A novel mutation ApoE2 Kurashiki (R158P) in a patient with lipoprotein glomerulopathy.

نویسندگان

  • Takehiko Tokura
  • Seiji Itano
  • Shinya Kobayashi
  • Atsunori Kuwabara
  • Sohachi Fujimoto
  • Hideyuki Horike
  • Minoru Satoh
  • Norio Komai
  • Naruya Tomita
  • Akira Matsunaga
  • Takao Saito
  • Tamaki Sasaki
  • Naoki Kashihara
چکیده

Lipoprotein glomerulopathy (LPG) is a rare glomerulopathy caused by lipoprotein thrombi. In almost all cases of LPG, several apolipoprotein (apo) E mutations were reported. Here, we present a case of LPG caused by a novel mutation that we named ApoE2 Kurashiki, which substitutes arginine with proline at apoE codon 158. ApoE2 polymorphism is well known for its relationship to type III hyperlipoproteinemia, and the common apoE2 isoform is encoded by the R158C allele. ApoE2 Kurashiki substitutes at the same codon and cannot be distinguished from common apoE2 by stan-dard apoE genotyping or phenotyping.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Macrophage Infiltration into the Glomeruli in Lipoprotein Glomerulopathy

Lipoprotein glomerulopathy (LPG) is characterized by histopathological features showing intra-glomerular lipoprotein thrombi and type III hyperlipoproteinemia (HLP), with heterozygote mutation of apolipoprotein (apo) E gene. On the other hand, as another renal lipidosis with type III HLP, apoE2 homozygote-related glomerulopathy (apoE2-GN) showing foamy macrophages has been reported. The case of...

متن کامل

A Novel Mutation in Exon 4 of the Low Density Lipoprotein (LDL) Receptor Gene in an Iranian Familial Hypercholesterolemia Patient

Familial hypercholesterolemia (FH) is an autosomal co-dominant disorder of lipid metabolism, caused by mutations in LDL receptor gene. The penetrance of FH is almost 100%, meaning that half of the offspring of affected parents born with disease. The patients are at risk of premature coronary heart disease (CHD). There is no report about the molecular basis of FH in Iran. Identification of mutat...

متن کامل

A rare cause of nephrotic syndrome: lipoprotein glomerulopathy.

Lipoprotein glomerulopathy is a rare kidney disease in which lipoprotein thrombi are seen in the glomerular capillaries. Most of these patients are found in Japan and East Asian countries. The presenting symptoms include proteinuria, an abnormal plasma lipoprotein profile that resembles type III hyperlipoproteinaemia, and a marked increase in serum apolipoprotein E concentration. Previous studi...

متن کامل

Familial Hypercholesterolemia in Iran: A Novel Frameshift Mutation in Low Density Lipoprotein Receptor (LDLR) Gene

  Background and Objective: Familial hypercholesterolemia (FH) is an autosomal trait, which is caused by mutations in Low Density Lipoprotein Receptor (LDLR) gene. FH penetrance is about 100% and worldwide prevalence for heterozygous subjects is almost 1 in 500 and for homozygous 1 in 1,000,000. The patients are at risk of premature coronary heart disease (CHD) due to defective LDLR a...

متن کامل

Human apoE is present on nearly all serum lipoproteins and plays a protective role in atherosclerosis by acting both as a ligand for receptor-mediated lipoprotein clearance and as an acceptor for cholesterol exported by peripheral cells

Journal of Lipid Research Volume 55, 2014 2073 Copyright © 2014 by the American Society for Biochemistry and Molecular Biology, Inc. Human apoE is present on nearly all serum lipoproteins and plays a protective role in atherosclerosis by acting both as a ligand for receptor-mediated lipoprotein clearance and as an acceptor for cholesterol exported by peripheral cells ( 1, 2 ). apoE on triglycer...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Journal of atherosclerosis and thrombosis

دوره 18 6  شماره 

صفحات  -

تاریخ انتشار 2011