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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of kidney transplantation in a variety of renal diseases have been analyzed. The diseases causing end-stage kidney failure in recipients were Alport syndrome, amyloidosis, cystinosis, diabetes mellitus, Fabry disease, familial nephritis, gout, medullary cystic disease, oxalosis, and systemic lupus erythematosus. The data indicate that renal transplantation is justifiable and parallels functional results for the more common causes of end-stage renal disease in all but Fabry disease and oxalosis. Although Fabry disease did not recur in any grafted kidney, only three patients have a functioning graft one year after transplantation. From a group of ten patients with oxalosis who received a total of 14 kidneys, only one survives. In no other metabolic disease, except one instance of primary amyloidosis, did the metabolic disease notably affect the transplant as it did in oxalosis.
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PMID:Renal transplantation in congenital and metabolic diseases. A report from the ASC/NIH renal transplant registry. 80 49

Recently, calcium oxalate crystals have been identified in the synovial fluid of patients with arthritis and end-stage renal failure. We describe 4 patients who, during the course of long-term hemodialysis, developed calcium oxalate crystal deposits in the synovium and skin. Clinical manifestations included podagra, tenosynovitis, olecranon bursitis, and acute and chronic synovitis of the large joints that were associated with chondrocalcinosis or subchondral bone erosions. Diffuse involvement of the hand, with chondrocalcinosis of the finger joints, miliary calcified deposits in the skin, and artery calcifications, was observed in 3 patients. The fourth patient had erosive arthropathy. Oxalosis secondary to end-stage renal failure in patients treated with long-term hemodialysis can present with articular manifestations that resemble those of gout, pseudogout, and apatite deposition disease. Other characteristic features of the synovitis associated with oxalosis secondary to end-stage renal disease were: predominant involvement of the hand, mild inflammatory changes in the synovial fluid and synovium, and poor response to administration of nonsteroidal antiinflammatory agents.
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PMID:Arthropathy and cutaneous calcinosis in hemodialysis oxalosis. 377 44

Morphologic characteristics of granulomatous inflammation in the heart and pericardium are discussed. In rheumatic fever, two types of myocardial lesion are present--a nonspecific myocarditis and a specific lesion characterized by granulomas known as Aschoff's nodules. The latter undergo a cycle of development and resolution; in their mature stage, they contain Aschoff's cells which are uni- or multinucleated histiocytes with a serrated nuclear chromatin bar. Ultrastructural studies do not suggest a relationship between these cells and cardiac or smooth muscle cells. In metabolic disorders, granulomas occur in Farber's disease (lipogranulomatosis), gout (in which tophi are associated with calcific deposits and with a foreign body cellular reaction), the various syndromes of oxalosis (in which oxalate deposits also lead to a foreign body reaction), and in chronic granulomatous disease of childhood. Foreign body giant-cells can also be found in association with calcification of necrotic myocytes and in the syndromes of "cholesterol pericarditis." Well-developed granulomas occur in sarcoidosis, giant cell myocarditis, as a reaction to foreign bodies and devices implanted within the cardiovascular system, and in certain diseased caused by infective agents (tuberculosis, fungal and parasitic disorders). Infiltration of the heart by nongranulomatous masses of histiocytes can occur in Whipple's disease, Niemann-Pick disease, the hyperlipoproteinemias, Gaucher's disease, and in proliferative disorders of the mononuclear phagocyte system (juvenile xanthogranuloma, Chester-Erdheim syndrome, and malignant histiocytosis).
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PMID:Granulomatous inflammation of the heart. 391 77

The responses of cultured rabbit synovial fibroblasts to amorphous and microcrystalline calcium oxalate were compared with responses to MSUM. Like urate crystals, crystalline calcium oxalate (but not amorphous oxalate) caused marked stimulation of secretion of latent collagenase and PGE2 after 3 days of culture without significant change in cell protein or gross cellular morphology. Collagenase rose from undetectable levels in control cultures to 32.4 +/- 6.0 and 27.4 +/- 7.9 U/mg of cell protein for crystalline calcium oxalate and MSUM, respectively. PGE2 rose from a control level of 0.24 +/- 0.14 to 19.47 +/- 5.15 and 23 +/- 4.84 micrograms/mg of cell protein for crystalline calcium oxalate and sodium urate compared to 1.22 +/- 0.48 microgram for amorphous calcium oxalate. Although the crystalline species studied caused LDH in the media to increase threefold, this was minimal. Cell stimulation by amorphous oxalate and the crystals did not correlate with membranolytic potential as measured with an erythrocyte lysis assay. Stimulation of resident synovial cells by crystalline calcium oxalate and sodium urate may contribute to the chronic inflammation and destruction of joint tissues that occurs in oxalosis and gout.
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PMID:Stimulation of synovial fibroblasts by calcium oxalate and monosodium urate monohydrate. A mechanism of connective tissue degradation in oxalosis and gout. 629 14

Immune triggered granulocyte (PMN)-endothelial interactions have been implicated in the pathogenesis of vascular diseases. While hyperuricemia and gout are associated with an increased risk of atherogenesis, we studied the modulation by monosodium-urate (MSU) crystals of PMN-endothelial interactions in vitro. The relationship between calcium oxalate (COX) crystals - implicated in the vasculitis of primary oxalosis - and immunologically mediated endothelial injury was also explored. Both MSU- and COX-crystal treated sera stimulate PMN to adhere to and induce significant 51Cr-release from endothelial cells in vitro. Platelets significantly increase crystal-triggered PMN endothelial cell adherence and 51Cr-release. This platelet augmenting effect depends on the release of platelet constituents (e.g. serotonin). Microcrystalline material present in vessel walls, thus may cause C-activation and may trigger PMN and platelets to damage endothelium in vitro and in vivo. These findings may have relevance to the understanding of the accelerated atherogenesis of hyperuricemia and the fulminant vasculitis of oxalosis or ethylene glycol poisoning.
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PMID:Mechanisms of vascular damage in gout and oxalosis: crystal induced, granulocyte mediated, endothelial injury. 663 34

This update develops the actual therapeutic options in the management of the joint involvement of calcium pyrophosphate deposition disease (CPPD), basic calcium phosphate (BCP) deposition disease, hemochromatosis (HH), ochronosis, oxalosis, and Wilson's disease. Conventional pharmaceutical treatment provides benefits for most diseases. Anti-interleukine-1 (IL-1) treatment could provide similar results in CPPD than in gout flares. There is only limited evidence about the efficacy of preventive long-term colchicine intake, methotrexate, and hydroxychloroquine in chronic CPPD. Needle aspiration and lavage have satisfactory short and midterm results in BCP. Extracorporeal shockwave therapy has also proved its efficacy for high-doses regimes. Phlebotomy does not seem to have shown real efficacy on joint involvement in HH so far. Iron chelators' effects have not been assessed on joint involvement either, while IL-1 blockade may prove useful. NSAIDs have limited efficacy on joint involvement of oxalosis, while colchicine and steroids have not been assessed either. The use of nitisinone for ochronotic arthropathy is still much debated, but it could provide beneficial effects on joint involvement. The effects of copper chelators have not been assessed either in the joint involvement of Wilson's disease. NSAIDs should be avoided because of the liver affection they may worsen.
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PMID:Treatment of nongout joint deposition diseases: an update. 2489 35