Fibromuscular dysplasia presenting as a renal infarction: a case report

<p>Abstract</p> <p>Introduction</p> <p>Fibromuscular dysplasia is a non-atherosclerotic, non-inflammatory disease that most commonly affects the renal and internal carotid arteries.</p> <p>Case presentation</p> <p>We present the case of a 44-year-old Caucasian man who was admitted with complaints of loin pain and hypertension. A computed tomography scan of the abdomen revealed a right renal infarction with a nodular aspect of the right renal artery. Subsequent renal angiography revealed a typical 'string of beads' pattern of the right renal artery with thrombus formation. Oral anticoagulation was started and the secondary hypertension was easily controlled with anti-hypertensive drugs. At follow-up, our patient refused percutaneous transluminal renal angioplasty as a definitive treatment.</p> <p>Conclusions</p> <p>Fibromuscular dysplasia is the most common cause of renovascular hypertension in patients under 50 years of age. Presentation with renal infarction is rare.</p> <p>In fibromuscular dysplasia, angioplasty has been proven to have, at least for some indications, an advantage over anti-hypertensive drugs. Therefore, hypertension secondary to fibromuscular dysplasia is the most common cause of curable hypertension.</p

Antigenic Complementarity in the Origins of Autoimmunity: A General Theory Illustrated With a Case Study of Idiopathic Thrombocytopenia Purpura

We describe a novel, testable theory of autoimmunity, outline novel predictions made by the theory, and illustrate its application to unravelling the possible causes of idiopathic thrombocytopenia purpura (ITP). Pairs of stereochemically complementary antigens induce complementary immune responses (antibody or T-cell) that create loss of regulation and civil war within the immune system itself. Antibodies attack antibodies creating circulating immune complexes; T-cells attack T-cells creating perivascular cuffing. This immunological civil war abrogates the self-nonself distinction. If at least one of the complementary antigens mimics a self antigen, then this unregulated immune response will target host tissues as well. Data demonstrating that complementary antigens are found in some animal models of autoimmunity and may be present in various human diseases, especially ITP, are reviewed. Specific mechanisms for preventing autoimmunity or suppressing existing autoimmunity are derived from the theory, and critical tests proposed. Finally, we argue that Koch's postulates are inadequate for establishing disease causation for multiple-antigen diseases and discuss the possibility that current research has failed to elucidate the causes of human autoimmune diseases because we are using the wrong criteria