*2.1. Study Patients' Characteristics*

All consecutive patients with primary NS admitted to our department between January 2017 and December 2017 were considered for inclusion, and only those with a histopathological diagnosis were further included in the study. NS was defined as a level of proteinuria over 3.5 g/day and hypoalbuminemia. Exclusion criteria were age under 18 years, presence of known secondary causes of NS (diabetes, hepatitis B or C virus infection, HIV infection, systemic lupus erythematosus), a previous VTE, disorders that interfere with the synthesis of hemostasis-related factors (severe hepatic impairment) and therapy that influences hemostasis (antiplatelet drugs, anticoagulants).

Baseline demographics and biochemical data collected included age at presentation, gender, proteinuria over 24 h, serum albumin, and creatinine level. Glomerular filtration rate (GFR) was estimated using the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation. The genetic testing panel included the assessment for polymorphisms of Factor V gene (G1691A, T1250C, Cambridge and Hong-Kong mutations), PAI gene (plasminogen activator inhibitor—4G/5G mutation), methylene tetrahydrofolate reductase (MTHFR) gene (C677T and A1298C mutations) and prothrombin gene (G20210A mutation). Genetic testing was performed using a real-time polymerase chain reaction method (RT-PCR).

The study was conducted in accordance with the Declaration of Helsinki, and the protocol was approved by the Ethics Committee of Fundeni Clinical Institute (No. 20638/30 March 2020).
