Titlebook: Urate Deposition in Man and its Clinical Consequences; Ursula Gresser,Nepomuk Z?llner Conference proceedings 1991 Springer Verlag, Berlin

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Acute Renal Insufficiency: Which Mechanisms Are Involved?,diotherapy, which lead to fast cell destruction. As a result of increased renal excretion, hyperuricemia can be responsible for acute renal insufficiency. Conger and Falk [1] reported a reduction of the glomerular filtration rate (GFR) due to tubular and vascular obstruction by urate deposition.

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Pathogenesis of Monosodium Urate Crystal-Induced Inflammation,lar and periarticular tissues, of crystals of the monosodium salt of uric acid (MSU). MSU crystals directly or indirectly activate a remarkable number of humoral and cellular inflammatory mediator systems, and this is reflected in the clinical features of a typical acute gouty paroxysm, i. e., acute

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Crystal-Associated Inflammation: Some Mechanisms of Cellular Activation,th in acute gouty arthritis and in experimentally induced crystal arthritis. Support for this hypothesis includes the massive accumulation of PMN in inflamed synovium and synovial fluid, the striking diminution of experimentally induced urate crystal synovitis following neutrophil depletion by cytot

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The Course of Chondrocalcinosis,gical view, chondrocalcinosis therefore is a pathomorphological or at most a roentgenological diagnosis. However, the term chondrocalcinosis was coined by clinicians. In 1958, Zitnan and Sitaj described the clinical and roentgenological features of what they called in Latin .. They described the fea

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Conference proceedings 1991r any of the otherconsequences of uratedeposition.At present, far too little is known about urate depositionand the mechanisms by which it occurs, as well as aboutitsclinical consequences, which include formation of toph; overthehelix of the ear or in bones close to joints that havenever exhibited a

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Urate Deposition in Man and its Clinical Consequences