Central serous chorioretinopathy after solid organ transplantation

Purpose: To describe the demographic and clinical characteristics of central serous chorioretinopathy (CSC) after solid organ transplantation. Design: Case series. Participants: Fifteen patients who presented to the authors with CSC after solid organ transplantation. Methods: We performed a retrospective chart review to identify patient demographics and clinical features of disease, including angiographic changes. Main Outcome Measures: Patterns of CSC. These patterns were compared with type of organ received, demographics, and visual outcome. Results: We identified 25 eyes of 7 women (46.7%) and 8 men (53.3%) that developed CSC after solid organ transplantation. Patient ages ranged from 27 to 55 years (median, 40). Seven of the 15 patients (46.7%) were Caucasian, including 3 Hispanic patients (20%). Of the 8 remaining patients (53.3%), 2 were African American (13.3%), 2 were Filipino (13.3%), and 4 were Asian (26.7%). The organs received included 13 kidneys (86.7%), 1 liver (6.7%), and 1 heart (6.7%). Systemic hypertension was reported in 14 of 15 patients (93.3%). All patients were receiving systemic immunosuppressive drugs at presentation; 14 of 15 (93.3%) were also receiving systemic corticosteroids. Visual acuity at presentation ranged from 20/20 to counting fingers. Patterns of CSC included (1) geographic or diffuse alterations in the retinal pigment epithelium (5 eyes; 2 bilateral, 1 unilateral), (2) focal CSC (6 eyes, all unilateral), (3) multifocal CSC (6 eyes; 2 bilateral, 2 unilateral), and (4) CSC with bullous retinal detachment (8 eyes, all bilateral). Follow-up, available for 21 affected eyes of 13 patients, ranged from 1 month to 6 years (median, 12 months). Compared with other solid organ transplant recipients at our institutions, renal transplant recipients (P = 0.003), as well as Hispanic and Asian patients (P = 0.05), were more prevalent in this cohort. Conclusion: Central serous chorioretinopathy after solid organ transplantation varies in presentation and severity. Our observations support a role for choroidal vascular compromise in the pathogenesis of this disorder.