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)

A 24-year-old white woman with a past history of recurrent venous thromboses of the lower extremities was admitted for hypertension and renal failure. She had a chronic cutaneous ulcer on the anterior side of the left leg and oral ulcers of the palatum. Laboratory tests demonstrated rapidly progressive renal failure and the presence of an anticardiolipin antibody (ELISA). Thrombosis of the inferior vena cava was shown by phlebocavography. Renal biopsy revealed typical thrombotic microangiopathy. Tissue-type plasminogen activator (tPA) was visualized by immunofluorescence in endothelial cells of renal arterioles and glomeruli. Normal plasma levels of tPA, urokinase and plasminogen activator inhibitor 1 were found by ELISA, and tPA antigen levels rose after desmopressin acetate infusion. Thus, in this case, the diffuse thrombotic process was not related to defective circulating or renal fibrinolytic systems and could be promoted by the procoagulant effect of antiphospholipid antibodies.
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PMID:Systemic and renal fibrinolytic activity in a patient with anticardiolipin syndrome and renal thrombotic microangiopathy. 211 23

When acute renal vein thrombosis is associated with renal failure, aggressive therapy to eliminate the venous obstruction is indicated. There are reports of successful treatment of this condition with thrombolytic agents administered systemically or directly into the renal vein. Renal arterial administration of urokinase was used successfully to treat acute renal vein thrombosis associated with renal failure in a 9 1/2-year-old child.
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PMID:Acute renal vein thrombosis: successful treatment with intraarterial urokinase. 318 91

A patient with systemic lupus erythematosus had severe hypertension, rapidly worsening renal failure, and multiple successive thrombotic cerebrovascular and retinal lesions develop. In a kidney biopsy specimen luminal thrombi were demonstrated in arteries and arterioles, without vasculitic or inflammatory changes. The patient's plasma was markedly deficient in both prostacyclin stimulating factor (PSF) and vascular plasminogen activator (VPA), and also contained a potent inhibitor of in vitro urokinase-induced fibrinolysis. Treatment with ancrod resulted in striking reversal of the progressive renal damage and clinical recovery from the thrombotic cerebrovascular and retinal lesions. This clinical improvement was associated with improved renal histologic appearance, correction of the PSF and VPA deficiencies, and disappearance of the urokinase inhibitor. Possible mechanisms of action of ancrod are discussed.
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PMID:Ancrod in systemic lupus erythematosus with thrombosis. Clinical and fibrinolysis effects. 622 28

The results of a controlled therapeutic trial comparing 2 groups of patients presenting with hemolytic-uremic syndrome (HUS) are reported. Group A (15 children) was given urokinase (UK) and heparin; group B (18 children) received no treatment. Ages of patients, the delay before admission, the severity of anemia, thrombocytopenia and initial renal failure were similar in both groups. UK was responsible for bleedings in 12 children, minimal in 8, severe in 4. No child died in group A, 3 children died in group B (n.s.). Durations of hemolysis, thrombocytopenia and anuria were similar in both groups. Long-term evolutions of renal function and arterial pressure were comparable in both groups. Needle kidney biopsy (26 cases) showed cortical necrosis in 3 children of group A and in 2 of group B, and glomerular thrombotic microangiopathy in 10 children of group A and in 11 of group B. The average ratio of injured glomeruli was 40 (19 to 80) in group A, and 38 (21 to 75) in group B. Two children in group A and 3 children in group B presented with 50 to 80% of glomerular lesions. This trial suggests that UK is of no significant value in the treatment of HUS.
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PMID:[Treatment of childhood hemolytic-uremic syndrome with urokinase. Cooperative controlled trial]. 637 29

A comprehensive study of haemostasis has been performed in a homogeneous group of 20 patients with nephrotic syndrome without renal failure. We have found unchanged number of platelets and a significant increase of platelet adhesiveness and aggregation; increased levels of activity and related antigen of fibrinogen, of factor VIII, of activity of factors II, VII and X and of antigens of factors XIII. Antithrombin III was unchanged in plasma and was detected in the urine. Euglobulin lysis times were decreased, and levels of plasminogen and its activators were increased after a venous occlusion test. At the same time urokinase inhibitors and antiplasmins were increased not only after, but also before a venous occlusion test. Fibrinogen degradation products have been found in the urine of all our patients but not in their sera.
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PMID:Comprehensive study of haemostasis in nephrotic syndrome. 640 81

Fibrinolytic parameters and von Willebrand factor (VWF) antigen were measured in 22 patients with glomerulonephritis (GN) who underwent renal biopsy after desmopressin (DDAVP) infusion. Blood was collected immediately before and after DDAVP infusion, after one week, and 3-6 months later. The main abnormalities on admission were the following: the mean baseline levels of t-PA antigen and VWF were significantly higher in GN patients than in 22 healthy controls; the median t-PA activity and the mean scu-PA level were significantly lower than normal. The t-PA response to DDAVP was impaired in 7 patients (32%), the response of VWF in 9 patients (41%), and the u-PA:Ag response in 11 patients (50%). When the patients were stratified according to creatinine clearance rate, significant differences between the subgroups with severely and moderately impaired renal function were noted: the baseline levels of PAI activity and VWF were higher in patients with severe renal failure and the VWF response to DDAVP was significantly lower. The response of u-PA (not of t-PA or VWF) to DDAVP appeared to correlate with urine flow during the first 24 h, suggesting the dependence of u-PA release on intact nephrons. A series of 18 patients with adult-type polycystic kidney disease (APKD) with creatinine clearance rates in the same abnormal range as the GN patients, had lower mean PAI and a significantly higher mean scu-PA level.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Blood fibrinolysis and the response to desmopressin in glomerulonephritis. 816 42

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

A 66-year-old woman presented with acute-onset rapid atrial fibrillation and right upper quadrant pain which had appeared 24 h prior to admission. The patient also manifested acute oliguric renal failure (serum creatinine 6.9 mg/dl). Selective renal angiography revealed total occlusion of the right renal artery with normal visualization of the left kidney vasculature. The patient was treated with intra-arterial urokinase and intravenous heparin, with no response. Intravenous administration of the prostacyclin analogue, iloprost, resulted in rapid resolution (within hours) of the oliguric acute renal failure, in spite of the continuing presence of a nonfunctioning right kidney. We conclude that the etiology of the acute renal insult in this patient is probably related to unilateral renal arterial embolization accompanied by arterial spasm of the unaffected kidney. The contralateral vasospasm can be reversed by iloprost, which then leads to a rapid recovery from acute renal failure. We are unaware of prior reports documenting the beneficial effect of iloprost in a clinical setting as described here.
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PMID:Acute oliguric renal failure associated with unilateral renal embolism: a successful treatment with iloprost. 973 May 73

In 1967 we reported for the first time five cases of an acquired bleeding disorder in humans which developed after contact with saturnidae caterpillars. Since that time, other cases have been reported in Brazil, French Guyana, Peru, Paraguay and Argentina. The caterpillars have been identified as Lonomia achelous (LA) in Venezuela and northern Brazil and as Lonomia obliqua (LO) in southern Brazil. All patients present pain and a burning sensation at the site of contact. Within a few hours hematomas and hematuria are seen in combination with intracerebral and intraperitoneal hemorrhage (in some cases also renal failure). Hematological tests show: mild anemia with leucocytosis; prolonged PT, PTT and ThT; decreased fibrinogen, factor V, factor XIII, plasminogen and alpha2-antiplasmin levels; increased factor VIII:c, von Willebrand factor, and FDPs/D-dimers levels with normal ATIII and platelets. Factor VII, factor II and PC levels varied. Several activities similar to or directed against blood clotting factors have been identified in LA: fibrinolytic enzymes, which degrade fibrinogen producing abnormal FDPs; prothrombin activators: one direct and one factor Xa-like; a thermostable factor V activator; a thermolabile factor V inhibitor; a factor XIII proteolytic/urokinase-like activity; and a kallikrein-like activitiy. In LO three activities have been described: a prothrombin activator called 'Lonomia obliqua prothrombin activator protease' (LOPAP); a factor X activator; and a phospholipase A(2)-like activity called Lonomiatoxin. No fibrinolytic activity has been described in LO. Subcutaneous injection of crude hemolymph and some chromatographic fractions of LA induce a decrease in fibrinogen, plasminogen and factor XIII. Intravenous injection of factor XIII proteolytic/urokinase-like activity induce a dose-dependent thrombolysis with a decrease in plasmatic factor XIII without hemorrhagic manifestations. Intradermal injection of LO bristle extracts in rats and rabbits produce incoagulability whereas intravenous injection of LOPAP induced DIC in mice.
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PMID:Lonomia genus caterpillar toxins: biochemical aspects. 1108 23


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