Predisposing Factors for Deep Venous Thrombosis in Children and Adolescents with Nephrotic Syndrome

Gabriela De Toledo Passos Candelaria,Vera Maria Santoro Belangero

doi:10.5402/2011/827483

Gabriela De Toledo Passos Candelaria, Vera Maria Santoro Belangero

Open Access

https://doi.org/10.5402/2011/827483

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Journal: ISRN Vascular Medicine	Publication Date: Nov 17, 2011
Citations: 30	License type: CC BY 3.0

Affiliation: Universidade Estadual de Campinas

Abstract

Nephrotic syndrome (NS) is a state of hypercoagulability. In this paper, we sought to determine risk factors for the occurrence of deep vein thrombosis (DVT) in children with NS. The “with DVT” group included patients with decompensated NS and diagnosed with DVT. The “without DVT” group included the same patients, six to eighteen months prior to the episode of DVT, with decompensated NS but without DVT. Different prediction variables were analyzed. The odds ratio for the occurrence of DVT in patients with triglyceride levels ≥300 mg/dL was 3.14 (95% CI 1.14 to 8.64). For hematocrit levels ≥43% and for the presence of infection or a severe systemic event, the odds ratio was 4.37 (95% CI 1.23 to 15.53). The presence of significant risk factors for the occurrence of DVT in children with NS may serve as a warning for the occurrence of venous thrombosis.

Highlights

Many studies have associated nephrotic syndrome (NS) with a multifactorial hypercoagulable state [1]
While some studies have shown lower serum levels of protein S and reduced activity of protein C in patients with NS [3], other studies point to increased levels and activity of these proteins [4, 5], possibly due to the variability in the severity of hypoalbuminemia and proteinuria and the time since last steroid use, which may bias the results of these studies
Two patients had two episodes of deep vein thrombosis (DVT) at different times, which yielded a total of 11 cases of thrombosis

Summary

Introduction

Many studies have associated nephrotic syndrome (NS) with a multifactorial hypercoagulable state [1] This NSassociated hypercoagulability is dependent on changes in pro- and anticoagulant factors and on hemodynamic characteristics that favor thrombosis, such as the tendency toward hypovolemia and hemoconcentration. NS can result in the urinary loss of proteins that inhibit the hemostatic system (e.g., antithrombin III) and the increased synthesis of factors that promote thrombosis (factors V, VIII, and fibrinogen) [2]. Conditions such as thrombocytosis, increased levels of von Willebrand factor, and increased formation of thromboxane A2 are observed in patients with the disease [3]. Thrombosis in NS has not been associated with genetic factors that lead to hypercoagulability [6]

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