Article Sidebar
Published:
Jan 11, 2013Keywords:
Atherosclerosis Fetuin-A Lupus nephritis SLE Vascular Calcification
Article Details
Issue
Section
Articles
Copyright belongs to The Arab Society of Nephrology and Renal Transplantation (ASNRT)
Main Article Content
Negative Correlation between Fetuin-A and Indices of Vascular Disease in Systemic Lupus Erythematosus Patients with and without Lupus Nephritis
Abstract
Introduction: Fetuin-A, a systemic calcification inhibitor, has been negatively related to vascular calcification (VC) and cardiovascular mortality. In this study we investigated the association between fetuin-A levels and atherosclerotic vascular complications in systemic lupus erythematosus (SLE) patients with and without lupus nephritis (LN).
Methods: We recruited 20 SLE patients without LN, 20 SLE patients with LN and 20 healthy controls. We determined serum creatinine, lipid profile, high sensitivity C-reactive protein (hsCRP), calcium, phosphate and fetuin-A levels, and calculated the calcification risk index (CRI) and SLE disease activity index (SLEDAI) for all subjects. Vascular disease burden was assessed by quantification of carotid artery intima-media-thickness (IMT) and the ankle-brachial index (ABI).
Results: Fetuin-A levels were significantly lower in LN patients (0.47 ± 0.1 g/L) compared to SLE patients without LN (0.54 ± 0.1 g/L) and both were significantly lower than controls (0.78 ± 0.2 g/L). CRI was significantly higher in LN patients (89.1 ± 12.1 mg/L) compared to SLE patients without LN (67.2 ± 9.3 mg/L) and both were significantly higher than controls (34.2 ± 6.2 mg/L). Peripheral arterial disease (ABI < 0.9) was significantly more common in LN patients (55%) compared to SLE patients without LN (30%) as well as controls (0%). Fetuin-A levels showed significant negative correlations with serum creatinine, hsCRP, CRI, IMT and ABI in SLE patients with and without LN.
Conclusion: Fetuin-A levels were decreased in SLE patients with and without LN and negatively correlated with vascular complications. This suggests a potentially important role for fetuin-A deficiency as marker of vascular disease in SLE patients with and without LN.
Keywords: Atherosclerosis; Fetuin-A; Lupus nephritis; SLE; Vascular Calcification.
Methods: We recruited 20 SLE patients without LN, 20 SLE patients with LN and 20 healthy controls. We determined serum creatinine, lipid profile, high sensitivity C-reactive protein (hsCRP), calcium, phosphate and fetuin-A levels, and calculated the calcification risk index (CRI) and SLE disease activity index (SLEDAI) for all subjects. Vascular disease burden was assessed by quantification of carotid artery intima-media-thickness (IMT) and the ankle-brachial index (ABI).
Results: Fetuin-A levels were significantly lower in LN patients (0.47 ± 0.1 g/L) compared to SLE patients without LN (0.54 ± 0.1 g/L) and both were significantly lower than controls (0.78 ± 0.2 g/L). CRI was significantly higher in LN patients (89.1 ± 12.1 mg/L) compared to SLE patients without LN (67.2 ± 9.3 mg/L) and both were significantly higher than controls (34.2 ± 6.2 mg/L). Peripheral arterial disease (ABI < 0.9) was significantly more common in LN patients (55%) compared to SLE patients without LN (30%) as well as controls (0%). Fetuin-A levels showed significant negative correlations with serum creatinine, hsCRP, CRI, IMT and ABI in SLE patients with and without LN.
Conclusion: Fetuin-A levels were decreased in SLE patients with and without LN and negatively correlated with vascular complications. This suggests a potentially important role for fetuin-A deficiency as marker of vascular disease in SLE patients with and without LN.
Keywords: Atherosclerosis; Fetuin-A; Lupus nephritis; SLE; Vascular Calcification.
