Abstract

Open-angle glaucoma (OAG) is a common ocularabnormality seen in patients with end-stage renaldisease (ESRD) [1]. Although the pathogenesis ofOAG is not yet fully understood, lowering intraocularpressure is the accepted treatment goal. Withoutadequate treatment, glaucoma can lead to visualdisability and eventual blindness [2].From a simplified viewpoint, intraocular pressure isdetermined by the balance between aqueous produc-tion from the ciliary body and drainage of the aqueoushumour through the trabecular meshwork. Normalintraocular pressure (IOP) ranges from 10 to21mmHg. IOP of 20–30mmHg usually results inchronic optic nerve damage. In cases of significantintraocular hypertension (40–50mmHg), rapid visualloss and retinovascular occlusion may occur.Intradialytic alteration of IOP by conventionalhaemodialysis (CHD) has been well-documented[3,4]. It is generally accepted that there are twoopposing forces, which may impact on IOP duringhaemodialysis: ultrafiltration and solute removal.Tokuyama et al. [3] documented a fall in IOP whichwas inversely correlated with the increase in plasmaoncotic pressure caused by ultrafiltration. In contrast,other authors speculated that the rapid removal ofuraemic toxins via CHD may lower plasma osmolalityat a rate in excess of changes in ocular osmolalityresulting in an acute rise in IOP [5].Nocturnal haemodialysis (NHD), which provides8–10h of renal replacement therapy during sleep,5–7 nights per week, is a form of intensive haemo-dialysis which approximates most closely to normalphysiology [6]. Here, we report our index case inwhich the conversion from CHD to NHD is associatedwith a restoration in IOP. We will further examinethe potential interactions between augmentation ofuraemia clearance, enhanced volume control andchanges in total peripheral resistance in the treatmentof glaucoma with NHD in ESRD patients.

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