Choroidal and Retinal Permeability Changes in Chronic Kidney Disease-A Literature Review

Purpose: This review consolidates current evidence on how chronic kidney disease (CKD)-especially end-stage kidney disease (ESKD) and its treatments-alters choroidal and retinal vascular permeability, leading to changes in intraocular fluid homeostasis. Methods: A literature search of Medical Literature Analysis and Retrieval System Online (MEDLINE), reference lists, and key ophthalmology-nephrology texts was performed for studies published between 1980 and 2025. One-hundred-forty-four articles (clinical trials, observational cohorts, and case reports) met the inclusion criteria. Data were abstracted on choroidal thickness changes, blood-retinal barrier integrity, incidence of Central Serous Chororioretinopathy (CSCR) and Serous Retinal Detachment (SRD) in dialysis and transplant populations, and systemic variables such as oncotic pressure, hypertension, and corticosteroid exposure, with special attention to retinal pigment epithelium (RPE) pump function. Findings were synthesized qualitatively and tabulated where appropriate. Results: ESKD induces a triad of lowered plasma oncotic pressure, fluctuating hydrostatic forces, and impaired RPE pump function that collectively drive subretinal fluid accumulation. Hemodialysis acutely reduces sub-foveal choroidal thickness by a mean of ≈15-25 µm yet shows inconsistent effects on retinal thickness. Large population data demonstrate a three- to four-fold higher SRD risk and ~1.5-fold higher CSCR risk in dialysis patients versus controls, with peritoneal dialysis conferring the greatest hazard. After kidney transplantation, CSCR prevalence approaches 6%, driven by combined stresses of surgery, hypertension, and long-term corticosteroid or calcineurin-inhibitor therapy. Most reported SRDs resolve as systemic parameters normalize, underscoring the importance of promptly identifying systemic drivers. Conclusions: Systemic fluid-pressure imbalances and treatment-related factors in CKD significantly perturb the outer blood-retinal barrier. Regular ophthalmic surveillance, early visual-symptom screening (e.g., Amsler grid), and close nephrologist-ophthalmologist collaboration are essential for timely detection and management. Future research should quantify the relative contribution of hypoalbuminemia, hypertension, and immunosuppression to ocular permeability changes, and evaluate preventive strategies tailored to high-risk CKD subgroups.