Epicardial and liver fat implications in albuminuria: a retrospective study

Abstract

Background: Albuminuria is considered an early and sensitive marker of kidney dysfunction, but also an independent cardiovascular risk factor. Considering the possible relationship among metabolic liver disease, cardiovascular disease and chronic kidney disease, we aimed to evaluate the risk of developing albuminuria regarding the presence of epicardial adipose tissue and the steatotic liver disease status.

Methods: A retrospective long-term longitudinal study including 181 patients was carried out. Epicardial adipose tissue and steatotic liver disease were assessed by computed tomography. The presence of albuminuria at follow-up was defined as the outcome.

Results: After a median follow up of 11.2 years, steatotic liver disease (HR 3.15; 95% CI, 1.20-8.26; p = 0.02) and excess amount of epicardial adipose tissue (HR 6.12; 95% CI, 1.69-22.19; p = 0.006) were associated with an increased risk of albuminuria after adjustment for visceral adipose tissue, sex, age, weight status, type 2 diabetes, prediabetes, hypertriglyceridemia, hypercholesterolemia, arterial hypertension, and cardiovascular prevention treatment at baseline. The presence of both conditions was associated with a higher risk of developing albuminuria compared to having steatotic liver disease alone (HR 5.91; 95% CI 1.15-30.41, p = 0.033). Compared with the first tertile of visceral adipose tissue, the proportion of subjects with liver steatosis and abnormal epicardial adipose tissue was significantly higher in the second and third tertile. We found a significant correlation between epicardial fat and steatotic liver disease (rho = 0.43 [p < 0.001]).

Conclusions: Identification and management/decrease of excess adiposity must be a target in the primary and secondary prevention of chronic kidney disease development and progression. Visceral adiposity assessment may be an adequate target in the daily clinical setting. Moreover, epicardial adipose tissue and steatotic liver disease assessment may aid in the primary prevention of renal dysfunction.

Keywords: Albuminuria; Cardiovascular disease; Chronic kidney disease; Epicardial adipose tissue; Steatotic liver disease; Visceral adipose tissue.

Fig. 1

Flowchart of patient participation. CT-WBS, Computed Tomography Whole Body Scan

Fig. 2

Adjusted proportion of participants with abnormal EATi and with SLD in each tertile of visceral adipose tissue. 95% CI, 95% confidence interval. T1: First tertile of VAT (median: 1847.41 [interquartilic range: 1135.21–2427.55]); T2: Second tertile of VAT (median: 3802.65 [interquartilic range: 3241.47–4128.8]); T3: Third tertile of VAT (median: 6007.045 [interquartilic range: 5221.755- 6719.845]). VAT, visceral adipose tissue

Fig. 3

Multivariable adjusted incidence rate of albuminuria at follow-up by the presence or not of SLD at baseline. SLD: steatotic liver disease

Fig. 4

Multivariable adjusted incidence rate of albuminuria at follow-up by level of epicardial adipose tissue. EAT: Epicardial adipose tissue

Fig. 5

Adipose tissue dysfunction continuum. Chronic overfeeding, sedentarism, intestinal dysbiosis and genetic susceptibilities may contribute to adipose tissue dysfunction hampering lipid metabolism and, thus, favoring visceral and liver fat accumulation. Liver fat accumulation and progression may lead to a pro-inflammatory state characterized by lipotoxicity, oxidative stress, elevated renin–angiotensin–aldosterone-system activity, and eventually endothelial and organ dysfunction. Epicardial adipose tissue and perirenal fat have mesothelial layers enriched in white adipose tissue progenitors thus adipose tissue dysfunction enhance a proinflammatory state in organs eventually leading to fibrosis and apoptosis. AT: adipose tissue; FFA: free fatty acid; RAS: renin-angiotensin system