Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0162871 (abdominal aortic aneurysm)
 8,664 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Relapsing polychondritis is purported to be an autoimmune disease characterized by inflammation of cartilaginous structures including the nose, ears, glottis, trachea, and mainstem bronchi. Arthropathy, aortopathy, scleritis, conjunctivitis, iritis, vertigo, otitis media, glomerulonephritis, and skin lesions are common manifestations. We have recently cared for an elderly nonsmoker with a history of abdominal aortic aneurysm repair and recurrent bouts of painful ear swelling who presented with a pulmonary infiltrate and pulmonary function studies suggestive of small airways disease. Subsequent transbronchial biopsy revealed no pathogens but was associated with excessive bleeding, perhaps suggestive of a vasculitic process in the lung. The pulmonary infiltrate cleared over a 2-month interval with the use of corticosteroids. Unusual in this otherwise classical case of relapsing polychondritis was that the pulmonary infiltrate and small airways disease were the prominent pulmonary manifestations and no tracheobronchial abnormalities were visualized.
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PMID:Relapsing polychondritis: new pulmonary manifestations. 157 23

We describe a 71-year-old man, who had been treated for hypertension, myocardial infarction and abdominal aortic aneurysm, and was admitted to our hospital because of proteinuria(3.9 g/day at the outpatient clinic and 1.5 g/day at the time of admission) and edema in the extremities. Light microscopic study of the kidney biopsy specimen revealed mesangial proliferative glomerulonephritis and glomerular paralysis. Electron microscopic findings showed endothelial damage, including widening of the subendothelial space and detachment of endothelial cells from the glomerular basement membrane. Deposition of immunoglobulins and complement was not detected by immunofluorescence studies. These pathological findings resemble the findings of thrombotic microangiopathy, but there were no clinical pictures of HUS/TTP. These findings suggest that hypertension, atherosclerosis and circulating turbulence caused by an aortic aneurysm induced severe glomerular endothelial damage leading to mesangial proliferative glomerulonephritis without an immune response.
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PMID:[A case of mesangial proliferative glomerulonephritis with endothelial damage]. 1247 92

We report a case of methicillin-resistant Staphylococcus aureus (MRSA)-associated glomerulonephritis treated with antibiotic therapy. A 67-year-old man was admitted to our hospital because of proteinuria, hematuria, purpura, and high fever one month after a graft replacement of an abdominal aortic aneurysm. MRSA was detected in specimens of his blood, sputum, and joint fluid. Before his operation, he had shown no renal abnormalities. He presented with a rapid deterioration of renal function following MRSA infection. Maximum level of proteinuria was 1.5 g/day, serum creatinine (Cr) was 3.5 mg/dl, and blood urea nitrogen was 57 mg/dl. Renal biopsy revealed necrotizing crescentic glomerulonephritis. Immunofluorescence examination showed IgA and C3 deposits. Clinical and pathological examinations showed the typical features of MRSA-associated glomerulonephritis. Vancomycin and fosfomycin were administered intravenously. The serum level of C-reactive protein fell from 22.0 mg/dl to 0.1 mg/dl. Proteinuria also decreased and the patient's renal function improved in parallel with the decreased activity of MRSA infection. After three months of antibiotic treatment, proteinuria was negative and the level of serum Cr had dropped to 0.9 mg/dl. These findings suggest that antibiotic treatment can lead to complete remission of MRSA-associated glomerulonephritis.
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PMID:[Successful treatment of MRSA-associated glomerulonephritis with antibiotic therapy]. 1268 Mar 19

Treatment options for crescentic glomerulonephritis include the use of steroids, cytotoxic therapy, and, in severe cases, intravenous immunoglobulins and plasmapheresis. Injury and lysis of capillary glomerular basement membrane, which is made up of type IV collagen, laminin, fibronectin, and proteoglycans, by serine proteinases and matrix metalloproteinases (MMPs) likely is an important participant in the pathogenesis of crescentic glomerulonephritis. Tetracycline derivatives inhibit not only the activity of MMPs, but also their production, and have been investigated for the treatment of disorders in which the MMP system becomes amplified, such as degenerative osteoarthritis, periodontitis, cancer, and abdominal aortic aneurysm. We report an interesting case of crescentic glomerulonephritis in a young man who was treated with cyclophosphamide and prednisone. The patient developed steroid-induced acne that was treated with long-term oral doxycycline therapy. During the period the patient was administered doxycycline, proteinuria decreased by 70% and recurred when doxycycline was stopped. To our knowledge, this is the first report of possible benefits of a metalloproteinase inhibitor (doxycycline) in glomerulonephritis in humans. Future studies are urgently required to explore the option of metalloproteinase inhibitors in the treatment of proliferative glomerulonephritis.
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PMID:Doxycycline decreases proteinuria in glomerulonephritis. 1290 Aug 22

A 53-year-old male who was being followed up by a nephrology department because of type V crescentic glomerulonephritis was admitted with abdominal pain to our clinic. He was diagnosed with abdominal aortic aneurysm after the examinations. Aortic repair with a tubular graft was performed. Pathological examination of the aneurysm tissue showed fungal hyphae. We started antifungal chemotherapy with amphotericin B. A separation of the graft body occurred, and the patient was reoperated on. An excision of the graft, ligation of the aorta, and axillobifemoral graft by-pass was performed. At the 15(th) month of his discharge, the patient was readmitted to the emergency room of our clinic suffering from hematemesis. According to the examinations, an aortoduodenal fistula was diagnosed, and we performed a partial duodenal resection and end-to-end duodenoduodenostomy. We want to share this unusual, interesting, and complicated case, operated on several times because of a mycotic aneurysm due to a fungal infection.
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PMID:A real mycotic aneurysm-mycotic aneurysm of the abdominal aorta due to fungal infection. 2593 34

Obesity-induced kidney injury contributes to albuminuria, which is characterized by a progressive decline in renal function leading to glomerulosclerosis and renal fibrosis. Matrix metalloproteinases (MMPs) modulate inflammation and fibrosis by degrading a variety of extracellular matrix and regulating the activities of effector proteins. Abnormal regulation of MMP-12 expression has been implicated in abdominal aortic aneurysm, atherosclerosis, and emphysema, but the underlying mechanisms remain unclear. The present study examined the function of MMP-12 in glomerular fibrogenesis and inflammation using apo E(-/-) or apo E(-/-)MMP-12(-/-) mice and maintained on a high-fat-diet (HFD) for 3, 6, or 9 months. MMP-12 deletion reduced glomerular matrix accumulation, and downregulated the expression of NADPH oxidase 4 and the subunit-p67(phox), indicating the inhibition of renal oxidative stress. In addition, the expression of the inflammation-associated molecule MCP-1 and macrophage marker-CD11b was decreased in glomeruli of apo E(-/-)MMP-12(-/-) mice fed HFD. MMP-12 produced by macrophages infiltrating into glomeruli contributed to the degradation of collagen type IV and fibronectin. Crescent formation due to renal oxidative stress in Bowman's space was a major factor in the development of fibrogenesis and inflammation. These results suggest that regulating MMP-12 activity could be a therapeutic strategy for the treatment of crescentic glomerulonephritis and fibrogenesis.
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PMID:Matrix metalloproteinase 12 modulates high-fat-diet induced glomerular fibrogenesis and inflammation in a mouse model of obesity. 2682 29