Renal outcomes following fundus fluorescein angiography in patients with diabetic nephropathy: Incidence, risk factors and three-month kidney function changes.
Source: PubMed, NCBI / U.S. National Library of Medicine
The aim of this study was to determine the incidence of contrast-associated acute kidney injury (CA-AKI) after fundus fluorescein angiography (FFA) in a high-risk diabetic nephropathy (DN) population, to identify clinical predictors of renal injury and to evaluate the effect of acute exacerbation on 3-month eGFR changes. This retrospective cohort study included 307 patients diagnosed with DN. CA-AKI was defined as an increase of ≥0.3 mg/dL in serum creatinine level within 48 h or ≥1.5-fold increase within 7 days after FFA exposure. Patients' medication history and 3-month post-procedure eGFR values were recorded. Independent factors predicting CA-AKI development were assessed using multivariate logistic regression, while long-term losses were evaluated using linear regression and ROC analysis. CA-AKI occurred in 5.2% of patients. Lower baseline eGFR and diuretic use were independent predictors of CA-AKI. ROC analysis identified a baseline eGFR threshold of ≤32 mL/min/1.73 mfor increased CA-AKI risk, and a combined model including eGFR and diuretic use demonstrated superior predictive accuracy. Although SGLT-2 inhibitor use was associated with CA-AKI in univariate analysis, it was not independently significant after adjustment. Notably, 13 of 16 patients (81.3%) who developed CA-AKI experienced persistent eGFR decline at 3 months, and CA-AKI was the strongest predictor of subsequent renal function deterioration. FF
Abstract
The aim of this study was to determine the incidence of contrast-associated acute kidney injury (CA-AKI) after fundus fluorescein angiography (FFA) in a high-risk diabetic nephropathy (DN) population, to identify clinical predictors of renal injury and to evaluate the effect of acute exacerbation on 3-month eGFR changes. This retrospective cohort study included 307 patients diagnosed with DN. CA-AKI was defined as an increase of ≥0.3 mg/dL in serum creatinine level within 48 h or ≥1.5-fold increase within 7 days after FFA exposure. Patients' medication history and 3-month post-procedure eGFR values were recorded. Independent factors predicting CA-AKI development were assessed using multivariate logistic regression, while long-term losses were evaluated using linear regression and ROC analysis. CA-AKI occurred in 5.2% of patients. Lower baseline eGFR and diuretic use were independent predictors of CA-AKI. ROC analysis identified a baseline eGFR threshold of ≤32 mL/min/1.73 mfor increased CA-AKI risk, and a combined model including eGFR and diuretic use demonstrated superior predictive accuracy. Although SGLT-2 inhibitor use was associated with CA-AKI in univariate analysis, it was not independently significant after adjustment. Notably, 13 of 16 patients (81.3%) who developed CA-AKI experienced persistent eGFR decline at 3 months, and CA-AKI was the strongest predictor of subsequent renal function deterioration. FFA is associated with a clinically meaningful risk of CA-AKI in patients with advanced DN, particularly in those with eGFR ≤32 mL/min/1.73 mand concurrent diuretic therapy. Careful pre-procedural risk stratification, individualized hydration and post-procedure renal monitoring are warranted.