Prostaglandin D amplifies lupus disease through basophil accumulation in lymphoid organs.

In systemic lupus erythematosus (SLE), autoantibody production can lead to kidney damage and failure, known as lupus nephritis. Basophils amplify the synthesis of autoantibodies by accumulating in secondary lymphoid organs. Here, we show a role for prostaglandin D (PGD) in the pathophysiology of SLE.

Basophils contribute to pristane-induced Lupus-like nephritis model.

Lupus nephritis (LN), one of the most severe outcomes of systemic lupus erythematosus (SLE), is initiated by glomerular deposition of immune-complexes leading to an inflammatory response and kidney failure. Autoantibodies to nuclear antigens and autoreactive B and T cells are central in SLE pathogenesis. Immune mechanisms amplifying this autoantibody production drive flares of the disease.

[Vascular steal syndrome due to the creation of an arteriovenous shunt for hemodialysis, patient information and nephrologist responsibility].

Although responsibility is a fundamental determinant in medical practice, physicians are generally unfamiliar with its principles. The same is true for disclosure requirements and requests for compensation in the event of physical injury. We report on a representative survey of iatrogenic complications that may arise after the implementation of vascular access for haemodialysis and that illustrate's the physician's responsibility and obligation to inform the patient.