**1. Introduction**

Venous thromboembolic events (VTEs) are serious complications of nephrotic syndrome (NS), associated with significant morbidity and mortality [1]. The reported incidence varies widely (5–50%), due primarily to the retrospective nature of most studies and the lack of an accurate screening method that eludes an important number of asymptomatic cases [1–4]. Current clinical guidelines have inadequate evidence to support prophylactic anticoagulation, taking into account only serum albumin level and proteinuria over 24 h as markers of VTE risk [5].

VTEs must be viewed as a multifactorial disorder with the underlying pathogenesis being a complex interplay of inherited and acquired risk factors [6]. Hemostasis imbalance secondary to the NS [7], chronic inflammation associated with certain glomerulonephritis [1], a genetic background [1,6], when associated, can trigger a VTE. Usually, an inherited thrombophilia does not result in a spontaneous VTE, until an acquired hypercoagulable state (nephrotic syndrome) determines the clinical expression of the prothrombotic tendency [6]. With past clinical trials focusing mainly on serum albumin or proteinuria to define the VTE risk [3,8–10], the magnitude of additional risk factors has been evaluated

only in small series, with conflicting results [2,11–14]. Additionally, polymorphisms associated with inherited thrombophilia seem to be relatively prevalent in the general population, and screening for these disorders remains debatable [2,6,15–17].

We conducted a retrospective, observational study that sought to identify the prevalence of inherited risk factors for VTEs in a population of NS patients and to define the risk of VTEs in such patients.
