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Query: UMLS:C0039483 (giant cell arteritis)
 3,204 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a case in which giant cell arteritis coexisted with microscopic polyarteritis nodosa and focal-local glomerulonephritis. We also review previous cases of renal abnormalities in giant cell arteritis. We believe that this association of inflammatory renal disease and giant cell arteritis has not been documented in the past.
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PMID:Giant cell arteritis with visceral angiitis. 0 17

We report a case of biopsy-proven temporal arteritis and polymyalgia rheumatica with improved clinical symptoms with steroid treatment but with subsequent renal failure while on steroids. Kidney biopsy showed focal segmental necrotizing glomerulonephritis with crescents and small-vessel vasculitis. Treatment with methylprednisolone and cyclophosphamide achieved normalization of renal function. We emphasize the importance of kidney biopsy because of its therapeutic implications. The previous literature concerning renal disease in temporal arteritis is discussed.
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PMID:Renal failure in temporal arteritis. 148 11

Medial arterial calcification, which has been increasingly recognized in end-stage renal disease (ESRD) patients, has been associated with acutely symptomatic vascular complications including calcific uremic arteriolopathy (calciphylaxis) and ischemic changes in the extremities. This report describes a 50-year-old ESRD patient on maintenance hemodialysis in whom medial arterial calcification developed with features mimicking the findings of temporal arteritis. He complained of persistent bilateral temporal area headaches with associated symptoms of blurred vision; pain in his shoulders, hips, and knees; and intermittent symptoms consistent with jaw claudication. He was not receiving calcium or vitamin D supplements. Superficial temporal arteries were dilated, tortuous, nodular, and tender to palpation. Ophthalmologic examination was unremarkable, except for the presence of peripapillary atrophy. Temporal artery biopsy results showed medial arterial calcification with mild inflammatory changes. No giant cells were identified. Additional long-term complications of medial arterial calcification have included the development of painful ischemic ulceration of the glans penis and extensive mitral annulus calcification detected by echocardiography. The findings in this patient show that clinical manifestations of medial artery calcification associated with ESRD can mimic those seen with other vascular diseases.
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PMID:Medial arterial calcification mimicking temporal arteritis. 1538 38

Temporal arteritis is easily diagnosed and responds gratifyingly to treatment. Renal complications are unusual, but nevertheless occur. Earlier, an association between pauci-immune glomerulonephritis and temporal arteritis was shown. We present a patient who clearly had temporal arteritis but also developed cerebral hemorrhage, pulmonary infiltrates related to granulomatous pulmonary vasculitis, and pauci-immune glomerulonephritis. We suggest that temporal arteritis is neither always localized nor temporal. Instead, the condition can be a lethal, systemic disease. Renal involvement in patients with temporal arteritis is not common and the presence of glomerulonephritis is rare [Jennette and Falk 1994]. Lenz et al. [1998] described a patient who developed vision loss, optic nerve atrophy, elevated erythrocyte sedimentation rate, a positive rheumatoid factor and terminal glomerulonephritis. The renal biopsy showed focal and segmental necrotizing glomerulonephritis, despite negative antineutrophil cytoplasmatic antibodies (ANCA), antinuclear antibodies and antiglomerular basement membrane antibodies. Giant cells were identified in the necrotic vessel walls within the kidney. Immunofluorescence was negative and a diagnosis of ANCA-negative pauci-immune glomerulonephritis was made. The patient did not respond to immunosuppression and developed end-stage renal disease. Although the clinical attributes were consistent with temporal arteritis, no temporal artery biopsy was done in that patient. We recently treated a patient with temporal arteritis and pauci-immune glomerulonephritis. Our patient's course was somewhat different in comparison to the patient described by Lenz et al. [1998].
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PMID:Temporal arteritis with pauci-immune glomerulonephritis: a systemic disease. 1557 Nov 85

We describe an 80-year-old woman who presented with headaches, bilateral jaw claudication and visual symptoms. She was diagnosed with giant cell arteritis, which was confirmed by temporal artery biopsy. She was treated with high-dose prednisone followed by a slow taper, with complete resolution of symptoms. Approximately 4 years later, she developed progressively worsening renal function associated with haematuria. Serological workup revealed a high-titre perinuclear antinuclear cytoplasmic antibody and antibodies to myeloperoxidase. Renal biopsy demonstrated a pauci-immune focal crescentic glomerulonephritis. Extensive review of systems, physical exam and diagnostic studies demonstrated no evidence of extra-renal disease, and she was diagnosed with renal-limited microscopic polyangiitis. High-dose prednisone was resumed, but she refused treatment with either cyclophosphamide or rituximab due to concern for toxicity. Her prednisone dose was tapered and renal function stabilised. Our case highlights the need to recognise the successive occurrence of two distinct vasculitides in a single patient and monitor accordingly.
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PMID:A tale of two vasculitides: biopsy-proven giant cell arteritis followed by the independent development of renal-limited microscopic polyangiitis. 2843 67

A 72-year-old woman with membranous glomerulonephritis and failed renal transplant on peritoneal dialysis presented with bilateral vision loss. She reported several months of diminishing right eye vision that worsened after cataract extraction. On presentation, visual acuity was hand motion in the right and 20/100 in the left eye with a right afferent pupillary defect. Confrontation visual fields were constricted bilaterally. Intraocular pressure was 23 in the right eye, and there was diffuse right eye central corneal opacity with iris neovascularization. Fundus examination revealed bilateral pale optic nerves with cotton wool spot inferior to the left optic disc and diffuse arteriolar whitening with crystalline deposits in the left macula. Given fundus appearance, concurrent ischemic optic neuropathy, and ocular ischemic syndrome, ocular calciphylaxis was suspected. The patient reported development of painful gluteal nodules a month prior, and biopsy revealed calcinosis cutis, a dermatopathologic finding on the spectrum of calcific vasculitides. Her vision continued to decline in both eyes with left eye vision of 20/400. Intravenous sodium thiosulfate through hemodialysis was started with initial improvement in left eye vision to 20/125, but subsequently declined despite treatment. Pathogenesis of systemic calciphylaxis is poorly understood but believed to result from upregulation of osteogenesis and decreased inhibition of vascular calcification in parathyroid axis dyscrasias due to end-stage renal disease. Excess serum calcium-phosphate deposits in blood vessels causing tissue infarction, most commonly in the skin. Prior case reports have described ischemic optic neuropathy mimicking giant cell arteritis and crystalline retinopathy with ocular ischemic syndrome separately. Treatment with empiric intravenous sodium thiosulfate and calcium chelation may preserve vision in some patients.
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PMID:Gazing Into the Crystal Ball: Calciphylaxis Causing Striking Retinal Vascular Calcification, Ocular Ischemic Syndrome, Crystalline Retinopathy, and Ischemic Optic Neuropathy. 3310 6