Epicardial adipose tissue volume and nephropathy in people living with type 2 diabetes: the Kidn-EAT study

Introduction Epicardial adipose tissue (EAT), a visceral adipose tissue located between the pericardium and the myocardium, has been linked to cardiac issues. The present study aimed to evaluate the association between EAT volume and the presence of nephropathy and its components, i.e. albuminuria/creatininuria ratio (ACR) and estimated glomerular filtration rate (eGFR) classes, in patients living with type 2 diabetes (PwT2D). Materials and methods The present study is a cross-sectional analysis of a retrospective cohort of 700 PwT2D who had a computed tomography scan to measure both their coronary artery calcium score and EAT volume (proprietary prototype, GE HealthCare), and available data for both eGFR and ACR. Results A total of 700 PwT2D (332 women) were included, of whom 295 patients had nephropathy (42.1%), including 87 (12.4%) with eGFR < 60 ml/min/1.73m 2 and 258 (36.9%) with ACR ≥ 3 mg/mmol. Mean age (± standard deviation) was 60.3 ± 10.4 years old and 44.8% had obesity. EAT volume was higher in patients with nephropathy compared to those without (respectively, 103.6 ± 39.8 versus 93.8 ± 36.8 cm 3 , p = 0.001). EAT volume differed across eGFR classes (≥ 60 versus < 60 mL/min/1.73m 2 ): respectively 96.6 ± 38.1 and 107.7 ± 39.2 (p = 0.012) and ACR classes (< 3; between 3 and 29.9; ≥ 30 mg/mmol): respectively 94.7 ± 36.9, 106.0 ± 40.2, and 95.7 ± 39.8 cm 3 (p = 0.004). EAT volume was weakly correlated to eGFR (r = -0.146; p < 0.001) and to ACR (r = 0.124; p = 0.001). After adjustment for major confounding factors, each 10 cm 3 increase of EAT volume was associated with a 5.8% increase in the odds of nephropathy (OR = 1.058 [95% CI 1.007–1.112], p = 0.026) and a 5.9% increase in the odds of ACR ≥ 3 mg/mmol (OR = 1.059 [95% CI 1.008–1.114], p = 0.024), but not with eGFR < 60 mL/min/1.73m 2 (OR = 1.047 [95% CI 0.975–1.123], p = 0.204). Conclusion EAT volume was associated with nephropathy and especially with increased ACR in PwT2D. This association may be partly explained by metabolic and inflammatory mechanisms, potentially driven by EAT and/or other associated ectopic fat depots in PwT2D.