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PubMed1994

Antiphospholipid antibodies and thrombosis.

Antiphospholipid antibodies are a diverse group of immunoglobulins initially thought to have specificity to phospholipid epitopes. It is apparent that autoimmune anticardiolipin antibodies require a serum cofactor beta-2-glycoprotein I (beta 2GPI) for their binding to phospholipids. Lupus anticoagulant also may bind to phospholipids by beta 2GPI or by prothrombin. The description of binding to protein-phospholipid epitopes may explain several perplexing features of these antibodies both in vitro and in vivo. Antiphospholipid antibodies have a well-established association with clinical disease--in particular thrombosis, thrombocytopenia and recurrent fetal loss. The mechanism of the predisposition to thrombosis seen with these antibodies is poorly understood. It has been suggested that they may cause endothelial dysfunction by causing increased tissue factor expression, by inhibiting prostacyclin secretion or by inhibiting fibrinolysis. Various platelet-activating activities have also been described. The evidence that antiphospholipid antibodies promote thrombosis by effects on endothelium or platelets is inconclusive. Inhibition of protein C activation, or of activated protein C action, has been demonstrated in vitro. A poor correlation between thrombosis in vivo and these inhibitory effects has been found. Beta-2-glycoprotein I has been identified as a cofactor for binding to phospholipid by thrombogenic anticardiolipin antibodies. That beta 2GPI may be a natural anticoagulant of importance remains to be proved. Inhibition by antiphospholipid antibodies of this anticoagulant function could explain the propensity to thrombosis seen in association with these antibodies.

Antibodies, Anticardiolipin↗
PubMed1995

Mesenteric vein thrombosis: is it one disease?

OBJECTIVES: to compare the clinical course and outcome of mesenteric vein thrombosis due to known causes and mesenteric vein thrombosis of unknown aetiology. DESIGN: a retrospective study. SETTING: two major general hospitals in Kuwait. SUBJECTS: 12 patients who had mesenteric vein thrombosis due to known causes and seven patients who had mesenteric vein thrombosis of unknown aetiology were treated over eight years. CHIEF OUTCOME MEASURES: severity of clinical findings and outcome. RESULTS: There was no statistical difference between the two groups in the clinical presentation or in outcome. CONCLUSION: 36% of mesenteric vein thrombosis occurred without an obvious cause although the disease appeared to be the same. More work on the aetiology of this condition is required.

Adult↗
PubMed2002

Low prevalence of femoral venous thrombosis after cardiac catheterizations in children: a prospective study.

OBJECTIVE: Cardiac catheterization is an important and frequent diagnostic intervention in children, but few systematic studies have explored the associated venous thrombotic complications. We have prospectively evaluated the prevalence of venous thrombosis, diagnosed by ultrasonography, in children catheterized at our department. MATERIALS AND METHODS: We examined 50 children with weight greater than seven kilograms for thrombosis of the femoral vessels. Prophylactic anticoagulation was given to half of the children who were to undergo left-sided catheterization. The enrolled children had ultrasonography of the site of puncture the day before, and the day after, the cardiac catheterization. During catheterization, blood samples were taken from 33 of the children for analysis of thrombophilic agents. RESULTS: The children, with a median age of 34 months, had been catheterized 103 times, comprising the 50 current and 53 previous procedures. Over the course of the current procedure, interventions of various types were performed in 18 children (36%). We diagnosed thrombophilic predispositions in four patients. Despite the thrombophilic tendencies, and a high frequency of interventions, we did not encounter a single case of femoral venous thrombosis. Nor did we find any evidence of arterial thrombosis. CONCLUSION: Our study indicates that catheterization procedures in children are currently associated with a low prevalence of femoral venous thrombosis. Continuous assessment of vascular complications, nonetheless, is still required to prevent late effects, and to ensure the best quality of cardiac catheterisations in children.

Adolescent↗
PubMed2005

Follow-up after deep venous thrombosis in azygos continuation.

BACKGROUND: To determine the sequelae of patients after deep venous thrombosis inpatients with azygos continuation defined as agenesis of the inferior vena cava with collateral flow. PATIENTS AND METHODS: Five patients post deep venous thrombosis in the context of azygos continuation were followed up clinically and with colour duplex ultrasonography. RESULTS: All five patients had to our knowledge after the initial deep venous thrombosis no further thromboembolic events. Three patients after isolated iliac thromboses are symptom free or nearly symptom free, two after more extended thromboses still sufferfrom venous claudication. Four patients are without anticoagulation, one patient is permanently orally anticoagulated. CONCLUSIONS: Azygos continuation may not influence the risk of recurrent venous thrombo-embolism nor the outcome of a deep venous thrombosis. Careful deep venous thrombosis prophylaxis in patients with azygos continuation may be sufficient when a risk factor is present but conclusions lack due to the small numbers of patients of enough supportive data.

Adult↗
PubMed2000

Partial venous thrombosis of the pancreatic allografts after simultaneous pancreas-kidney transplantation.

Despite new advances in transplantation, complete venous thrombosis (VT) of the pancreas after simultaneous pancreas kidney (SPK) transplantation usually results in graft loss. Data are limited regarding the outcome and treatment of partial VT of the pancreas allograft. From July 1994 to December 1999, 126 patients with IDDM/end-stage renal disease underwent SPK with systemic bladder drainage at the University of Miami. We retrospectively reviewed our experience regarding the outcome and treatment options of partial VT of the pancreas allografts. From July 1994 to April 1997, partial VT was not seen in the first 66 SPK patients induced with anti-CD3 rnAb and oral or intravenous (i.v.) tacrolimus (TAC) in the operating room. From May 1997 to June 1999, 14 (29%) out of 48 patients had VT. These cases were identified following the i.v. use of TAC with anti-IL-2R antibody-induction therapy (7/15) or without (7/33). Partial thrombosis of the splenic vein (PTSV) was documented in 10 patients, 2 had complete thrombosis of the splenic vein (CTSV), 1 had partial thrombosis of the superior mesenteric vein (PTSMV), and 1 patient had PTSV and PTSMV. These were identified incidentally during routine color Doppler ultrasonography (CDU). None of these SPK recipients demonstrates a change in clinical parameters. The first 8 patients were systemically heparinized, followed by oral anticoagulation, except 1 patient with CTSV. He progressed to complete thrombosis of the pancreas allograft and was treated with percutaneous thrombectomy and urokinase infusion, followed by heparinization and oral anticoagulation. One patient required exploration for bleeding. In an attempt to reduce the morbidity of heparinization, we treated the next 6 patients with PTSV with aspirin followed by serial CDU. All 14 patients had preservation of the endocrine and exocrine pancreatic functions. CDU showed resolution with recanalization of the thrombosed vein(s). From July 1999 to December 1999, 12 SPK recipients were administered TAC orally with or without induction therapy with anti-IL-2R antibody. So far, in this group, VT has not been identified. In summary, a total of 14 out of 126 patients (11%) had isolated VT with a mean follow-up of 36.4 months. Based on our experience, we suggest that extensive VT after pancreas transplantation, including splenic and superior mesenteric VT, be treated with heparin and subsequent oral anticoagulation for 3 months. For more limited, partial splenic VT, aspirin may be sufficient. Follow-up CDU is critical for a successful outcome. The i.v. use of TAC appears to be a risk factor for the increased incidence of VT. Currently, using IL-2rmAb as induction, TAC is started orally on postoperative days 3 or 4 and aspirin on postoperative day 2.

Adult↗
PubMed2006

Therapy Insight: venous-catheter-related thrombosis in cancer patients.

Central venous catheters (CVCs) have improved the management of patients with cancer substantially, by facilitating chemotherapy and supportive therapy. The use of CVCs is associated with complications such as infection and upper-limb deep vein thrombosis (UL-DVT). The incidence of clinically overt UL-DVT related to the use of CVCs ranges between 2% and 4%. In the most recent study, the incidence of CVC-related thrombosis, as screened by venography, was approximately 18% in the absence of prophylaxis. In cancer patients with CVC-related UL-DVT, the incidence of clinically overt pulmonary embolism was between 15% and 25%, and the incidence of autopsy-proven pulmonary embolism was up to 50%. Pathogenic factors for CVC-related thrombosis include vessel injury caused by the CVC insertion procedure, venous stasis because of the indwelling CVC, and hypercoagulability associated with cancer. Recent studies have not confirmed a benefit for prophylaxis with antithrombotic agents for CVC-related thrombosis. The recommended treatment for CVC-related thrombosis is based on long-term anticoagulant therapy, with or without catheter removal.

Catheterization, Central Venous↗
PubMed2005

Nanoparticle-induced platelet aggregation and vascular thrombosis.

Ever increasing use of engineered carbon nanoparticles in nanopharmacology for selective imaging, sensor or drug delivery systems has increased the potential for blood platelet-nanoparticle interactions. We studied the effects of engineered and combustion-derived carbon nanoparticles on human platelet aggregation in vitro and rat vascular thrombosis in vivo. Multiplewall (MWNT), singlewall (SWNT) nanotubes, C60 fullerenes (C60CS) and mixed carbon nanoparticles (MCN) (0.2-300 microg ml(-1)) were investigated. Nanoparticles were compared with standard urban particulate matter (SRM1648, average size 1.4 microm). Platelet function was studied using lumi aggregometry, phase-contrast, immunofluorescence and transmission electron microscopy, flow cytometry, zymography and pharmacological inhibitors of platelet aggregation. Vascular thrombosis was induced by ferric chloride and the rate of thrombosis was measured, in the presence of carbon particles, with an ultrasonic flow probe. Carbon particles, except C60CS, stimulated platelet aggregation (MCN>or=SWNT>MWNT>SRM1648) and accelerated the rate of vascular thrombosis in rat carotid arteries with a similar rank order of efficacy. All particles resulted in upregulation of GPIIb/IIIa in platelets. In contrast, particles differentially affected the release of platelet granules, as well as the activity of thromboxane-, ADP, matrix metalloproteinase- and protein kinase C-dependent pathways of aggregation. Furthermore, particle-induced aggregation was inhibited by prostacyclin and S-nitroso-glutathione, but not by aspirin. Thus, some carbon nanoparticles and microparticles have the ability to activate platelets and enhance vascular thrombosis. These observations are of importance for the pharmacological use of carbon nanoparticles and pathology of urban particulate matter.

Animals↗
PubMed2000

MR angiographic diagnosis of cerebral venous sinus thrombosis following allogeneic bone marrow transplantation.

Allogeneic bone marrow transplantation is frequently associated with neurological complications, particularly intracerebral bleeds and infections. Cerebral venous sinus thrombosis has only rarely been reported following allogeneic transplants. We report three cases of cortical venous thrombosis following allografting for acute lymphoblastic leukaemia. Two patients received marrow from HLA-identical siblings and one from an unrelated donor. Two of the patients presented with grand mal seizures and one presented with a headache. No neurological abnormalities were found upon clinical examination and lumbar puncture was normal in all three cases. In two of the patients computed tomography (CT) of the brain was normal and in the third showed non-specific abnormalities. Magnetic resonance imaging (MRI) with MR angiography (MRA) demonstrated cerebral venous sinus thrombosis in all three patients. In conclusion, cerebral venous sinus thrombosis should be considered in the differential diagnosis when neurological symptoms occur following allogeneic bone marrow transplantation. We therefore advocate the use of MRA for unexplained neurological symptoms post-allograft since without it cerebral venous sinus thrombosis may easily be missed.

Adolescent↗
PubMed2004

Effect of genetic variation in the human S-adenosylhomocysteine hydrolase gene on total homocysteine concentrations and risk of recurrent venous thrombosis.

Hyperhomocysteinemia is an independent and graded risk factor for arterial vascular disease and venous thrombosis. It is still debated via which mechanism homocysteine (Hcy) causes vascular disease. S-adenosylhomocysteine hydrolase (AHCY) catalyses the reversible hydrolysis of S-adenosylhomocysteine (AdoHcy) to Hcy. As an increase in AdoHcy, a strong inhibitor of many methyltransferases, is observed in hyperhomocysteinemic individuals, AdoHcy may play a role in the development of cardiovascular diseases by inhibiting transmethylation reactions. We sequenced the entire coding region and parts of the untranslated regions (UTRs) of the AHCY gene of 20 patients with recurrent venous thrombosis in order to identify genetic variation within this gene. We identified three sequence variants in the AHCY gene: a C > T transition in the 5' UTR (-34 bp C > T), a missense mutation in exon 2, which mandates an amino-acid conversion at codon 38 (112 C > T; Arg38Trp) and a silent mutation in exon 4 (390 C > T; Asp130Asp). We studied the effect of the first two variants on total plasma Hcy and venous thrombosis risk in a case-control study on recurrent venous thrombosis. The two polymorphisms under study seem to have no evident effect on tHcy. The adjusted relative risk of venous thrombosis associated with the 112CT genotype compared with 112CC individuals was 1.27 (95% CI 0.55-2.94), whereas the -34CT genotype confers a risk of 1.25 (95% CI 0.44-3.52) compared with the wild-type genotype at this locus. However, the wide confidence intervals do not allow firm conclusions to be drawn.

Adenosylhomocysteinase↗
PubMed2006

Frequency and risk factors for thrombosis in idiopathic myelofibrosis: analysis in a series of 155 patients from a single institution.

Thrombosis is a frequent complication of polycythemia vera and essential thrombocythemia, but its incidence and predisposing factors in idiopathic myelofibrosis (IM) are unknown. In 18 (11.6%) of 155 patients diagnosed with IM in a single institution, 31 thrombotic events (19 arterial, 12 venous) were registered after a mean follow-up of 4.2 (s.d.: 4.5) years. In six patients, the thrombosis was simultaneous to or appeared a few months before IM diagnosis and 14 had one or more thrombotic episodes. When compared with the general population, a significant increase was observed in the incidence of venous thrombosis (odds ratio 17.5, 95% confidence interval: 10.3-31.4). At multivariate analysis, the initial variables associated with an increased risk of thrombosis were thrombocytosis (platelets >450 x 10(9)/l, P=0.001), presence of one cardiovascular risk factor (arterial hypertension, smoking, hypercholesterolemia, or diabetes, P=0.003), cellular phase of myelofibrosis (P=0.005), and Hb >11 g/dl (P=0.02). Considering post-diagnosis events, the 5-year thrombosis-free survival probability was 90.4% in the series, 80.6% for patients with platelets >450 x 10(9)/l, 82.6% for patients with one cardiovascular risk factor, and 85.1% for those in cellular phase. These results indicate an increased thrombotic risk for IM patients with hyperproliferative features and/or coexistent cardiovascular risk factors.

Adolescent↗
PubMed2002

Hormonal replacement therapy, prothrombotic mutations and the risk of venous thrombosis.

Hormone replacement therapy (HRT) increases the risk of venous thrombosis. We investigated whether this risk is affected by carriership of hereditary prothrombotic abnormalities. Therefore, we determined the two most common prothrombotic mutations, factor V Leiden and prothrombin 20210A in women who participated in a case-control study on venous thrombosis. Relative risks were expressed as odds ratios (OR) with 95% confidence intervals (CI95). Among 77 women aged 45-64 years with a first venous thrombosis, 51% were receiving HRT at the time of thrombosis, compared with 24% of control women (OR = 3.3, CI95 1.8-5.8). Among the patients, 23% had a prothrombotic defect, versus 7% among the control women (OR = 3.8, CI95 1.7-8.5). Women who had factor V Leiden and used HRT had a 15-fold increased risk (OR = 15.5, CI95 3.1-77), which exceeded the expected joint odds ratio of 6.1 (under an additive model). We conclude that the thrombotic risk of HRT may particularly affect women with prothrombotic mutations. Efforts to avoid HRT in women with increased risk of thrombosis are advisable.

Case-Control Studies↗
PubMed2002

Low risk of thrombosis in family members of patients with hyperhomocysteinaemia.

Mild to moderate hyperhomocysteinaemia, a metabolic disorder due to genetic and/or acquired factors, is associated with an increased risk of venous and arterial thrombosis. To establish whether measuring homocysteine in members of families of hyperhomocysteinaemic patients is warranted, we investigated 169 relatives of patients diagnosed with hyperhomocysteinaemia after they developed arterial or venous thrombosis. The prevalence of hyperhomocysteinaemia was 16.6%; the relative risk of thrombosis in relatives with hyperhomocysteinaemia compared to those without was 1.2 (odds ratio; 95% CI 0.24-4.2), with similarly low absolute annual incidences of thrombosis (0.28% and 0.24%). The low prevalence of hyperhomocysteinaemia among relatives of patients with this metabolic disorder, and their low risk of thrombosis, do not justify family screening.

Adolescent↗
PubMed2002

Protein C inhibitor (plasminogen activator inhibitor-3) and the risk of venous thrombosis.

Protein C inhibitor (PCI), also known as plasminogen activator inhibitor-3, is a serine proteinase inhibitor that can inhibit enzymes in blood coagulation, fibrinolysis and fertility. The role of PCI in regulating the blood coagulation mechanism is not known, as it can inhibit both procoagulant (thrombin, factor Xa, factor XIa) and anticoagulant (activated protein C, thrombin-thrombomodulin, urokinase) enzymes. To determine the relevance of this inhibitor in thrombosis, PCI levels were assessed in the Leiden Thrombophilia Study, a case-control study of venous thrombosis in 473 patients with a first deep-vein thrombosis and 474 age- and sex-matched control subjects. PCI levels above the 95th percentile of the controls (136.1%) increased the risk 1.6-fold compared with PCI levels below the 95th percentile (95% confidence interval 0.9-2.8). There was a gradual increase in risk of thrombosis with further increasing levels of PCI. Adjustment for a number of possible confounders led to a reduction of the risk estimates associated with PCI. However, it is unclear whether adjustment for such factors in the risk models is justified. These results indicate that high levels of PCI may constitute a mild risk factor for venous thrombosis.

Adolescent↗
PubMed1999

Deep venous thrombosis in peripheral vascular disease.

BACKGROUND: This prospective study aimed to determine the prevalence of lower limb deep venous thrombosis in patients with peripheral vascular disease (PVD). METHODS: Some 136 patients admitted for arteriography, angioplasty or arterial reconstruction with limiting claudication (n = 72), ischaemic rest pain (n = 26) or gangrene (n = 38) and 40 control subjects admitted for general surgical procedures but without evidence of PVD were screened with colour duplex ultrasonography for the presence of venous thrombosis in the lower limb deep veins before any surgical or radiological procedures were undertaken. Patient age, the ankle : brachial pressure index (ABPI) and the presence of other risk factors for venous thromboembolism were also recorded. RESULTS: Venous thrombosis was found in 27 of 136 patients with PVD and two of 40 control patients (P = 0.03). Logistic regression analysis demonstrated that decreasing ABPI independently contributed to an increased risk of deep venous thrombosis. CONCLUSION: There was a high prevalence of venous thrombosis among patients with PVD which was related to the severity of the ischaemia. Presented to the South West Vascular Surgeons Meeting in Newport, UK, March 1998

Adult↗
PubMed2001

Lupus anticoagulant and history of thrombosis are not associated with persistent endothelial cell activation in systemic lupus erythematosus.

Antiphospholipid antibodies (aPL), especially lupus anticoagulant (LAC), characterize systemic lupus erythematosus (SLE) patients at increased risk for arterial and venous thromboembolic complications. It has been reported that purified human anti-phospholipid antibodies cause endothelial cell activation in in vitro experiments. In order to investigate whether increased endothelial cell activation is associated with thromboembolic events in SLE patients with LAC, we measured plasma levels of thrombomodulin (TM), von Willebrand factor (vWf), sP-selectin, vascular cell adhesion molecule-1 (sVCAM-1) and ED1-fibronectin in a study of 76 patients with SLE. Patients were subdivided on the basis of: no history of thrombosis and LAC-negative (n = 22) or LAC-positive (n = 17); positive history of thrombosis and LAC-negative (n = 16) or LAC-positive (n = 21). The median SLE disease activity index (SLEDAI) was 4. Although concentrations of sTM, vWf, sP-selectin and sVCAM-1 were significantly elevated in SLE compared with values in healthy controls, they did not differ between the four groups, between patients with or without history of thrombosis, and between patients with or without LAC. Presence of anticardiolipin antibodies could not explain these negative findings. Adjustment of the concentrations for significantly associated variables, such as age, hypertension, smoking, immunosuppressive treatment and concentrations of creatinine, cholesterol and homocysteine, did not change the main results of the study. Only sTM was significantly lower in patients with both LAC and thrombosis than in patients without both these features after adjustment for serum creatinine concentrations. In conclusion, we did not find an association between endothelial cell activation and presence of LAC or history of thrombosis in SLE.

Adult↗
PubMed1996

Behcet's disease: presentation with sagittal sinus thrombosis diagnosed noninvasively.

The standard evaluation of patients with intracranial hypertension frequently does not reveal a discrete pathophysiologic process, leading in these cases to classification of the syndrome as "benign." We present a 35-year-old woman with a recent diagnosis of pseudotumor cerebri who presented with headache, emesis, and blurring of vision. Her symptoms were progressive despite two lumbar punctures that revealed normal cerebrospinal fluid under high pressure. Contrast and noncontrast CT scans were normal; both the cerebrospinal fluid and CT neuroimaging were thus consistent with benign intracranial hypertension. An MRI, however, supported the presence of sagittal sinus thrombosis, a finding which was confirmed by MR venography. Further workup for an underlying cause of sinus thrombosis disclosed symptoms and signs fulfilling the diagnostic criteria for Behcet's disease. Cerebral venous (or sinus) thrombosis should be considered in the differential diagnosis of intracranial hypertension. Behcet's disease, while extremely rare, should be considered as a potential cause of cerebral venous thrombosis. Magnetic resonance venography can serve as a useful diagnostic study in situations where confirmation or exclusion of sinus thrombosis is required.

Acute Disease↗
PubMed2003

Applications of percutaneous mechanical thrombectomy in transjugular intrahepatic portosystemic shunt and portal vein thrombosis.

Portal vein thrombosis (PVT) is an uncommon cause for presinusoidal portal hypertension. PVT can be caused by one of three broad mechanisms: (1) spontaneous thrombosis when thrombosis develops in the absence of mechanical obstruction, usually in the presence of inherited or acquired hypercoagulable states; (2) intrinsic mechanical obstruction because of vascular injury and scarring or invasion by an intrahepatic or adjacent tumor; or (3) extrinsic constriction by adjacent tumor, lymphadenopathy or inflammatory process. Usually, several combined factors are necessary to result in PVT. The consequences of portal vein thrombosis are mostly related to the extension of the clot within the vein. Gastrointestinal bleeding from gastroesophageal varices is the most frequent presentation. Noninvasive imaging techniques are currently used for the screening of patients and the initial diagnosis of PVT. The invasive techniques are reserved for cases when noninvasive techniques are inconclusive, before percutaneous interventional treatment, or in preoperative assessment of patients who are candidates for surgery. Recanalization of the portal vein with anticoagulation alone may not be consistent or appropriate in highly symptomatic patients. Catheterization of the superior mesenteric artery (SMA) is helpful for diagnosis as well as for therapy by allowing the intra-arterial infusion of thrombolytic drugs in the same setting. Direct transhepatic portography allows precise determination of the degree of stenosis and extension within the portal vein, as well as pressure measurements. Thrombotic occlusions of the portal, mesenteric, and splenic veins can be managed by mechanical thrombectomy (MT) or pharmacologic thrombolysis. Underlying occlusions because of organized or refractory thrombus or fixed venous stenosis are best corrected by balloon angioplasty and stent placement. Access into the portal venous system can also be established through creating a transjugular intrahepatic portosystemic shunt (TIPS). Creating a TIPS is also important in the setting of PVT associated with cirrhosis to decompress portal hypertension and improve portal venous flow. PVT involving the portal, splenic, and/or mesenteric veins can also complicate a preexisting TIPS in which case the shunt can be readily used as therapy access. Several techniques may be used to recanalize the shunt and portal venous system, including thrombolytic therapy, balloon angioplasty/embolectomy, suction embolectomy, basket extraction of clots, and mechanical thrombectomy with a variety of devices. Advantages of MT include the potential to rapidly remove thrombus without the need for prolonged thrombolytic infusions, and reducing the potential life-threatening complications of thrombolytic therapy. Possible drawbacks include the risk of intimal or vascular trauma to the portal vein, which may promote recurrent thrombosis.

Humans↗
PubMed1978

[Thrombectomy for acute renal-vein thrombosis (author's transl)].

Three personal cases are presented to indicate the growing need for thrombectomy as a method of treatment of renal-vein thrombosis. In addition to known causes of renal-vein thrombosis (e.g. iatrogenic, post-traumatic) there is the so-called spontaneous renal-vein thrombosis especially in newborns. The possibility of renal-vein thrombosis must be considered in the presence of sudden, circumscribed pain in the flanks, haematuria and albuminuria, large kidney shadow radiologically, loss of renal function. Reported cases and the three personal ones suggest a trial of thrombectomy. It is not known how long the kidneys can tolerate venous occlusion. But the personal observations suggest that even occlusion lasting for serveral days may be reversible. In one patient with renal-vein thrombosis after unrecognised misplacement of a Mobin-Uddin filter into the right renal vein, surgical restoration of venous drainage after several weeks indicates that long-term observations are necessary to judge final results.

Acute Disease↗