scholarly journals Effects of family history of heart disease, apolipoprotein E phenotype, and lipoprotein(a) on the response of children’s plasma lipids to change in dietary lipids

1997 ◽  
Vol 66 (5) ◽  
pp. 1207-1217 ◽  
Author(s):  
L B Dixon ◽  
B M Shannon ◽  
A M Tershakovec ◽  
M J Bennett ◽  
P M Coates ◽  
...  
Keyword(s):  
Heart Disease ◽  
Family History ◽  
Apolipoprotein E ◽  
Plasma Lipids ◽  
Dietary Lipids ◽  
Lipoprotein A ◽  
History Of

Lipoprotein(a) plasma concentrations, apolipoprotein (a) polymorphism and family history of coronary heart disease in patients with essential hypertension

1996 ◽  
Vol 3 (2) ◽  
pp. 191-197 ◽  
Author(s):  
Carmine Gazzaruso ◽  
Paola Buscaglia ◽  
Adriana Garzaniti ◽  
Graziella Bonetti ◽  
Sandra Savino ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Essential Hypertension ◽  
Family History ◽  
Plasma Concentrations ◽  
Lipoprotein A ◽  
Apolipoprotein A ◽  
History Of

scholarly journals LIPOPROTEIN (a) DOES NOT PREDICT FAMILY HISTORY OF EARLY HEART DISEASE IN HYPERLIPIDEMIC CHILDREN. † 117

1996 ◽  
Vol 39 ◽  
pp. 22-22
Author(s):  
Jay A Barth ◽  
Richard J Deckelbaum ◽  
Thomas J Starc ◽  
Lisa Cohn ◽  
Steven Shea ◽  
...  
Keyword(s):  
Heart Disease ◽  
Family History ◽  
Lipoprotein A ◽  
History Of

scholarly journals Relationship of lipoprotein(a) levels to physical activity and family history of coronary heart disease.

1999 ◽  
Vol 89 (3) ◽  
pp. 383-385 ◽  
Author(s):  
S Martín ◽  
R Elosua ◽  
M I Covas ◽  
M Pavesi ◽  
J Vila ◽  
...  
Keyword(s):  
Physical Activity ◽  
Coronary Heart Disease ◽  
Heart Disease ◽  
Family History ◽  
Lipoprotein A ◽  
History Of ◽  
Relationship Of

scholarly journals Lipoprotein(a) and Coronary Artery Disease Risk Without a Family History of Heart Disease

2021 ◽  
Author(s):  
Phoebe Finneran ◽  
Akhil Pampana ◽  
Sumeet A. Khetarpal ◽  
Mark Trinder ◽  
Aniruddh P. Patel ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Heart Disease ◽  
Coronary Artery ◽  
Family History ◽  
Disease Risk ◽  
Coronary Artery Disease Risk ◽  
Lipoprotein A ◽  
History Of ◽  
Artery Disease

scholarly journals Lipoprotein glomerulopathy associated with the Osaka/Kurashiki APOE variant: two cases identified in Latin America

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Joaquim Nelito da Silveira-Neto ◽  
Guilherme Jinson de Oliveira Ahn ◽  
Precil Diego Miranda de Menezes Neves ◽  
Vinicius Augusto Ferreira Baptista ◽  
Stanley de Almeida Araújo ◽  
...  
Keyword(s):  
Latin America ◽  
Family History ◽  
Kidney Disease ◽  
Genetic Analysis ◽  
Apolipoprotein E ◽  
Total Cholesterol ◽  
Kidney Biopsy ◽  
Lipoprotein Glomerulopathy ◽  
History Of ◽  
Secondary Causes

Abstract Background Lipoprotein glomerulopathy (LPG) is a rare autosomal dominant disease caused by mutations in APOE, the gene which encodes apolipoprotein E. LPG mainly affects Asian individuals, however occasional cases have also been described in Americans and Europeans. Herein we report two unrelated Brazilian patients with LPG in whom genetic analyses revealed the APOE-Osaka/Kurashiki variant. Case presentation - case 1 A 29-year-old Caucasian male sought medical attention with complaints of face swelling and foamy urine for the last 3 months. He denied a family history of kidney disease, consanguinity, or Asian ancestry. His tests showed proteinuria of 12.5 g/24 h, hematuria, serum creatinine 0.94 mg/dL, albumin 2.3 g/dl, total cholesterol 284 mg/dL, LDL 200 mg/dL, triglycerides 175 mg/dL, and negative screening for secondary causes of glomerulopathy. A kidney biopsy revealed intraluminal, laminated deposits of hyaline material in glomerular capillaries consistent with lipoprotein thrombi. These findings were confirmed by electron microscopy, establishing the diagnosis of LPG. His apolipoprotein E serum level was 72 mg/dL and genetic analysis revealed the APOE pathogenic variant c.527G > C, p.Arg176Pro in heterozygosis, known as the Osaka/Kurashiki mutation and positioned nearby the LDL receptor binding site. Case 2 A 34-year-old Caucasian man sought medical assessment for renal dysfunction and hypertension. He reported intermittent episodes of lower-limb edema for 3 years and a family history of kidney disease, but denied Asian ancestry. Laboratorial tests showed BUN 99 mg/dL, creatinine 10.7 mg/dL, total cholesterol 155 mg/dL, LDL 79 mg/dL, triglycerides 277 mg/dL, albumin 3.1 g/dL, proteinuria 2.7 g/24 h, and negative screening for secondary causes of glomerulopathy. His kidney biopsy was consistent with advanced chronic nephropathy secondary to LPG. A genetic analysis also revealed the Osaka/Kurashiki variant. He was transplanted a year ago, displaying no signs of disease relapse. Conclusion We report two unrelated cases of Brazilian patients with a diagnosis of lipoprotein glomerulopathy whose genetic assessment identified the APOE-Osaka/Kurashiki pathogenic variant, previously only described in eastern Asians. While this is the second report of LPG in Latin America, the identification of two unrelated cases by our medical team raises the possibility that LPG may be less rare in this part of the world than currently thought, and should definitely be considered when nephrotic syndrome is associated with suggestive kidney biopsy findings.

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