지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 저널정보
- 대한병리학회 Journal of Pathology and Translational Medicine Journal of Pathology and Translational Medicine 제50권 제6호
- 발행연도
- 2016.1
- 수록면
- 405 - 410 (6page)
이용수
초록· 키워드
오류제보하기
Focal segmental glomerulosclerosis (FSGS) is characterized by focal and segmental obliteration of glomerular capillary tufts with increased matrix. FSGS is classified as collapsing, tip, cellular, perihilar and not otherwise specified variants according to the location and character of the sclerotic lesion. Primary or idiopathic FSGS is considered to be related to podocyte injury, and the pathogenesis of podocyte injury has been actively investigated. Several circulating factors affecting podocyte permeability barrier have been proposed, but not proven to cause FSGS. FSGS may also be caused by genetic alterations. These genes are mainly those regulating slit diaphragm structure, actin cytoskeleton of podocytes, and foot process structure. The mode of inheritance and age of onset are different according to the gene involved. Recently, the role of parietal epithelial cells (PECs) has been highlighted. Podocytes and PECs have common mesenchymal progenitors, therefore, PECs could be a source of podocyte repopulation after podocyte injury. Activated PECs migrate along adhesion to the glomerular tuft and may also contribute to the progression of sclerosis. Markers of activated PECs, including CD44, could be used to distinguish FSGS from minimal change disease. The pathogenesis of FSGS is very complex; however, understanding basic mechanisms of podocyte injury is important not only for basic research, but also for daily diagnostic pathology practice.
목차
등록된 정보가 없습니다.
참고문헌 (71)
참고문헌 신청
D’Agati VD / 2004 / Pathologic classification of focal segmental glomerulosclerosis: a working proposal / Am J Kidney Dis 43:368~382
Weiss MA / 1986 / Nephrotic syndrome, progressive irreversible renal failure, and glomerular “collapse”: a new clinicopathologic entity? / Am J Kidney Dis 7:20~28
Moudgil A / 2001 / Association of parvovirus B19 infection with idiopathic collapsing glomerulopathy / Kidney Int 59:2126~2133
Markowitz GS / 2001 / Collapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate / J Am Soc Nephrol 12:1164~1172
Markowitz GS / 2010 / Treatment with IFN-α, -β, or -γ is associated with collapsing focal segmental glomerulosclerosis / Clin J Am Soc Nephrol 5:607~615
Weiss MA / 1986 / Nephrotic syndrome, progressive irreversible renal failure, and glomerular “collapse”: a new clinicopathologic entity? / Am J Kidney Dis 7:20~28
Moudgil A / 2001 / Association of parvovirus B19 infection with idiopathic collapsing glomerulopathy / Kidney Int 59:2126~2133
Markowitz GS / 2001 / Collapsing focal segmental glomerulosclerosis following treatment with high-dose pamidronate / J Am Soc Nephrol 12:1164~1172
Markowitz GS / 2010 / Treatment with IFN-α, -β, or -γ is associated with collapsing focal segmental glomerulosclerosis / Clin J Am Soc Nephrol 5:607~615
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