1.Calcitropic Hormones and Systemic Factors of Vascular Calcification.
Journal of Korean Society of Endocrinology 2005;20(6):561-570
No Abstract available.
Vascular Calcification*
2.The Classification and Mechanism of Vascular Calcification.
Journal of Korean Society of Endocrinology 2005;20(6):556-560
No Abstract available.
Classification*
;
Vascular Calcification*
3.Osteoporosis and Vascular Calcification: Lesson from OPG KO Mice.
Journal of Korean Society of Endocrinology 2005;20(6):571-588
No Abstract available.
Animals
;
Mice*
;
Osteoporosis*
;
Vascular Calcification*
4.Chronic Kidney Disease and Vascular Calcification.
Korean Journal of Nephrology 2009;28(5):393-396
No abstract available.
Renal Insufficiency, Chronic
;
Vascular Calcification
6.Activin/myostatin receptor signaling and vascular calcifications in chronic kidney disease: A “liaison dangereuse”?
Giacomo GARIBOTTO ; Pasquale ESPOSITO ; Daniela PICCIOTTO ; Daniela VERZOLA
Kidney Research and Clinical Practice 2019;38(4):407-410
No abstract available.
Renal Insufficiency, Chronic
;
Vascular Calcification
8.The mechanisms of medial vascular calcification.
Acta Physiologica Sinica 2016;68(5):592-610
Vascular calcification is an active, invertible and highly regulated pathophysiological process, characterized by the deposition of hydroxyapatite crystal in vascular wall. Vascular calcification is classified into two types based on the sites of calcification: intimal atherosclerotic calcification and Mönckeberg's medial calcification. Medial vascular calcification is a pathological phenomenon commonly existed in diabetes, chronic kidney failure and aging. The current review summarizes the mechanisms of medial vascular calcification.
Calcinosis
;
Humans
;
Tunica Intima
;
Vascular Calcification
9.Vascular Calcification in Patients with End-Stage Renal Disease.
Korean Journal of Nephrology 2010;29(6):847-850
No abstract available.
Humans
;
Kidney Failure, Chronic
;
Vascular Calcification
10.Persistent hypertension for two months in a preterm infant.
Yun-Feng LIU ; Tong-Yan HAN ; Xiao-Mei TONG ; Jing WANG ; Ya-Nan TANG ; Li-Gang CUI ; Xiao-Hui ZHU ; Mei-Hua PIAO ; Qing-Qing WANG ; Hui WU
Chinese Journal of Contemporary Pediatrics 2018;20(11):939-943
A boy aged 2 months (born at 36 weeks of gestation) was admitted due to cough and dyspnea. After admission, he was found to have persistent hypertension, proteinuria, and persistent convulsion, and imaging examination showed extensive calcification of the aorta and major branches and stenosis of local lumens of the abdominal aorta and the right renal artery with increased blood flow velocity. The boy was admitted during the neonatal period due to wet lung and pulmonary arterial hypertension and was found to have hypertension and proteinuria. High-throughput whole-exome sequencing was performed and found two compound heterozygous mutations in the ENPP1 gene from his parents, c.130C>T (p.Q44X) and c.1112A>T (p.Y371F). c.130C>T was a nonsense mutation, which could cause partial deletion of protein from 44 amino acids, and was defined as a primary pathogenic mutation. c.1112A>T was a missense mutation which had been reported as a pathogenic mutation associated with idiopathic infantile arterial calcification (IIAC). Therefore, he was diagnosed with IIAC. He was given phosphonate drugs, antihypertensive drugs, anticonvulsion treatment, and respiratory support. Blood pressure was maintained at the upper limit of normal value. There was no deterioration of arterial calcification. It is concluded that IIAC should be considered for infants with persistent hypertension and extensive vascular calcification, and imaging and genetic examinations should be performed as early as possible to make a confirmed diagnosis.
Humans
;
Hypertension
;
Infant
;
Infant, Premature
;
Male
;
Mutation
;
Vascular Calcification