Adipokines in rheumatoid arthritis patients suffering glomerulonephritis

Abstract

Background: Beside their eminent role in metabolic syndrome, white adipose tissue (WAT) derived adipokines might have a distinguished role in autoimmune and rheumatic diseases. In addition, increased level of many adipokines is observed in patients suffering glomerulonephritis. The status of adipokines was not studied in rheumatoid arthritis patients (RA) suffering glomerulonephritis (GN). Objective: To study serum level of adiponectin, leptin, and Visfatin in RA patients suffering GN in a trial to elucidate if they play a role on metabolic or endothelial function. Cases and methods: In this cross-sectional case control observational study, we compared serum level of adiponectin, leptin, and Visfatin in fifty RA patients (group I) in coparison to fifty RA cases suffering chronic GN (group II) and fifty normal control subjects. In addition, we looked for kidney function tests and 24 urine protein (UP), serum calcium, phosphorus, alkaline phosphatase (AP), 25 hydroxy vitamin D (25 OH vit. D), parathyroid hormone (PTH), C-reactive protein (CRP), interleukin 6(IL6), lipid profile, and Homa insulin resistanc (Homa IR). RA cases were further investigated for rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) carotid arteries intima media thickness (IMT), brachial artery flow mediated Dilation (BA-FMD), health assessment questionnaire (HAQ), disease activity score calculator (DASC), simple disease activity index (SDAI), and clinical disease activity index (CDAI). Percutaneous kidney biopsies were obtained in group II patients. Results: Serum adiponectin and Visfatin are significantly higher and serum leptin is significantly lower in Group II compared to group I and the control group (20.3 vs. 18.6 and 12.3, 24,5 vs. 20.9 and 9.8, and 3.6 vs. 4.6 and 7.8 ng/mL for median serum adiponectin, visfatin, and leptin in group II vs group I and control group respectively, P<0.001 in all). Serum level of 25 (OH) vit D is significantly lower, while serum AP, PTH and Homa IR are significantly higher in group I compared to control subjects (18 vs. 37 ng/mL, 140.5 vs, 57 u/L, 63 vs 47.8 ng/mL, and 13.2 vs 4 respectively, P<0.001 in all) whilst there is no significant difference in these parameters between the RA groups. BA-FMD is significantly lower in group II vs group I (3% vs 4%, P=0.02) but there are no significant differences between these two groups in IMT of carotid arteries, HAQ, DASC, SDAI or CDAI. Moreover, there is no difference in any of the studied parameters within patients of group II according to renal histopathology. Conclusion: Studied adipokines have no relation to metabolic or vascular complications of RA. Changes of serum adipokines in GN patients are unrelated to inflammation. This pilot study would stimulate further research looking for the possible role of different adipokines in GN complicating RA.