Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.5 (thrombin)
 33,306 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The point prevalence and clinical significance of renal vein thrombosis (RVT) was evaluated in 27 of 33 consecutive nephrotic patients with idiopathic membranous glomerulopathy. A technique of retrograde venography after the injection of epinephrine into the main renal artery to decrease renal blood flow was used. Two patients had histories compatible with a thromboembolic event, and the excretory urogram was not suggestive of RVT in any patient. RVT was noted in 13 patients; in eight it was bilateral. All patients with RVT received anticoagulant drugs for a minimum of 1 year after the study, and no thromboembolic events occurred in this group. No patient was treated with corticosteroids. Follow-up observation of an average of 2.5 years has not revealed a significant difference in the rate of renal function deterioration or change in degree of proteinuria between patients with and without RVT. Coagulation abnormalities included elevated platelet counts and plasma fibrinogen levels and prolonged reptilase and thrombin times. These were noted in all 14 patients studied, six of whom had RVT. In patients experiencing a nephrotic remission, coagulation abnormalities reverted to normal. RVT is common in idiopathic membranous glomerulopathy with nephrosis and is associated with few clinical markers. Its influence on renal function and proteinuria is of questionable significance. Coagulation abnormalities may be a causative factor of RVT in this setting.
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PMID:Renal vein thrombosis in idiopathic membranous glomerulopathy and nephrotic syndrome: incidence and significance. 684 62

Endothelin (ET) isopeptides are synthetized in the kidney and act as local hormones with an impressive number of diverse autocrine and paracrine functions. A variety of proinflammatory and vasoactive agents including thrombin, transforming growth factor beta, angiotensin II as well as mechanical forces enhance the renal synthesis of ET. Two receptor subtypes, ETA and ETB, are widely expressed in the kidney, coupled to multiple intracellular signal transduction pathways that mediate distinct activities. Renal vessels are peculiarly sensitive to the vasoconstrictive effect of ET, which, infused in the kidney, decreases renal blood flow and glomerular filtration rate. This effect, together with the capability of ET to induce contraction and proliferation of mesangial cells, as well as accumulation of mesangial matrix proteins, have suggested that ET may participate in the renal events that lead to renal disease progression. Evidence is now available that renal ET does play a role in the process of progressive renal injury in chronic models of renal disease to the extent that the selective pharmacological manipulation of ET pathway has a major positive impact on the progression of the disease. By contrast, more work is necessary to define the role of ET in the pathophysiology of human glomerulopathy. The recent availability of orally active compounds with potential human use, may hopefully speed progress in the area.
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PMID:Endothelin in the progressive renal disease of glomerulopathies. 756 77

The mechanisms of glomerular injury can be separated into nonimmunologically mediated glomerulonephritis (GN) such as diabetes, leading to glomerular hypertension and into immunologically mediated GN. The immunologically mediated GN may induce chronic glomerulopathy such as membranous GN or proliferative GN. The final pathway of these two types of GN is proteinuria and renal failure linked to glomerulosclerosis. In inflammatory GN, most of the mediators could be synthesized either by infiltrating cells or by resident glomerular cells. They include cytokines, lymphokines, complement activation, generation of superoxyde anions, arachidonic acid metabolites, and fibrin deposition. (a) We have investigated the interaction between isolated glomeruli and platelets and have demonstrated that lipidic and proteic extracts of glomeruli enhance thromboxane B2 platelet synthesis. This fact is related to the generation by isolated glomeruli of saturated fatty acids and tissue factor. (b) We investigated the interaction between rat isolated glomeruli and peritoneal macrophages. We have demonstrated that 12-HETE synthesized by isolated glomeruli induce macrophage prostaglandin synthesis which, in turn, inhibits the 12-HETE synthesis. (c) We have demonstrated, using human glomerular epithelial cells, that alpha-thrombin, the active form of thrombin, generated before fibrin formation, is able to induce cell proliferation and abolishes the profibrinolytic activity of these cells. In summary, the mechanisms of glomerular injury are complex, certainly acting by multiple pathways. So far, the mediators leading to proteinuria and renal failure after glomerular injury remain under investigation.
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PMID:Mechanisms of glomerular injury: overview and relation with hemostasis. 851 88