High postdialysis urea rebound can predict intradialytic increase in intraocular pressure in dialysis patients with lowered intradialytic hemoconcentration.

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Abstract

Intradialytic (ID) decrease in intraocular pressure (IOP) parallel to ultrafiltration-induced hemoconcentration has been recently reported. However, exacerbation of glaucoma in hemodialysis (HD) patients during HD sessions is occasionally observed. Postdialysis urea rebound (PDUR) is induced by the lag in urea removal from the cells to urea removal from the extracellular fluid, which when increased can result in ID drag of water to intracellular compartment. It is our hypothesis that similar lag in urea removal from ocular compartments may also be reflected by PDUR, and may induce drag of water into ocular compartments counteracting the effect of hemoconcentration. Our assumption was, therefore, that PDUR might predict ID increase in IOP.

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Vascular aspects in the pathophysiology of glaucomatous optic neuropathy.

Hak Chung, Alon Harris, David Evans … (1999)

Glaucoma remains a major eye illness with unknown etiology. Although elevated intraocular pressure is clearly a major risk factor, vascular deficits may contribute to initiation and progression of glaucoma. When intraocular pressure is acutely elevated in healthy individuals, the resistance index (derived from the peak systolic and end-diastolic velocities and an indirect index of vascular resistance distal to the site of measurement) in the central retinal and posterior ciliary arteries increases progressively. This result implies that mechanical and vascular factors may be coupled in such a way that perfusion of the retina and optic nerve head may be influenced by changes in the intraocular pressure. Further, at night, when ophthalmic artery flow velocities fall as arterial blood pressure falls in glaucoma patients, the risk of disease progression may be increased. The constancy of these same flow velocities in age-matched healthy individuals points to a possible vascular autoregulatory defect in glaucoma. In addition, in normal-tension glaucoma, vasodilation (CO2 inhalation) normalizes retrobulbar arterial flow velocities, hinting that some vascular deficits in glaucoma may be reversible. Finally, Ca2+ channel blockade improves contrast sensitivity in patients with normal-tension glaucoma, who also show increased retrobulbar vessel flow velocities, a result suggesting that visual function loss may be linked to ocular ischemia. Emerging evidence points to a role of ischemia in the pathogenesis of glaucoma, suggesting that treatments designed to improve ocular blood flow may benefit glaucoma patients.

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Progress in measurement of ocular blood flow and relevance to our understanding of glaucoma and age-related macular degeneration.

H.S. Chung, A. Harris, T.A. Ciulla … (1999)

New technologies have facilitated the study of the ocular circulation. These modalities and analysis techniques facilitate very precise and comprehensive study of retinal, choroidal, and retrobulbar circulations. These techniques include: 1. Vessel caliber assessment; 2. Scanning laser ophthalmoscopic fluorescein angiography and indocyanine green angiography to image and evaluate the retinal circulation and choroidal circulation respectively; 3. Laser Doppler flowmetry and confocal scanning laser Doppler flowmetry to measure blood flow in the optic nerve head and retinal capillary beds; 4. Ocular pulse measurement; and 5. color Doppler imaging to measure blood flow velocities in the central retinal artery, the ciliary arteries and the ophthalmic artery. These technique have greatly enhanced the ability to quantify ocular perfusion defects in many disorders, including glaucoma and age-related macular degeneration, two of the most prevalent causes of blindness in the industrialized world. Recently it has become clear, in animal models of glaucoma, that retinal ganglion cells die via apoptosis. The factors that initiate apoptosis in these cells remain obscure, but ischemia may play a central role. Patients with either primary open-angle glaucoma or normal-tension glaucoma experience various ocular blood flow deficits. With regard to age-related macular degeneration, the etiology remains unknown although some theories include primary retinal pigment epithelial senescence, genetic defects such as those found in the ABCR gene which is also defective in Stargardt's disease and ocular perfusion abnormalities. As the choriocapillaris supplies the metabolic needs of the retinal pigment epithelium and the outer retina, perfusion defect in the choriocapillaris could account for some of the physiologic and pathologic changes in AMD. Vascular defects have been identified in both nonexudative and exudative AMD patients using new technologies. This paper is a comprehensive update describing modalities available for the measurement of all new ocular blood flow in human and the clinical use.

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Author and article information

Journal

Journal ID (iso-abbrev): Nephron

Title: Nephron

Publisher: S. Karger AG

ISSN: 1660-8151

ISSN (Print): 1660-8151

Publication date (Electronic): Feb 2002

Volume: 90

Issue: 2

Affiliations

[1 ] Department of Nephrology, Soroka Medical Center, Ben-Gurion University, Beer-Sheva, Israel. dtovbin@bgumail.bgu.ac.il

Article

Publisher Item ID: nef90181

DOI: 10.1159/000049040

PubMed ID: 11818703

SO-VID: 0d67406f-c842-4804-9bcf-732c9d0d8a3d

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