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Thrombosis, renal venous

Twenty-five percent ofthrombophilic patients develop thrombosis at unusual sites resulting in cerebral venous thrombosis, mesenteric vein thrombosis, hepatic venous thrombosis, retinal vein thrombosis, purpura fulminans, splenic vein thrombosis, portal vein thrombosis, renal vein thrombosis, or axillary vein thrombosis. The thrombotic disorders may involve inflammatory factors that contribute to the vascular deficit. In addition, embolic events also play a role in the development of these thrombotic complications. [Pg.17]

Lam AH, Warren PS (1981) Ultrasonographic diagnosis of neonatal renal venous thrombosis. (Diagnostic chographique de la thrombose des veines renales du nouveau-n ). Ann Radiol 24 7-12 Latta K, Brodehl J (1990) Primary hyperoxaluria type I. Eur J Pediatr 149 518-522... [Pg.399]

Kosch A, Kuwertz-Broking E, Heller C et al (2004) Renal venous thrombosis in neonates prothrombotic risk factors and long-term follow-up. Blood 104 1356-1360 Kolonko A, Wiecek A, Kokot F (1998) The nonselective adenosine antagonist theophylline does prevent renal dysfunction induced by radiographic contrast agents. J Nephrol 11 151-156... [Pg.428]

Messinger Y, Sheaffer JW, Mrozek J et al (2006) Renal outcome of neonatal renal venous thrombosis review of 28 patients and effectiveness of fibrinolytics an ad heparin in 10 patients. Pediatrics 118 el478-el484 Murphy SW, Barrett BJ, Parfrey PS (2000) Contrast nephropathy. J Am Soc Nephrol 11 177-182 Nakamura M, Yokota K, Chen C et al (1999) Hyperechoic renal papillae as a physiological finding in neonates. Clin Radiol 54 233-236... [Pg.428]

Pohl M, Zimmerhackl LB, Heinen F et al (1998) Bilateral renal vein thrombosis and venous sinus thrombosis in a neonate with factor V mutation (FV Leiden). J Pediatr 132 159-161... [Pg.429]

Winyard PJD, Bharucha T, De Bruyn R et al (2006) Perinatal renal venous thrombosis presenting renal length predicts outcome. Arch Dis Child Fetal Neonatal Ed 91 F273-F278... [Pg.429]

Recombinant human erythropoietin (rHuEpo) may increase the risk of thrombosis (201). It has been reported that patients with carcinoma of the cervix who received chemotherapy and rHuEpo have an increased risk of symptomatic venous thrombosis (201). In clinical trials where the maintenance hematocrit was 3% on PROCRIT clotting of the arteriovenous shunts occurred at an annual rate of about 0.25 events per patient per year. However, other thrombotic conditions such as cerebrovascular events, transient ischemic attacks, myocardial infarction, or pulmonary embolism occurred at a rate of 0,04 events per patient per year (202). In a separate study of I, I I I untreated patients on hemodialysis, clotting of arteriovenous shunts occurred at a rate of 0.5 events per patient per year. In patients with chronic renal failure on hemodialysis who also had congestive heart failure, ischemic heart disease and venous thrombosis were increased in patients who were treated with PROCRIT targeted to a hematocrit level of 42 3% compared to those targeted to 30 3% (202). It has also been reported... [Pg.16]

Hepatic venous thrombosis, also known as Budd-Chiari syndrome, is caused by hypercoagulable disorders precipitated by pregnancy, infection, and birth control medication. An acute painful abdomen, sudden enlargement of the liver, and the presence of ascites make up a triad of clinical symptoms that are important in the diagnosis of this syndrome. Myeloproliferative disorders such as polycythemia vera and paroxysmal nocturnal dyspnea were previously thought to be responsible. Factor V Leiden and prothrombin 20210 mutations are also known to be responsible, Other intraabdominal thromboses include portal vein thrombosis, mesenteric vein thrombosis and renal vein thrombosis. [Pg.17]

The scope of the medical problems which require the use of anticoagulant drugs cannot be overstated. Arterial thrombosis is a major contributor to the number one (acute myocardial infarction), number three (stroke) and number four (renal) causes of death in the United States (1J. Venous thromboembolism is the most common non-surgical cause of death in patients hospitalized for major orthopedic procedures, the most frequent non-obstetrical cause of postpartum death, and a major cause of death in patients with chronic cardiac and pulmonary disease (1 ). Venous thrombosis is estimated to lead to the hospitalization of approximately... [Pg.417]

A 51-year-old man was given piperacillin 2 g bd for osteomyelitis. After close to 4 weeks he developed acute renal insufficiency and superior mesenteric venous thrombosis. His coagulation profile showed disseminated intravascular coagulation. Withdrawal of piperacillin and anticoagulation therapy resulted in clinical improvement and normalization of the laboratory data. [Pg.2759]

There are many synthetic chemicals that have been reported to increase lysis activity, chloroform being one of the earliest reported.68 More recently acid anti-inflammatory,87 antidiabetogenic,BS vasoactive,81 and diuretic agents,86 and anabolic steroids60 have been reported to have some effect on the lysis system. Even whiskey (alcohol) has been reported to enhance lysis.61 Hedner, et al.62 reported that ethyloestrend (8 mg/ day) increased spontaneous lysis in 45 patients with deep venous thrombosis and pulmonary embolism after 3 months of treatment. Euphillin (amino-phylline) was reported to increase abnormally low fibrinolysis in human patients and in rabbits with venous thrombosis.09 When 40 mg of furose-mide was injected i.v. into 33 healthy people, the euglobulin lysis time was shortened.64 Since this activation was not found in patients with uremia and nephrectomy, an intact renal system appears necessary. [Pg.86]

Deep venous thrombosis occurred in a bed-bound patient, and acute renal failure in a patient with diabetic nephropathy after intravenous immunoglobulin [40 ]. [Pg.516]

A 58-year-old man had a gastric varix injected twice with a mixture of enbucrilate plus hpiodol and subsequently needed anticoagulant therapy for four episodes of venous thromboembolism. A CT scan showed a linear hyper-dense lesion in the left renal vein due to the presence of enbucrilate and renal vein thrombosis. The thrombus extended into the inferior vena cava and there was splenic infarction [37 ]. [Pg.1015]

Fig. 3.24a-c. Renal vein thrombosis, a Color flow sonography shows thrombosed segmental veins within the renal sinus (arrow) and b transcapsular venous drainage, towards the external iliac vein, at the lower pole of the kidney, c The venous phase of renal DSA shows the absence of venous drainage through the normal renal vein and a heterogeneous renal parenchyma... [Pg.76]


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See also in sourсe #XX -- [ Pg.424 , Pg.425 ]




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