Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The urinary kallikrein activity (KA) was measured to investigate its significance in the renal diseases by using tosyl-arginine methyl ester (TAME) as a substrate. The examinees were 94 patients with renal diseases and 25 normal persons. The daily urinary kallikrein excretion (KE, KE=KAxdaily urinary volume) is less in chronic glomerulonephritis and outstandingly less in chronic renal failure than in the normal controls. The KE also shows a positive correlation moderately to 15-min PSP excretion and relatively to creatinine clearance. KE is closely related to renal function and decreases with the degree of renal damage. KA has no relation to the concentration of urine protein, but it was parallel, in general, to the urokinase activity. In nephrotic syndrome, KA tends to show a negative correlation to the urinary alpha 1-antitrypsin. alpha 1-antitrypsin may have a function as an inhibitor to the urinary kallikrein.
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PMID:A clinical study on urinary kallikrein in patients with renal diseases. 51 49

Plasma fibrinopeptide B beta 15-42 was significantly high in undialyzed and hemodialyzed chronic renal failure (CRF) patients, indicating that the fibrinolytic system as well as the coagulation system is stimulated. There are two kinds of plasminogen activators (PA) for the fibrinolytic system: urokinase (UK) and tissue-type PA (t-PA). PA activity of peripheral leukocytes from healthy volunteers, continuous ambulatory peritoneal dialysis (CAPD) patients and hemodialysis (HD) patients was measured and compared. Peripheral leukocyte PA in the euglobulin fraction was purified using zinc-chelate-Sepharose 6B column and Concanavalin A-Sepharose column chromatography. The different PA activity was quantitatively identified by electrophoretic enzymography and was confirmed using antibody against UK and t-PA. PA activity of peripheral leukocytes was significantly higher in HD patients on the cupro-ammonium processing membrane dialyzer than in CAPD patients and healthy volunteers. All PA activity in the three groups was UK, and t-PA was not detected. This suggested that the inflammatory response was continuously induced in HD patients, resulting in the induction of PA activity of the leukocytes and plasma, and that different mechanisms were involved for the synthesis or secretion of UK and t-PA.
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PMID:Leukocyte tissue-type plasminogen activator activity in dialysis patients. 249 42

A case of renal granulomatous sarcoidosis that presented with chronic renal failure (CRF) is described. Renal biopsy specimens revealed typical features of sarcoidosis in light microscopy and immunofluorescence microscopy examinations. The absence of bilateral hilar lymphadenopathy (BHL) was a distinctly unusual feature of sarcoidosis although uveitis and rectal granuloma were observed during the clinical course. A dramatic response occurred on corticosteroid and urokinase therapy, characterized by a fall of serum creatinine levels.
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PMID:A case of granulomatous renal sarcoidosis with a dramatic response to corticosteroid and urokinase therapy. 665 47

After placement of a Gianturco-Roubin metallic, coiled coronary stent(s) following balloon angioplasty (PTCA), a pre-discharge (7 day) angiogram determined the patency of the old coronary bypass vein graft(s) (SVG) (> or = 5 years remote from their last surgery, mean age: 8.5 +/- 1.8 years). Metallic, coiled stents were successfully deployed in 95/96 (99%) patients within 100/101 (99%) SVGs. The indications for deployment were threatened [81 patients (84%)] or acute [15 patients (16%)] vein graft closure following PTCA. Intragraft urokinase infusion was performed in 17 patients (17%) [6 patients with baseline occlusions; 11 with abrupt closure post PTCA]. Complications encountered included three (3%) in-hospital deaths (two procedure related) two (2%) Q wave myocardial infarctions, six (6%) non-Q wave myocardial infarctions, and 22 (22%) bleeding problems. These included, not mutually exclusively, 21 (22%) requiring transfusions, six (6%) cases of gastrointestinal bleeding, six (6%) pseudoaneurysms, five (5%) retroperitoneal haemorrhages and two (2%) cerebrovascular accidents. All patients received dipyridamole, aspirin, dextran, and anticoagulation (heparin 10-20,000 U intra-procedurally); a heparin infusion was continued for 5 +/- 1 days, despite warfarin administration which attained a therapeutic prothrombin time (PT) (1.5-2 times control) by 3 +/- 1 days. Out of the 95 successfully treated patients, six with eight stented grafts were ineligible for pre-discharge angiography. Of the six, three died in hospital (four SVGs), one had an intracerebral haemorrhage (one SVG), and two were asymptomatic patients with chronic renal failure (three SVGs).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The use of Gianturco-Roubin flexible metallic coronary stents in old saphenous vein grafts: in-hospital outcome and 7 day angiographic patency. 783 59

Thirty-nine neonates with renal vein thrombosis diagnosed in our hospital department between 1973 and 1991 were studied retrospectively. Twenty-five patients were and 14 were not treated with urokinase (UK). Among the five deaths (13%), four occurred at the acute stage from non-renal complications and one occurred at the age of three months from end-stage renal failure. Eight patients (21%) have moderate renal failure after a mean follow-up of 7.4 years; a single patient (2%) developed end-stage renal failure after 7.9 years and 25 patients (64%) have a normal glomerular filtration rate after a mean follow-up of 4.5 years. Rates of death and chronic renal failure were 8% and 32%, respectively, in the group given UK and 21% and 7%, respectively, in the group not given UK. Among 54 involved kidneys, only 10 (19%) recovered normal function and morphological features. Functional impairment was seen in 11 of 37 (30%) kidneys treated by UK and 10 of 17 (59%) kidneys not treated by UK. Although these data suggest that UK may be effective in promoting recanalization of renal veins obstructed by thrombosis, confirmatory evidence could be obtained only by performing a prospective therapeutic trial.
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PMID:[Thrombosis of the renal veins in the newborn: treatment and long term prognosis]. 845 36

A pathogenetic role for fibrin deposition and platelet activation in the kidney is thought to play a role in the pathogenesis of acute renal failure (ARF). Thus, some fibrinolytic parameters and platelet function have been studied in 17 patients with ARF and compared to healthy volunteers and subjects with chronic renal failure (CRF). Since serotonin may participate in pathological processes resulting from platelet/vessel wall interactions, its level in the whole blood and plasma was also assayed. In ARF and CRF platelet aggregatory responses in both whole blood and in platelet rich plasma upon stimulation with various agonists (collagen, arachidonic acid, ADP, ristocetin) were lower than those obtained in healthy volunteers. Increased levels of lipoprotein (a), von Willebrand factor (vWF) and fibronectin were found in ARF relative to controls. Protein C activity was significantly lower in patients with ARF. Euglobulin clot lysis time was prolonged in ARF and CRF, reflecting a decreased overall fibrinolytic activity. Activity of tissue plasminogen activator (tPA) inhibitor (PAI) and PAI:Ag were higher in ARF, whereas tPA:Ag, urokinase, tPA/PAI complexes, thrombin-antithrombin complexes (TAT), plasmin-antiplasmin (PAP) complexes, fibrinogen, and F1+2 did not differ between ARF and controls. In CRF elevated levels of TAT, PAP, fibrinogen and prothrombin fragments F1+2 were found, whereas concentration of fibronectin was lowered when compared to controls. In both groups of renal failure patients increased levels of fibrin monomers and d-dimer were found relative to healthy volunteers. Whole blood serotonin was significantly lower, whereas plasma serotonin was significantly higher in patients with ARF and CRF relative to controls. Serotonin uptake and its release from platelets were markedly diminished in patients with ARF and CRF. Chronic renal failure exhibit a slightly different pattern of coagulopathies that acute renal failure.
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PMID:Hemostasis, platelet function and serotonin in acute and chronic renal failure. 887 44

The necessity of maintaining a strict schedule of dialysis treatments in patients with chronic renal failure dictates that occluded access catheters be restored to full function in a timely and cost-effective manner. The records of 22 consecutive patients receiving outpatient treatment for occluded hemodialysis catheters at Osteopathic Medical Center of Texas were reviewed by the authors. Each patient had 100,000 units of urokinase in 50 ml normal saline instilled over 30 minutes through the occluded catheter. In most instances the dose was divided to allow 35 ml to the proximal port and 15 ml to the distal port. The maximum sustained blood flow rate on dialysis was recorded for each patient. The mean maximum sustained blood flow rate improved from 150 ml/min +/- 79 ml to 261 ml/min +/- 62 ml. Following infusion, improvement was obtained in 19 of 22 patients, with 14 catheters delivering blood flow greater than 250 ml/min. The total cost per treatment was $316. No adverse events were experienced. Thrombotic occlusion of extended use hemodialysis catheters can be rapidly and safely relieved in a cost-effective manner with little delay in scheduled dialysis treatments.
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PMID:Short-term continuous infusion thrombolytic therapy for occluded central nervous venous dialysis catheters. 1016 60

Hepatocyte growth factor (HGF) was purified as a potent mitogen for rat hepatocytes in primary culture and is believed to be the most physiological hepatotrophic factor that triggers liver regeneration. HGF is one of the largest disulfide-linked cytokines, consisting of a 60-kDa heavy chain and a 35-kDa light chain. Human HGF is synthesized as a single polypeptide chain precursor of 728 amino acid residues that has an appreciable homology with plasminogen, and it is processed proteolytically to release an N-terminal signal peptide of 31 amino acids and to generate an active heterodimer after secretion. The novel serine protease HGF activator and urokinase-type plasminogen activator (u-PA) are responsible for the latter extracellular processing. HGF stimulates the proliferation of rat hepatocytes in primary culture at concentrations as low as 10 pM. It also stimulates the growth of various epithelial cells, endothelial cells, and some kinds of mesenchymal cells. HGF inhibits the proliferation of several tumor cell lines and induces apoptosis of some of them. It also has motogenic, morphogenic, anti-apoptotic, angiogenic, and immunoregulatory activities. The receptor of HGF is the product of c-met proto-oncogene with tyrosine kinase activity that mediates the transduction of multiple biological signals of HGF. During liver regeneration, HGF gene expression in the liver, spleen, and lung and HGF levels in the blood and liver increase prior to the induction of liver DNA synthesis. Liver regeneration is markedly inhibited by continuous administration of a neutralizing anti-HGF antibody. HGF production in cultured cells is induced by PKC-activating agents, cAMP-elevating agents, PKA-activating agents, growth factors, and inflammatory cytokines; and it is inhibited by TGF-beta, glucocorticoids, 1,25-dihydroxyvitamin D3, and retinoic acid. There are many reports on potential application of HGF as a therapeutic agent for organ diseases that are difficult to cure such as liver cirrhosis, chronic renal failure, pulmonary fibrosis, myocardial infarction, and arteriosclerosis obliterans utilizing its potent growth-stimulating activity for a wide variety of cells. ELISA kits for assays of serum and plasma HGF levels are clinically used to prognosticate the development of fulminant hepatic failure.
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PMID:[Function and regulation of production of hepatocyte growth factor (HGF)]. 1206 Nov 40

In the hemodialysis patient, hemostasis changes may occur. The contribution of fibrinolysis in pathogenesis of these disorders is unclear. The aim of the study was to estimate intrinsic fibrinolysis pathway in patients treated with hemodialysis (HD) because of chronic renal failure caused by chronic glomerulonephritis. The study was performed with 43 patients; the control group consisted of 51 healthy volunteers chosen by sex and age. The following parameters were determined: concentration of the urokinase plasminogen activator antigen (uPA:Ag), plasmin--antiplasmin complexes (PAP), fibrin and fibrinogen degradation products (FDP), activity of prekallikrein (PK) and C1-inhibitor (C1-INH) and also euglobulin clot lysis time (ELT). The above parameters were assessed in the patients before and after HD and were compared with the control group. In the HD patients, in comparison with the control group, prolonged statistically ELT [153 (125;215) vs. 105 (75;142) min.; p<0.001], with increase of PAP (508.6 +/- 274.7 vs. 184.7 +/- 69.4 microg/L; p<0.001) and FDP concentrations [5 (5;15) vs. 2.5 (0;0.3) microg/mL; p<0.05] before the procedure were determined. It suggests increased plasmin production and fibrin digestion despite determination of decreased general fibrinolytic activity. The C1-INH activity before HD was also significantly increased as compared with the control group [157 (136;171) vs. 107 (100;124)%; p<0.001], and its significant decreased after the HD is 157.7 +/- 23.9 vs. 122.3 +/- 20.3%; p<0.001, as it seems to be a nondirect proof of intrinsic pathway contribution in fibrinolysis activation in the HD patients. The remaining examined parameters did not change significantly after the dialysis procedure.
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PMID:The role of intrinsic fibrinolytic system activation in pathogenesis of hemostasis disturbances in hemodialyzed patients with chronic renal failure. 1535 69

A 74-year-old man with hypertension and diabetes mellitus was admitted to our hospital because of acute exacerbation of chronic renal failure after treatment with urokinase for a cerebral infarction. A percutaneous renal biopsy was performed to examine the cause of renal damage, revealing glomerulosclerosis and cholesterol clefts in the small arteries. Subsequently eosinophil was increased to 21% and livedo reticularis was found in the patient's foot. A skin biopsy was performed, and cholesterol clefts were again found in the small arteries. For the reason, our diagnosis was cholesterol crystal embolism. Although 30 mg of prednisolone was administered, the patient's renal function did not improve and maintenance hemodialysis therapy was necessary. This is a rare case of cholesterol crystal embolism caused by urokinase without any invasive vascular procedures.
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PMID:[Case of cholesterol crystal embolism occurring after treatment of cerebral infarction with urokinase]. 1677 2


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