Kallikrein-kinin activation by altered vitreous pH: New perspectives for treatment and pathogenesis of diabetic macular edema? : Comment on: Gao BB et al. Extracellular carbonic anhydrase mediates hemorrhagic retinal and cerebral vascular permeability through prekallikrein activation. Nat Med. 2007 Feb;13(2):181-8.

O Zeitz, M Keserü

Journal: Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie 2008;245(12):1745-7

PMID: 17823811

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Abstract

Recently, Gao et al. published an experimental study based on the pathophysiology of diabetic macular edema in Nature Medicine (Nat Med. 2007 Feb;13(2):181-8). They found an increased amount of carbonic anhydrase in the vitreous, which causes a pH shift. This activates the kallikrein-kinin system and leads to increased retinal vascular permeability. In this comment the clinical implications of this article are discussed.

Address: Klinik und Poliklinik für Augenheilkunde, Universitätklinikum Hamburg-Eppendorf, Martinitsr. 52, Hamburg 20246, Germany. [email protected]

DOI: 10.1007/s00417-007-0673-7

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https://dx.doi.org/10.1007/s00417-007-0673-7

MeSH Terms: Capillary Permeability, Carbonic Anhydrases, Diabetic Retinopathy, Humans, Hydrogen-Ion Concentration, Kallikrein-Kinin System, Macular Edema, Retinal Vessels, Vitreous Body