Abstract
ABSTRACTUveitic glaucoma consists one of the most serious complications of intraocular inflammation and, despite its rarity, is considered as one of the leading causes of preventable loss of vision worldwide. It has been associated with a wide spectrum of inflammatory diseases, but its pathogenesis is still not fully comprehended. It appears that the type of inflammation, the steroid-response and the anatomical alterations of the anterior chamber play a pivotal role. To our knowledge, the mechanisms may be both acute and chronic. The main targets of the treatment are to control the inflammation and reduce the intraocular pressure (IOP). The management of glaucoma associated with uveitis remains an extremely challenging condition for ophthalmologists. The successful treatment of uveitic glaucoma is inextricably correlated with prompt and immediate therapeutic decisions. Very often a solid collaboration between clinicians from different specialties may be required for treating the underlying disease.Further understanding of its pathogenesis can indicate therapeutic targets and may lead to the development of new and more efficient therapeutic approaches. New glaucoma surgical modalities may ameliorate the prognosis after surgical intervention, but this calls for further evaluation. This study aims to highlight the complexity of uveitic glaucoma analyzing the main pathogenetic mechanisms and the correlations with the inflammatory response.How to cite this articleKalogeropoulos D, Sung VCT. Pathogenesis of Uveitic Glaucoma. J Curr Glaucoma Pract 2018;12(3):125-138.
Highlights
How to cite this article: Bhagat P, Bharti S, Gupta P, Minz RW, Joshi K, Chhabra S
Antineutrophil cytoplasmic antibody-mediated GN is typically referred to as “pauci-immune”; some immune complex (IC) deposition may be found within the glomeruli on direct immunofluorescence (DIF) or on electron microscopy (EM)
Pauci-immune glomerulonephritis is associated with circulating Antineutrophil cytoplasmic antibody (ANCA) predominantly directed against either myeloperoxidase (MPO) or proteinase 3 (PR3)
Summary
For complement components on DIF and few or no electron-dense deposits on electron microscopy (EM).[1,2] Antineutrophil cytoplasmic antibody-mediated GN is typically referred to as “pauci-immune”; some immune complex (IC) deposition may be found within the glomeruli on DIF or on EM. The composition as well as clinical and pathological significance of IC deposits in ANCA-associated GN is not well known, they are believed to promote development of more severe GN These ANCA-associated GN cases with immune deposits are often referred to as ANCA-positive IC-GN.[3]. This study was done to determine the frequency of IC deposits in 35 renal biopsies from ANCA-positive patients and to study their histopathological features
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