Ocular Hemodynamic Variations in Chronic Kidney Disease Patients on Hemodialysis - An Observational Study

Glaucoma is the worldwide leading cause of irreversible blindness. The global prevalence of glaucoma for the age range 40-80 years is between 3 and 4%, which will result in approximately 110–120 million glaucoma patients in 2040.1

It is an optic neuropathy with multifactorial etiology of which elevated intraocular pressure (IOP) remains the focus of its treatment. But some glaucoma patients continue to experience optic nerve damage despite decreased IOP.2

However, risk factors other than IOP, such as impaired microvascular circulation, vascular injury, and oxidative stress or hypoxia, are also related to the pathogenesis of glaucoma.3

Altered ocular blood flow was reported to accelerate the development and progression of the disease in such patients. Also, medical conditions that negatively affect ocular blood flow will obviously cause ischemia and reperfusion damage in glaucoma patients and in individuals prone to glaucoma.

Hemodialysis (HD) an important component of the treatment of Chronic Kidney Disease (CKD) that eliminates osmotically active materials, resulting in fluid loss of the body and blood osmolarity.4 And intensive ultrafiltration is usually the factor that precipitates arterial hypotension in these patients.

A strong correlation exists between glaucomatous optic nerve damage and the presence of low diastolic arterial pressure, which gives rise to inadequate ocular perfusion pressure (OPP) explained by the "vascular hypothesis” which suggests that abnormal perfusion of the optic disc is a primary cause of glaucomatous damage.5

Some studies indicate varying effects on IOP during hemodialysis—some report increases, some decreases, and others note no significant changes.

Hence, we intend to study the effect of hemodialysis on the intraocular pressure, ocular perfusion pressure, systolic and diastolic arterial pressures in patients with end-stage renal disease.

The kidney and eye share striking structural, developmental, physiological, and pathogenic pathways. For example, both the glomerulus and choroid have extensive vascular networks of similar structure; the inner retina and glomerular filtration barrier share similar developmental pathways, and the renin–angiotensin–aldosterone hormonal cascade is found in both the eye and the kidney.

The composition and osmolarity of the aqueous humor are similar to the plasma; nevertheless, it has a lower protein concentration and a lower concentration of glucose and urea.

It is thought that an electrolyte and osmolarity disequilibrium might lead to a rise in IOP, since with the reductions in body fluid volume and osmotic pressure caused by HD, the amount of aqueous humor declines mainly by changes in intraocular osmotic pressure rather than plasma osmolality.6

Several studies have investigated how HD affects IOP, but the results have not been consistent. Some studies suggest that it increases during HD, while others indicate that it decreases or remains unchanged during or after the procedure.7

Also, there are instances of transient vision blurring, increased IOP, glaucoma, and retroocular pain during hemodialysis.8

In a retrospective study Glaucoma consecutively developed in 4.3% in the CKD group and 2.8% in the control group (P < 0.0001). CKD increased the risk of glaucoma development.3

Hemodialysis can lead to changes in fluid balance and hemodynamic status, which can affect ocular perfusion and potentially lead to changes in retinal and peripapillary retinal nerve fiber layer thickness. 9