Albuminuria Is Associated with Open-Angle Glaucoma in Nondiabetic Korean Subjects: A Cross-Sectional Study

Abstract

OBJECTIVE: Systemic vascular dysfunction has been suggested to contribute to glaucomatous damage. Albuminuria is a surrogate marker of endothelial injury, including vessels. However, their relationship is not well understood. This study aimed to investigate the association between albuminuria and the prevalence of open-angle glaucoma (OAG) in nondiabetic subjects.

METHODS: We conducted a cross-sectional study of 4186 nondiabetic participants aged 19 years or older from the 2011-2012 Korea National Health and Nutrition Examination Survey. OAG was defined based on the criteria of the International Society for Geographic and Epidemiologic Ophthalmology. Urinary albumin excretion was assessed by the urinary albumin-to-creatinine ratio (UACR). A multivariate logistic regression analysis was performed to evaluate the relationship between albuminuria and OAG.

RESULTS: Among the subjects, 124 had OAG. The weighted prevalences of microalbuminuria (UACR of 30-299 mg/g creatinine [Cr]) and macroalbuminuria (UACR ≥ 300 mg/g Cr) were 3.2 ± 0.3% and 0.4 ± 0.1%, respectively. The percentages of OAG increased in accordance with increasing UACR tertiles. Compared with subjects in the lower UACR tertile, those in the upper tertile showed an increased prevalence of OAG (odds ratio, 1.963; 95% confidence interval 1.072-3.595, P = 0.029) after adjusting for demographic factors, laboratory parameters, kidney function, and intraocular pressure. Furthermore, even after excluding 155 subjects with microalbuminuria and 19 subjects with macroalbuminuria, a positive association persisted between the upper UACR tertile (low-grade albuminuria) and an increased prevalence of OAG (odds ratio, 2.170; 95% confidence interval, 1.174-4.010, P = 0.014).

CONCLUSION: Albuminuria, even low-grade, was significantly associated with OAG in nondiabetic subjects. This result implies the role of vascular endothelial dysfunction in the pathogenic mechanism of OAG and suggests that careful monitoring of OAG is required in nondiabetic subjects with albuminuria.