Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal involvement is unusual in giant cell (temporal) arteritis (GCA). Microscopic hematuria and minimal proteinuria responsive to steroid therapy have been described as the most frequent renal alterations. The nephrotic syndrome in GCA has been rarely reported. We describe 2 cases of GCA with nephrotic syndrome, one at the time of diagnosis, the other 2 years after treatment. Percutaneous renal biopsy in both cases disclosed secondary renal amyloidosis confirmed by permanganate sensitivity and immunohistochemical analysis. To our knowledge, cases of GCA and secondary amyloidosis have not been reported.
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PMID:Giant cell (temporal) arteritis and secondary renal amyloidosis: report of 2 cases. 955 98

Patients with different forms of systemic vasculitis experience long-term morbidity and mortality caused by cardiovascular disease due to premature atherosclerosis. Epidemiologic reports of patients with GCA suggest that long-term mortality in this disease is not increased compared with the general population of the same age. The risk of a stroke, however, in particular in the vertebrobasilar territory, is increased. In addition, the occurrence of aortic aneurysmal disease and aortic dissection is also clearly increased in GCA. Mortality due to ischaemic heart disease, however, is not increased. In Takayasu arteritis accelerated atherosclerosis has been clearly documented both clinically and in autopsy reports. Atherosclerotic plaques in the carotid artery may be present in the carotid arteries especially in patients with a documented history of arteritis involving the carotid artery. It is controversial whether Kawasaki disease is associated with accelerated atherosclerosis. Young adults with a history of Kawasaki disease may have abnormal brachial artery reactivity, increased carotid IMT values and increased arterial stiffness. At autopsy examinations of KD patients, however, no significant atherosclerotic lesions are detected and carotid IMT measurements were found to be clearly different from those in young adults with familiar hypercholesterolaemia, suggesting that the remodeling process in KD is different from atherosclerosis. In ANCA-associated vasculitis (AAV), an increased mortality as a consequence of cardiovascular disease is well-documented. In these patients the relative risk for coronary heart disease is two- to fourfold that in control subjects. In addition, a similar relative risk has been found for stroke. Diabetes, hypertension, dyslipidemia, abdominal obesity (metabolic syndrome), impaired renal function, persistent proteinuria and increased production of C-reactive protein are common risk factors for premature atherosclerosis in patients with systemic vasculitis. Furthermore, cholesterol and its modifications play a pivotal role in the pathogenesis of accelerated atherosclerosis in vasculitis. The (preventive) therapy for accelerated atherosclerosis in systemic vasculitis is based on an aggressive approach against inflammation and against risk factors of premature atherosclerosis such as smoking, inactivity, obesity and unhealthy diet. In addition, patients should be treated with angiotensin-converting enzyme inhibitors and/or angiotensin receptor-1 blockers for hypertension and statins for dyslipidemia. Finally, low dose acetylsalicylic acid should be prescribed in patients with large vessel vasculitis, i.e., both in GCA and TA, who do not have contraindications for ASA.
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PMID:Cardiovascular disease due to accelerated atherosclerosis in systemic vasculitides. 2350 55

BACKGROUND Systemic vasculitis can present with a multitude of symptoms involving multiple organ systems. Clinicians should avoid anchoring bias and be cognizant that different types of vasculitides can be present in the same patient and that the diagnosis of one should not preclude the subsequent diagnosis of another. CASE REPORT A 67-year-old woman was referred for evaluation of episodes of epistaxis and recurrent severe sinusitis. Her physical examination showed nasal congestion and purpuric rash on the lower extremities. CT of the sinuses showed severe mucosal thickening. ANCA serologies were positive with a c-ANCA titer of 1: 5120 and anti-proteinase-3 (anti-PR3) antibodies of 1061 units. Serum creatinine was elevated at 1.32 mg/dL (GFR of 40.62 ml/min). Urine analysis showed proteinuria and hematuria. The patient declined treatment initially, but while awaiting kidney biopsy she developed episodes of headache and blurry vision. She underwent right temporal artery biopsy 4 days later, which confirmed the diagnosis of GCA. The biopsy showed characteristic histopathology findings and she was started on 60 mg of prednisone daily. The kidney biopsy showed pauci-immune crescentic glomerulonephritis (PICGN) consistent with ANCA-associated vasculitis. We identified all the cases of co-presentation of GCA and GPA in the literature and summarized their clinical features in this report. CONCLUSIONS Astute clinicians should be cognizant of overlapping and atypical presentations of vasculitides to avoid delayed diagnosis and errors in management.
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PMID:Co-Presentation of Giant Cell Arteritis and Granulomatosis with Polyangiitis: A Case Report and Review of Literature. 2987 33