High Postdialysis Urea Rebound Can Predict Intradialytic Increase in Intraocular Pressure in Dialysis Patients with Lowered Intradialytic Hemoconcentration

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Abstract

Background: 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. Methods: IOP, serum urea and hematocrit levels were measured at the start, end and 1 h postdialysis, in 19 chronic HD patients with normal IOP. Results: PDUR was positively correlated with mean (both eyes) ID changes in IOP (MIDIOP) (r = 0.5, p = 0.03) and % MIDIOP (r = 0.55, p = 0.02). ID increase in IOP was observed only in the 7 patients with relatively higher PDUR (≧9 mg%), who had also a relatively lower % ID change in Hct (<8%). MIDIOP was negatively correlated with % ID changes in Hct (r = –0.65, p = 0.03) in the 12 patients with PDUR ≧9 mg, and positively correlated with PDUR (r = 0.57, p = 0.03) in the 14 patients with % ID change in Hct <8%. Conclusion: High PDUR may predict susceptibility to ID increase in IOP in patients with lowered ID hemoconcentration.

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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 (publisher-id): NEF

Journal ID (nlm-ta): Nephron

Journal ID (doi): 10.1159/issn.1660-8151

Title: Nephron

Publisher: S. Karger AG

ISSN (Print): 1660-8151

ISSN (Electronic): 2235-3186

Publication date Subscription-year: 2002

Publication date (Print): February 2002

Publication date (Electronic): 30 January 2002

Volume: 90

Issue: 2

Pages: 181-187

Affiliations

Departments of ^aNephrology, ^bEpidemiology and Health Service Evaluation, and ^cOphthalmology, Soroka Medical Center, Ben-Gurion University, Beer-Sheva, Israel

Article

Publisher ID: 49040 Other ID: Nephron 2002;90:181–187

DOI: 10.1159/000049040

PubMed ID: 11818703

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

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Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

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Figures: 2, Tables: 2, References: 22, Pages: 7

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