Patients with Systemic lupus erythematosus (SLE) are known to present an increased risk of osteoporosis and cardiovascular calcification. It has also been suggested that bone remodelling and cardiovascular calcification are regulated by the same mechanisms, but inversely in terms of calcium deposition, as osteoporosis is often associated with cardiovascular calcification. Inflammatory and immune factors have been implicated in these two processes.

The role of the RANKL/OPG system in osteoclast differentiation has been elucidated over the last ten years. RANKL induces differentiation of monocytes-macrophages into osteoclasts, while, inversely, OPG exerts an inhibitory role by inactivating RANKL. Differentiation of smooth muscle cells into osteoblasts in the vessel wall induces calcification, and this phenomenon is counterbalanced by differentiation of monocytes into osteoclasts. Although the role of the RANKL/OPG ratio in the pathogenesis of osteoporosis has now been clearly established, its role in vascular calcification is only hypothetical at the present time.

This study will focus on patients with SLE diagnosed and followed in the Amiens University Hospital Internal Medicine and Nephrology departments

Inclusion Criteria:

• Women over 18 years old
• suffering from systemic lupus erythematosus.

Exclusion Criteria:

underlying diseases that can lead to bone and cardiovascular metabolic disturbances :

• Malignancies such as cancer metastasized
• Autoimmune disease other than LED or of overlap syndrome ( rhupus , MCTD )
• Infection by HIV, hepatitis B and C
• Hepatic Cirrhosis
• Chronic renal failure
• Parathyroid disorders