Impact of Adipokines in Brachial Artery Flow-mediated Dilatation in Lupus Nephritis

Abstract

Endothelial dysfunction is evident in systemic lupus erythematosus (SLE). Pro-inflammatory adipokines are involved in endothelial derangement and premature atherosclerosis, particularly in lupus nephritis (LN). This study aimed to investigate the impact of LN on endothelial function by estimating the serum levels of adiponectin, leptin, visfatin, and homeostatic model assessment-insulin resistance (HOMA-IR) and calculating the flow-mediated dilatation (FMD) of the brachial artery. This is a case–control study in which 190 systemic lupus patients who were fulfilling the American College of Rheumatology revised classification were enrolled. The patients were divided into 100 LN patients and 90 lupus non-nephritis patients. Demographic data, clinical parameters, and SLE activity were reported. Serum adiponectin, leptin, visfatin, and HOMA-IR were measured. The endothelial dysfunction was assessed by calculating the FMD of the brachial artery. The mean age of participants was 25.62 ± 5.81 years. Elevated levels of adiponectin, leptin, visfatin, and HOMA-IR were observed in LN cases (12.2 ± 0.3, 20.1 ± 0.5, 16.8 ± 0.1, and 12.0 ± 3.8, respectively) compared to non-nephritis cases (12.2 ± 0.3, 8.5 ± 0.5, 16.8 ± 0.5, and 9.0 ± 3.8, respectively) with a more reduced FMD percentage in LN cases with a statistical significance. Brachial artery FMD is negatively correlated with lipid profile, adipokines, and HOMA. Visfatin has better sensitivity (82.1%) and specificity (81%) with the area under a curve of 0.893, compared to other biomarkers. LN patients are characterized by impaired endothelial function. Elevated serum adiponectin, visfatin, and HOMA-IR were significantly correlated with poor FMD of the brachial artery. Visfatin has a better performance in detecting atherosclerosis.