#3668 Adiposopathy, inflammation and perirenal fat

Abstract Background and Aims Patients with chronic kidney disease (CKD) show high cardiovascular complication rates. There are classical cardiovascular risk factors, such as obesity, dyslipidemia, and diabetes affecting general and renal disease populations. Moreover, non-classical factors of risk such as meta-inflammation (chronic low-grade inflammation) are also present in renal-affected patients. In this sick scenario, visceral adiposity has been shown as another threat to the general and CKD population. Although it has not been widely evaluated, the adipose tissue surrounding the kidneys (perirenal fat [PRF]) could provide additional information of interest in the CKD population. The present study aims to assess the relationship between biomarkers of adiposopathy, inflammation, and PRF in patients with mild CKD stages. Method An observational and cross-sectional study was designed. Patients were evaluated at the outpatient clinic in Vithas Consuelo Hospital in Valencia Spain (January–November 2024). Forty-eight patients with different stages of CKD (G1A1 to G3A3) were included. All the patient's data from electronic medical and analytical records were entered into a protocol sheet. The patients that met the inclusion criteria (eGFR ≤90 or >30 ml/min/1.73 m2; age ≥18 years at the time of signing informed consent, and a life expectancy higher than 1 year) were eligible to participate in the study. As exclusion criteria, patients with active inflammatory processes such as infection, active cancer, or other inflammatory states were excluded beyond those mentioned in inclusion. Patients with an AKI, ADPKD, or CKD requiring RRT were also excluded. Patients were discriminated according to the levels of serum leptin (higher or lower than the mean). The thickness of the PRF was measured in centimeters (cm) through a B-mode ultrasound with a 3.5-MHz convex transductor (Alpinion®E-CUBE9; Alpinion Medical Systems, Seoul, Korea). Patients underwent a bilateral renal ultrasound, and the kidneys were measured anteroposteriorly, transversally, and longitudinally. PRF was measured in the distal third between the cortex and the hepatic border and/or spleen. Results The mean age of the patients was 61.7 ± 16 years and the weight and BMI mean were 77.7 Kg and 27.6 Kg/m2, respectively. Patients with higher leptin levels (mean 25.8 ng/ml) showed a correlation with higher levels of triglycerides (146.7 vs 90.3 mg/dl), TNF-α (9.1 vs 8.5 pg/mL), IL-6 (4.3 vs 3.8 pg/mL), and PCR (5.6 vs 4.2 mg/L) than those patients with low levels. The mean PRF thickness of the right and the left kidney was 1.65 and 1.29 cm (SD ± 0.30) respectively (general PRF mean 1.47 cm). Of note, those patients with higher leptin levels show greater accumulation of PRF (1.7 vs 1.1 cm; p 0.005). There was no association between other adiposopathy and kidney function biomarkers (TFGe, creatinine and/or albuminuria. However, as expected, we found a positive correlation between CKD stages and inflammatory markers. Thus, stage G1: TNF-α 6.6 pg/mL and IL-6 3.0 pg/mL; stage G2: TNF-α 8.0 pg/mL and IL-6 3.9 pg/mL; stage G3: TNF-α 10.2 pg/mL, IL-6 5.4 pg/mL. Conclusion These preliminary results show a positive relationship between adiposopathy biomarkers and the inflammatory load in CKD patients. Besides, we found a link between higher levels of leptin and the thickness of PRF. Finally, achieving a decrease in the latter could reduce visceral adipose tissue, thus reducing the cardiovascular risk in CKD-affected patients. Further research with larger sample sizes and longitudinal designs is warranted to validate these findings and explore the underlying mechanisms.