18F-FAPI PET/CT and Cardiac Magnetic Resonance for Cardiac Fibrotic Process in End-stage Renal Disease

Background: End-stage renal disease (ESRD) increases the risk of myocardial fibrosis. This study aimed to detect cardiac fibroblast activation and fibrosis in ESRD using 18 F-labeled fibroblast activation protein inhibitor (FAPI) PET/CT and cardiac magnetic resonance (CMR). Patients and Methods: This prospective clinical trial (NCT07107919) enrolled 33 ESRD patients who underwent 18 F-FAPI PET/CT, with 19 patients undergoing CMR. Myocardial FAPI activity was quantified. Cardiac function [left ventricular ejection fraction (LVEF), right ventricular ejection fraction (RVEF), left atrial ejection fraction (LAEF)] and tissue parameters [native T1, extracellular volume (ECV), late gadolinium enhancement (LGE)] were assessed by CMR. Spearman correlation analysis assessed correlations between 18 F-FAPI uptake and CMR parameters. Results: A total of 75.76% (25/33) of ESRD patients showed myocardial FAPI uptake, significantly higher than the controls ( P < 0.05). 18 F-FAPI-42 PET identified more segments with evidence of fibroblast activation than CMR-late gadolinium enhancement detected fibrosis (82 vs. 71). Compared with FAPI-negative patients, FAPI-positive patients had increased native-T1, decreased LVEF, LAEF and RVEF ( P < 0.05). FAPI-positive segments showed higher native-T1 and extracellular volume % than FAPI-negative segments ( P < 0.05). FAPI activity correlated with LVEF, RVEF, LAEF and native-T1. Higher myocardial FAPI uptake was associated with lower LVEF and longer dialysis duration. Conclusions: 18 F-FAPI PET enables in vivo detection of cardiac fibroblast activation in ESRD and correlates with functional and tissue parameters by CMR. FAPI uptake may serve as an imaging biomarker for cardiac remodeling. Further studies are warranted to clarify the role of 18 F-FAPI PET in evaluating the efficacy of anti-fibrotic treatment and in assisting cardiac risk stratification in ESRD patients.