Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “THROMBOEMBOLISM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,243 records · Page 69Linked to original sources
PubMed2002

The nonpeptide glycoprotein IIb/IIIa platelet receptor antagonist SM-20302 reduces tissue plasminogen activator-induced intracerebral hemorrhage after thromboembolic stroke.

BACKGROUND AND PURPOSE: Platelet activation and deposition in brain microvessels appear to be key events in the pathogenesis of ischemia-induced neuronal degeneration and behavioral deficits. It has been hypothesized that activated platelets in combination with polymorphonuclear leukocytes and fibrin may play a role in vessel reocclusion leading to the "no-reflow" phenomenon after administration of the thrombolytic tissue plasminogen activator (tPA). We studied the effects of the novel glycoprotein IIb/IIIa platelet receptor antagonist SM-20302 when administered in combination with tPA on infarct and hemorrhage rate and volume to determine whether activated platelets are involved in either infarct or hemorrhage generation after a thromboembolic stroke. METHODS: One hundred thirty-two male New Zealand White rabbits were included in the present study. Rabbits were embolized by injecting a blood clot into the middle cerebral artery via a catheter. Five or 65 minutes after embolization, SM-20302 (5 mg/kg) was infused intravenously. In drug combination studies, tPA was infused intravenously for 30 minutes starting 60 minutes after embolization, and SM-20302 was administered 5 or 65 minutes after embolization. Postmortem analysis included assessment of hemorrhage, infarct size and location, and clot lysis. RESULTS: In the vehicle control group, the hemorrhage rate after a thromboembolic stroke was 33%. There was a significant increase (109%) in the hemorrhage rate in the group of rabbits treated with the thrombolytic tPA. SM-20302 by itself did not significantly alter the embolism-induced hemorrhage rate when administered either 5 or 65 minutes after embolism. The SM-20302 groups had a 42% and 33% incidence of hemorrhage in the 5- and 65-minute groups, respectively. In groups treated with a combination of drugs, the SM-20302/tPA group had a 31% and 71% incidence of hemorrhage when SM-20302 was administered 5 and 65 minutes after embolization, respectively. SM-20302 in combination with tPA also significantly increased infarct rate, but not hemorrhage or infarct volume. CONCLUSIONS: This study suggests that treatment of thromboembolic stroke with the combination of a platelet inhibitor and tPA may have a beneficial outcome on the basis of the following: First, acute administration of SM-20302 did not significantly increase hemorrhage rate. Second, SM-20302 in combination with tPA significantly reduced tPA-induced intracerebral hemorrhage. Third, there appears to be a specific window of opportunity when a platelet inhibitor must be administered to produce a beneficial effect. Overall, on the basis of our results, we hypothesize that the increased rate of intracerebral hemorrhage observed after tPA administration may be partly due to increased reocclusion of cerebral vessels following lysis of the emboli and that reocclusion can be controlled by administration of a platelet inhibitor.

Animals↗
PubMed1995

Large vessel pulmonary arteritis mimicking chronic thromboembolic disease.

Chronic obstruction of pulmonary arteries can be due to a variety of disease processes, including chronic thromboembolic disease, fibrosing mediastinitis, or neoplasia. Large vessel arteritis is another unusual cause of pulmonary artery obstruction and can be difficult to distinguish from the above-listed etiologies. We present four patients referred to our institution with the provisional diagnosis of chronic thromboembolic pulmonary hypertension who were subsequently diagnosed with Takayasu's arteritis involving the pulmonary arteries. We review the historical, physical examination, and radiologic characteristics that help distinguish Takayasu's arteritis from chronic thromboembolic disease.

Adult↗
PubMed1998

Hereditary thrombophilia and venous thromboembolism.

The hereditary thrombophilias are a group of inherited conditions that predispose to thrombosis. Heritable deficiencies of the endogenous anticoagulants protein C, protein S, and antithrombin have been recognized for some years, but their prevalence, even among patients with familial thrombosis, is low. The recent discoveries of two relatively common thrombophilias, resistance to activated protein C associated with an abnormal factor V gene (factor V Leiden), and prothrombin gene variant 20210A, have substantially increased the likelihood of identifying a heritable predisposing factor in patients with thromboembolism. Modestly elevated levels of plasma homocysteine, which are in part genetically determined, have also recently been associated with an increased risk for venous thromboembolism. A predisposition to thrombosis can now be identified in a substantial minority of patients with venous thromboembolism, and in the majority of patients with familial thrombosis, and there is accumulating evidence that multiple coexisting defects are present in persons with the most marked tendency to thrombosis. The most common causes of hereditary thrombophilia are reviewed with an emphasis on resistance to activated protein C, prothrombin variant 20210A, and hyperhomocystinemia, and the current status of laboratory testing for thrombophilia is discussed.

Antithrombin III Deficiency↗
PubMed1992

Gene analysis of heterozygous protein C deficiency in a patient with pulmonary arterial thromboembolism.

A 16-yr-old male patient with heterozygous protein C deficiency developed acute pulmonary thromboembolism. The patient had low levels of plasma protein C antigen and activity (33 and 35% of normal, respectively). Analysis of the protein C gene by polymerase chain reaction (PCR) and direct sequencing revealed a nucleotide substitution (Arg169CGG----Trp169 TGG) in exon VII. This mutation is identical with protein C Tochigi, and the substituted amino acid is located at the cleavage site of the activation peptide of protein C. The mutant sequence was also detected in the mRNA transcripts of protein C gene. These results suggest that the possible mechanism of plasma protein C reduction is impaired stability or susceptibility to protein degradation during intracellular processing or after secretion into plasma. As this is a third independent case of protein C Tochigi with thromboembolism, the mutation of Arg169 (CGG) to Trp169 (TGG) in the protein C gene may be a "hot spot" and a common type of genetic lesion in congenital protein C deficiency with thromboembolic complications.

Adolescent↗
PubMed1998

Long-term, low-dose warfarin among venous thrombosis patients with and without factor V Leiden mutation: rationale and design for the Prevention of Recurrent Venous Thromboembolism (PREVENT) trial.

Standard therapy for patients with deep venous thrombosis and pulmonary embolism typically includes anticoagulation for a 3-6 month period with full dose warfarin. However, patients following this regimen experience high rates of recurrent thrombosis, re-hospitalization and mortality in the years immediately following cessation of anticoagulation. This is true for patients at average risk of disease recurrence, and for patients at elevated risk due to the presence of inherited defects of anticoagulation such as factor V Leiden mutation. Unfortunately, no clinical regimen currently available has proven to have sufficient benefit to support long-term prophylaxis. In particular, full dose warfarin is associated with substantially increased risks of hemorrhage when used on a long term basis. In contrast, while targeted low-dose warfarin (INR 1.5-2.0) is safe for long-term therapy, the efficacy of this approach in the prevention of recurrent venous thromboembolic disease has remained untested. The Prevention of Recurrent Venous Thromboembolism (PREVENT) trial will evaluate the efficacy of prolonged treatment with low-dose warfarin in the secondary prevention of venous thromboembolism (VTE). Patients with a history of documented idiopathic venous thrombosis who have completed a standard course of anticoagulation therapy will be enrolled in a randomized, double-blind, placebo-controlled trial comparing usual care plus targeted low-dose warfarin to usual care plus placebo for a period of up to 4 years. Trial endpoints will include recurrent VTE, major bleeding episodes and all-cause mortality in the total patient population and separately in those patients with factor V Leiden. The potential clinical impact of the PREVENT trial is broad since a positive finding would strongly support chronic low-intensity anticoagulation among patients with venous thrombosis who are at risk for recurrence following cessation of standard outpatient anticoagulation.

Adult↗
PubMed2005

Association of clinical features with HLA in chronic pulmonary thromboembolism.

The aetiology of chronic thromboembolic pulmonary hypertension (CTEPH) is largely unknown and may be heterogeneous, because there are several ethnic differences in the clinical characteristics of CTEPH. Female predominance and a higher ratio of chronic to acute pulmonary thromboembolism have been reported in Japan as compared with the USA. Because such ethnic differences may be controlled by genetic factors, the current study investigated HLA polymorphisms in Japanese patients with CTEPH. HLA typing by serological and/or DNA typing methods was performed (for HLA-A, B, DPB1, DRB1) in 80 patients and 678 controls, and the association of clinical characteristics with HLA alleles was studied. The frequencies of HLA-B*5201 (40 versus 24%) and DPB1*0202 (19 versus 6%) were significantly higher in the patients. HLA-B*5201 positive patients showed a significant female predominance. Total pulmonary vascular resistance and mixed venous oxygen tension were better in the HLA-B*5201 positive patients. In contrast, cardiac index and gas exchange parameters were worse in the HLA-DPB1*0202 positive patients. In the patients carrying HLA-B*5201 and/or -DPB1*0202, the frequency of deep vein thrombosis was significantly lower than the other patients. These observations suggested that both the susceptibility and clinical characteristics of chronic thromboembolic pulmonary hypertension were controlled in part by the HLA-B and -DPB1 loci.

Adult↗
PubMed2005

Incidence and risk factors of venous thromboembolism (VTD) in patients with amyloidosis.

BACKGROUND: Coagulation problems in amyloidosis are historically associated with bleeding tendencies (mostly Factor X abnormalities). Increased clotting was observed in isolated cases diagnosed with low-grade disseminated intravascular coagulation (DIC). Problem of venous thromboembolic disaease (VTD) in amyloidosis was not systematically investigated. METHODS: We evaluated frequency of VTD and risk factors for VTD in 56 consecutive amyloidosis patients with a documented disease evaluated and followed up at our Center from 1991-2001. Data was collected in 5 categories: (a) demographics, (b) disease and treatment, (c) thrombosis case information, (d) major risk factors for thrombosis and (e) baseline laboratory data. Univariable correlates of VTD were assessed using Kaplan-Meier analysis and Cox proportional hazards analysis. RESULTS: Mean age of the patients was 67 (years range 21-83). Male/female percentage ratio was 70/30. 29% of the patients had high creatinine level (> 1.4 mg/dl). Personal or family history of VTD was recorded in 2 and 0% of patients, respectively. Known hypercoagulable state was present in 1 patient (2%). 8% of patients were smokers. Of 56 patients, 6 developed VTD (11%). Median time from diagnosis of amyloidosis to VTD was 12.5 month (range 1-107). Treatment was given within a median of 1 month (range 0-4) from the development of thrombosis. Only sites of VTD were lower extremities. No cases were associated with I.V. line. 1 case (17%) was identified postoperatively. We identified several univariable correlates of VTD in amyloid patients, including greater age at diagnosis (HR-2.99, P = .041), personal history of DVT (HR-47.7, P = .006) and immobility (HR-11.78, P = .006). Presence of circulating serum M-protein had protective role in our analysis (HR-.08, P = .031). There was no correlation with the type of treatment patients were receiving. CONCLUSION: Risk for thromboembolic diseases in patients with amyloidosis is similar to one previously described for multiple myeloma. Additional studies with higher number of thromboembolic events could help to further elucidate risk factors for VTD in this population of patients.

Journal Article↗
PubMed2006

Endovascular treatment of unruptured intracranial aneurysms: occurrence of thromboembolic events.

OBJECTIVE: The purpose of this study was to evaluate the frequency and causes of thromboembolic events associated with endovascular embolization of asymptomatic aneurysms. Correlations between radiological findings (aneurysm size, localization, embolization time, number of coils used, as well as patient age) were evaluated with the occurrence of thromboembolic events and clinical findings. METHODS: Sixty-eight patients treated for unruptured intracranial aneurysms (mean age, 49 yr) were evaluated. Hyperintense lesions on diffusion weighted imaging were analyzed in 50 patients. Aneurysm size was 3 to 15 mm. RESULTS: Complete occlusion of the aneurysms was achieved in 55 of 68 (82%). One patient had a transient paresis. There was one infarction and one aneurysm rupture during the procedure with no consecutive neurological symptoms. We found new hyperintense lesions in 21 of 50 (42%) diffusion weighted imaging studies. In 43% of these, there was only one lesion smaller than 2 mm. In 33%, there was more than one lesion less than 2 mm; in 19%, we found a lesion of 2 to 10 mm in size. In one case, a lesion greater than 10 mm occurred. There was no correlation between aneurysm location and the occurrence of lesions or among the number of coils used, the size of the aneurysm, patient age, or embolization time. Mortality rate was 0%, morbidity 4.0%. If the 18 aneurysms where no diffusion weighted imaging was obtained are included, morbidity is 2.9%. CONCLUSION: The high rate of thromboembolic events suggests that heparin is not sufficient to prevent ischemic lesions. An antiplatelet therapy, started before or during intervention, might diminish thrombus formation.

Adult↗
PubMed2005

3. Sudden death due to pulmonary thromboembolism after car driving: a case report.

An autopsy case of sudden death due to pulmonary thromboembolism after a car trip is reported. A 56-year-old Japanese man with hypertension and atrial fibrillation suddenly died immediately after having driven for two and a half hours. At autopsy, the pulmonary arteries were found to be filled with dark-red, coiling thrombi consisting of fibrin and red blood cells. In the dilated right popliteal vein, a thrombus consisting of fibroblasts, a large number of collagen fibres, and newly formed capillaries was attached to the vessel wall. The cause of death was determined to be pulmonary embolism due to the thrombus of the right popliteal vein. Two and a half hours of prolonged sitting while driving a car encouraged thrombus formation. We believe that this case, the first autopsy case of fatal pulmonary thromboembolism after a car trip to be reported, highlights the importance of predicting venous thrombosis of the leg or fatal venous thromboembolism after a car trip.

Automobile Driving↗
PubMed2005

Recent advances in interventional radiology for acute massive pulmonary thromboembolism.

Acute massive pulmonary thromboembolism is life-threatening and requires vigorous treatment. Anticoagulation is the most traditional treatment for pulmonary thromboembolism, but may not be sufficient for massive thromboemboli. Systemic thrombolytic therapy and surgical thrombectomy are the traditional therapeutic options in this situation. Catheter-directed thrombolysis, percutaneous embolectomy and, more recently, percutaneous thrombus fragmentation techniques using specialized devices are now available to treat the most severe cases of massive pulmonary thromboembolism. The success of these techniques depends on a thorough understanding of the mechanism of action of each of the devices and familiarity with the relevant catheterization techniques. We present a review of currently available equipment and techniques, and describe our work with hybrid treatment using a combination of mechanical fragmentation, localized fibrinolysis and clot aspiration.

Acute Disease↗
PubMed1996

Parenchymal scarring is associated with restrictive spirometric defects in patients with chronic thromboembolic pulmonary hypertension.

UNLABELLED: The finding of a restrictive pulmonary defect may divert clinicians from considering the diagnosis of chronic thromboembolic pulmonary hypertension because lung volumes are usually normal in this disorder. We have, however, encountered a significant number of these patients with reduced lung volumes. Furthermore, we have observed many patients who have developed parenchymal scars and/or pleural thickening. To determine whether such findings are associated with lung volume restriction, we analyzed patients evaluated at our institution for chronic thromboembolic pulmonary hypertension over a 20-month period in whom thoracic high-resolution CT scans and pulmonary function testing had been performed. Patients with obstructive or restrictive lung disease from another cause were excluded. We compared the presence of lung restriction (total lung capacity below 80% of predicted) with the extent of parenchymal scarring, pleural thickening, and pulmonary artery diameter on CT scans. Of 191 patients evaluated, 51 met criteria for entry. Eleven patients (22%) had lung restriction. Parenchymal scarring was highly associated with lung restriction (p = 0.01). Neither pleural thickening (p = 0.08) nor pulmonary artery diameter (p = 0.80) was associated with lung restriction. CONCLUSIONS: A significant number of patients with chronic thromboembolic pulmonary hypertension may have restrictive lung defects. The restriction may be due to parenchymal scarring.

Adult↗
PubMed2000

Effects of nitric oxide inhalation after pulmonary thromboendarterectomy for chronic pulmonary thromboembolism.

STUDY OBJECTIVES: To examine the hypothesis that nitric oxide (NO) inhalation improves hemodynamics and gas exchange in patients with chronic pulmonary thromboembolism after pulmonary thromboendarterectomy. DESIGN: Prospective crossover clinical study. SETTING: : Surgical ICU in a national education and research hospital. PATIENTS: : Seven patients (mean age +/- SD, 54 +/- 11 years) who underwent elective pulmonary thromboendarterectomy for chronic pulmonary thromboembolism. INTERVENTIONS: Patients breathed 20 parts per million of NO gas for 30 min at 12-h intervals until extubation of the trachea. MEASUREMENTS AND RESULTS: Hemodynamics and arterial blood gas levels were analyzed before, during, and after NO inhalation. Waveform of pulmonary artery pressure (PAP) was evaluated using fractional pulse pressure (PPf): (systolic PAP - diastolic PAP)/mean PAP. After surgery, pulmonary vascular resistance decreased, PPf decreased, and cardiac index increased significantly. At the first trial, NO inhalation resulted in a slight improvement in arterial oxygen tension (from 173 +/- 33 to 196 +/- 44 mm Hg; p < 0.05), while hemodynamics did not change significantly. Twelve hours later, NO inhalation decreased pulmonary vascular resistance index (from 312 +/- 98 to 277 +/- 93 dyne.s. cm(-5)/m(2); p < 0.01), while the change in oxygenation was not significant. CONCLUSIONS: Immediately after pulmonary thromboendarterectomy for chronic pulmonary thromboembolism, NO inhalation improved oxygenation; at 12 h after surgery, NO inhalation resulted in decreased pulmonary vascular resistance, although both changes were small.

Aged↗
PubMed2002

Unilateral chronic thromboembolic pulmonary disease associated with combined inherited thrombophilia.

Chronic thromboembolic pulmonary hypertension (CTEPH) is considered to be an extreme variant of pulmonary thromboembolism. The underlying mechanisms for the failure of thrombus resolution are still unclear. In looking for inherited thrombophilia, an association with a lupus anticoagulant has been described repeatedly, and single cases of anticoagulant deficiencies (ie, antithrombin [AT], protein C, and protein S) have been reported. We describe a young patient with type I AT deficiency, the heterozygous prothrombin G20210A mutation, and unilateral chronic thromboembolic pulmonary disease presenting after a single thrombotic event. Pulmonary vascular patency was restored successfully by surgical pulmonary thromboendarterectomy. This case is unique because unilateral CTEPH is extremely uncommon, and it illustrates the severe clinical sequelae of the cosegregation of inherited thrombophilic defects.

Adult↗
PubMed2006

Incidence and prevalence of chronic thromboembolic pulmonary hypertension: from acute to chronic pulmonary embolism.

The incidence and prevalence of chronic thromboembolic pulmonary hypertension (CTEPH) are yet to be accurately determined and may be significantly underestimated. Historically, the occurrence of CTEPH in patients diagnosed with acute pulmonary embolism (PE) has been considered rare. Data from autopsy studies estimated the incidence of CTEPH at 1-3% overall and at 0.1-0.5% in patients surviving acute PE. Data indicate that each year in the United States, approximately 600,000 individuals suffer an acute pulmonary embolic event and that the annual number of new CTEPH cases in the United States is between 500 and 2,500. This may underestimate the true frequency of CTEPH because the disease is often misdiagnosed due to nonspecific symptoms and variable disease course. A monocenter, prospective, longitudinal study assessing symptomatic CTEPH in patients with acute PE but without prior venous thromboembolism recently estimated the cumulative incidence of CTEPH to be 1.0% 6 mo after PE, 3.1% after 1 yr, and 3.8% after 2 yr; overall post-PE incidence was approximately 3%. Further studies are needed to better define the true rate of CTEPH. Acute embolic events can occur without symptoms, and symptomatic PE is often overlooked or misdiagnosed in practice. CTEPH is often identified during diagnostic work-up in patients with unexplained pulmonary hypertension, many of whom lack medical history suggesting previous PE. In a recent study in 142 consecutive patients with CTEPH, 90 (63%) had no previous history of symptomatic venous thromboembolism. Further prospective epidemiologic studies are needed to better define the incidence and prevalence of CTEPH.

Acute Disease↗
PubMed2003

Safety of low molecular weight heparins in the treatment of venous thromboembolism.

Low molecular weight heparins (LMWHs) are commonly employed as a substitute for unfractionated heparin (UFH) in the treatment of venous thromboembolic events. Despite their higher cost, the preferential use of LMWHs seemed justified initially as, based on the results of earlier meta-analyses, these compounds were deemed to be more effective and safer than UFH. Although, in this respect, their purported superiority over UFH could not be confirmed by subsequent large, randomised trials and updated meta-analyses, other peculiar features of LMWHs were highlighted, favouring their preferential utilisation in patients with venous thromboembolism. Among these, the possibility of once-daily administration on an out-patient basis, the lower incidence of Type II heparin-induced thrombocytopenia and the lower likelihood of osteoporosis after prolonged treatment periods, appear to be especially prominent. This review attempts to evaluate the available evidence focusing on the safety of LMWHs for the treatment of venous thromboembolism and the current therapeutic options and potential advantages of LMWHs, either in general or in selected patient populations.

Anticoagulants↗
PubMed2006

Pulmonary thromboembolism in AIDS patient with chronic venous insufficiency, pulmonary tuberculosis and breast cancer: a case report and pathophysiology review.

Recent literature reports thrombotic episodes occurring in patients with HIV infection associated with other abnormalities including neoplasms and infections predisposing to a hypercoagulable state. We report a 47-year-old woman who developed pulmonary thromboembolism in association with HIV infection, pulmonary tuberculosis and breast cancer. She was treated with rifampin, isoniazid, pyrazinamide; heparin, phenprocoumon, zidovudine, lamivudine and efavirenz. Acid fast bacilli were visualized in a sputum smear and three months after, Mycobacterium tuberculosis was isolated from lymph node biopsy during a episode of immune reconstitution. The isolated mycobacteria showed sensitivity to all first-line drugs. HIV infection, breast cancer and pulmonary tuberculosis have several mechanisms that induce hypercoagulable state and can lead to thromboembolic complications. Pulmonary thromboembolism in this patient was a diagnostic challenge because of all the other severe diseases that she experienced at the same time.

Acquired Immunodeficiency Syndrome↗
PubMed2003

Thromboembolism following total hip replacement.

Total hip replacement is an operation that is prone to thromboembolic complications, with potentially life-threatening consequences. However, the risk has declined substantially in the past three decades, reflecting advances in the understanding of the pathophysiology of thromboembolism and perioperative prophylaxis. The old concept of deciding thromboembolic prophylaxis after the completion of surgery is obsolete. In this review, we will concentrate on the main preventive measures that the medical and surgical team should implement prior to, during, and immediately after surgery.

Arthroplasty, Replacement, Hip↗
PubMedDate not supplied

Prognostic factors for mortality and thromboembolism in canine immune-mediated hemolytic anemia: a retrospective study of 72 dogs.

Medical records of 72 dogs diagnosed with immune-mediated hemolytic anemia (IMHA) were reviewed to find risk factors for the disease, for mortality, and for thromboembolism. Coagulation data of 32 patients were evaluated for mortality or thromboembolism risk factors. Cocker Spaniels were at increased risk for IMHA (P = .012). Timing of vaccination was not associated with development of IMHA. PCV ranged from 5 to 33%, with a mean of 16 +/- 5%. Autoagglutination was present in 42% of the dogs. Platelet counts (n = 60) varied from 3,000 to 793,000/microL (mean, 160,117 +/- 133,571; median, 144,000). Thrombocytopenia (platelet count, <200,000/microL) was present in 70% of the dogs, with severe thrombocytopenia (platelet count, <50,000/microL) being present in 22%. One-step prothrombin time (OSPT) was prolonged in 28% of the dogs tested, and activated partial thromboplastin time (APTT) was prolonged in 47% of the dogs tested. Fibrin(ogen) degradation products (FDPs) were detected in 16 of 28 dogs tested (57%). Disseminated intravascular coagulation (DIC) was diagnosed in 10 of 31 (32%) dogs and was suspected in 8 dogs. Thromboemboli were found in 20 of 25 dogs given postmortem examinations. Mortality rate was 58%. Thrombocytopenia (P = .008) and serum bilirubin concentration of >5 mg/dL (P = .015) were risk factors for mortality, and hypoalbuminemia approached significance (P = .053). Severe thrombocytopenia (P = .046), serum bilirubin concentration of >5 mg/dL (P = .038), and hypoalbuminemia (P = .016) were risk factors for thromboembolism. On evaluation of continuous data, decreased platelet count (P = .057), increased bilirubin (P = .062), and decreased albumin (P = .054) approached significance for decreased survival. A higher risk for thrombosis was found with increased alkaline phosphatase (ALKP) (P = .042), increased bilirubin (P = .047), and decreased albumin (P = .012).

Anemia, Hemolytic↗