Hypercoagulability and Nephrotic Syndrome

Gigante, Antonietta; Barbano, Biagio; Sardo, Liborio; Martina, Paola; Gasperini, Maria Ludovica; Labbadia, Raffaella; Liberatori, Marta; Amoroso, Antonio; Cianci, Rosario

doi:10.2174/157016111203140518172048

Cited by 63 publications

(43 citation statements)

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“…In NS, the changes that produce the hypercoagulable state and potential thrombosis occur due to a combination of hormonal changes, the use of diuretics, and disturbances of the clotting mechanism [9]. The hypercoagulable state is a serious concern in patients with nephrotic syndrome; Renal Venous Thrombosis (RVT) and deep venous thrombosis are serious problems associated with it.…”

Section: Discussionmentioning

confidence: 99%

Children with Nephrotic Syndrome Suffer from Cerebral Venous Thrombosis

Peng¹

2014

J Nephrol Ther

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Hypercoagulability is a common complication in children with nephrotic syndrome and may cause venous thrombosis. This study explored the effectiveness of urokinase and low-molecular-weight (LMW) heparin used in conjunction in seven children with nephrotic syndrome complicated by intracranial venous thrombosis. The urokinase dose was 2,000-4,000 u/kg/day initially, with a pulse dose of 20,000-40,000 u given within 15-30 minutes and the remainder was pump-infused. From day 2, a dose of 2,000 u/kg/day was infused via the pump, and the total course duration was 3 to 7 days. During treatment, thrombin time (TT) and activated partial thromboplastin time (APTT) were tested three times per week, and particular attention was given to any bleeding. LMW heparin was used at a dosage of 100-120 anti-Xa IU/kg once or twice per day, given by abdominal subcutaneous injection for two weeks. The antiplatelet drug, dipyridamole 3-5 mg/kg, was also given orally two or three times per day for three months. In this study, the early use of urokinase, LMW heparin and anti-platelet drugs had good effect, the need for preventive therapy and early diagnosis of this complication in nephrotic syndrome should be given wider clinical consideration.

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Section: Discussionmentioning

confidence: 99%

Children with Nephrotic Syndrome Suffer from Cerebral Venous Thrombosis

Peng¹

2014

J Nephrol Ther

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“…pro-thrombotic factors (fibrinogen, factor V, factor VIII, platelets, von Willebrand factor, fibrinolytic system, plasminogen activator inhibitor fibrinogen) with associated abnormalities in platelet activation that promote in situ thrombosis in deep veins or arteries (7).…”

Section: Discussionmentioning

confidence: 99%

Nephrotic Syndrome and Stroke

Gigante

Barbano

Liberatori

et al. 2013

Int J Immunopathol Pharmacol

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The hypercoagulability of patients with nephrotic syndrome could be an important trigger for arterial and venous thrombotic events. Arterial thromboses are less frequent than venous thromboses and the most common locations are femoral arteries. The association of stroke and nephrotic syndrome is extremely rare. Here we report the case of a patient with stroke as first manifestation of nephrotic syndrome. Ischemic stroke can be the first manifestation of nephrotic syndrome and should be considered as a possible complication of the syndrome, when the commonest causes of ischemic stroke are excluded and especially in presence of pre-existing glomerular disease.Arterial and venous thromboses related to coagulation defects are potential complications of nephrotic syndrome (NS). This phenomenon has been attributed to a "hypercoagulable" state in which an imbalance between pro-coagulant/pro-thrombotic factors and anti-coagulant! antithrombotic factors promote in situ thromboses in deep veins or arteries. Arterial thromboses are less frequent than venous thromboses and the most common locations are femoral arteries, although other arteries may be involved (1-3). Stroke associated with nephrotic syndrome has rarely been reported (4). It has been suggested that arterial thromboses in NS patients are often associated with steroid and diuretic administration (5). Case reportA 71-year-old man was admitted to the Emergency Department for the onset of aphasia and crooked mouth. His past medical history revealed pharmacologically-treated mild hypertension for five years and autoimmune haemolytic anemia on treatment with low-dose steroids for ten years; he was not a smoker, and his BMI was 22.Brain CT scan and carotid echo color-Doppler did not show any sign-related abnormalities (Carotid intima media thickness was 1.1 mm in absence of stenosis bilaterally). Therefore, a brain MR scan was performed, revealing bilateral peri-ventricular multiple ischemic areas and a recent wide left fronto-temporal cortico-subcortical ischemic lesion (Fig. I). Electrocardiogram and transthoracic echocardiography were normal; subsequently a transesophageal echocardiography excluded cardiogenic thromboembolism or unstable aortic plaque.At the time of hospitalization, physical examination revealed edema of the lower legs and laboratory investigations showed proteinuria (21 g/24h), hypoalbuminemia (2 g/dL), decrease of plasma proteins (5.1 g/dL), hyperlipidemia (total cholesterol 405 mg/dL, LDL cholesterol 360 mg/dL,

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“…Currently, little has been known about the pathogenesis of PNS, although cellular mechanisms, inflammatory mediators, immune disorders, and genetic molecules are involved, with major contributions from immune induction and inflammatory damage (Gigante et al, 2014;Wu et al, 2014). As a result, the role of immune inflammatory response-mediating factors, including nuclear factor-kB, tumor necrosis factor-a, interleukin-1, interleukin-6, and interleukin-8, in the pathogenesis and development of PNS has become an active field in clinical studies and has received considerable attention (Urbonaviciute et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Analysis of the expression of HMGB-1, CXCL16, miRNA-30a, and TGF-β1 in primary nephritic syndrome patients and its significance

Wang¹,

Qu²,

Xi³

et al. 2015

Genet. Mol. Res.

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ABSTRACT. We investigated the expression levels of high-mobility group box protein 1 (HMGB-1), CXC chemokine ligand 16 (CXCL16), microRNA (miRNA)-30a and transforming growth factor b1 (TGF-b1) in primary nephritic syndrome (PNS) patients and the clinical significance of this expression. A total of 56 patients with PNS were included in the PNS group, while 50 healthy subjects formed the normal control group. Serum levels of HMGB-1, CXCL16, miRNA-30a, and urinary TGF-b1 concentrations were quantified along with other biochemical indices, including serum albumin, triglyceride (TG), total cholesterol (TC), lowdensity lipoprotein (LDL), high-density lipoprotein, and urinary proteins. The correlation between levels of HMGB-1, CXCL16, miRNA-30a, and TGF-b1 and biochemical indexes was further analyzed. PNS group patients had significantly higher levels of HMGB-1, CXCL16, miRNA30a, and TGF-b1 compared to the control group (P < 0.05). PNS patients also had higher 24-h urinary protein, TG, TC, and LDL levels but lower serum albumin compared to subjects in the control group (P < 0.05). Serum HMGB-1, CXCL16, miRNA-30a, and urinary TGF-b1 levels were all negatively correlated with serum albumin levels, but were positively correlated with TG, TC, LDL, and 24-h urinary protein (P < 0.05 in all cases). Additionally, a positive correlation existed among serum HMGB-1, CXCL16, miRNA-30a, and urinary TGF-b1 levels (P < 0.01). HMGB-1, CXCL16, miRNA-30a, and urinary TGF-b1 were highly expressed in PNS patients and may play important roles in the pathogenesis and development of PNS.

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Hypercoagulability and Nephrotic Syndrome

Cited by 63 publications

References 0 publications

Children with Nephrotic Syndrome Suffer from Cerebral Venous Thrombosis

Children with Nephrotic Syndrome Suffer from Cerebral Venous Thrombosis

Nephrotic Syndrome and Stroke

Analysis of the expression of HMGB-1, CXCL16, miRNA-30a, and TGF-β1 in primary nephritic syndrome patients and its significance

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