hyperlipidemia-renal injuries induced by a high-fat diet: a literature review

“…This effect may be due to the difference between mesangial expansion and mesangial cell activation ( Joles et al, 2000 ). Mesangial expansion is not only a case of mesangial proliferation, but may also be the recruitment and activation of macrophages in the mesangial area ( Li et al, 2022a ). Bruneval et al.…”

A case report of youth-onset lipoprotein glomerulopathy with APOE Chicago mutation

“…LPG epidemiology is mostly based on case reports, of which are more concentrated in East Asia. The estimated prevalence of LPG in Japan is approximately 3.74 per 10 million people and in China is 1.43 per 10 million people [ 3 ]. Among them, Chinese LPG patients have the highest incidence of APOE Kyoto (Arg25Cys) mutations, while Japanese LPG patients mainly have APOE Sendai (Arg145Pro) mutations [ 3 , 4 ].…”