Biological Collection in Nephrology for the Study of the Links Between Kidney Disease, Immunity System and Cardiovascular Complications

Kidney damage to systemic lupus erythematosus (SLE), anti-cytoplasmic neutrophil cytoplasmic (ANCA) vasculitis or systemic amyloidosis, expose patients to:

• a risk of renal insufficiency, which depends on the severity of the attack, the delay in the initiation of treatment, and the possible occurrence of relapses, which may leave fibrous sequelae and lead to the development of insufficiency chronic renal disease (CKD)
• a risk of immunosuppression and infectious complications, linked to the renal insufficiency itself or to the toxicity of immunosuppressive treatments aimed at controlling renal disease
• an increased risk of cardiovascular complications, linked on the one hand to the activity of the systemic disease and to the endothelial dysfunction it may entail, and on the other hand to the cardiovascular risk associated with the IRC .

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease, evolving in relapses interrupted by periods of remission. Renal impairment of SLE is common (20-30% of patients in Europe) [1] and severe [2], with an impact on patient survival [3] and a risk of progression to chronic renal insufficiency (IRC). Thus, nearly 40% of patients with severe form develop IRC [4], and 5-10% have terminal IRC at 10 years [5,6]. The classification of renal involvement according to the International Society of Nephrology / Renal Pathology Society (ISN / RPS) [7] distinguishes active proliferative forms, requiring immunosuppressive therapy [8], nonproliferative or purely chronic forms. However, renal biopsy remains an invasive procedure [9], which can hardly be repeatedly performed, let alone pre-emptively, although the onset of tissue damage precedes the emergence of clinically detectable proteinuria [10] . In addition, the response of proliferative lupus nephropathy to immunosuppressive therapy is difficult to predict. The progression in treatment is favorable in 70 to 80% of patients with proliferative form, but 20-30% are refractory to the standard treatment, while others retain important chronic lesions leading to chronic renal insufficiency.

There is therefore a crucial need for non-invasive biomarkers to identify lupus patients at risk for developing renal disease and to predict the severity of histological involvement and response to immunosuppressive therapy.

The investigators believe that the pathophysiological complexity of lupus nephropathy can not be summarized to a single biomarker, and that a global "omic" approach could capture this complexity or identify new pathways.