Women with preeclampsia (PE) form a vulnerable group for vitamin D3 deficiency. Reabsorption of vitamin D3 occurs in the proximal tubule after being endocytosed in combination with DBP (vitamin D binding protein) by the megalin/cubilin receptor. Because proteinuria promotes tubule injury and dysfunction, we hypothesized that the proteinuria present in pe could promote the loss of these components into the urine. Twenty preeclamptic patients and ten normal pregnant women with a gestational age greater than 20 weeks composed three groups: NC, normotensive control pregnant patients; PE, non-proteinuric preeclamptic patients; and PPE, preeclamptic patients with proteinuria. When proteinuria was absent, preeclampsia was diagnosed accordingly to the American college of Obstetricians and Gynecologists' (ACOG) guideline. The presence of 24-hour proteinuria equal to or greater than 300 mg was considered to form the PPE group. Urinary cubilin, megalin, and DBP were measured by ELISA and normalized by urinary creatinine. Regarding gestational age, there was no difference between the groups. NC group had arterial pressure within normal values, whereas PE and PPE groups had a significant increase (p < 0.01). As expected, PPE group presented elevated ACR (p < 0.05), accompanied by large amounts of cubilin and DBP in the urine (p < 0.05 vs. NC and PE). No difference was found in urinary megalin. PPE patients showed more chance of shedding cubilin into the urine compared to non-proteinuric patients (odds ratio 12.7 (1.2-136.3). In conclusion, this study further tightens the relationship between pe and vitamin D 3 deficiency, since proteinuria present in pe induces the loss of molecules responsible for renal tubular vitamin D 3 reabsorption for subsequent activation. Combined with other factors, the proteinuria may intensify vitamin D 3 deficiency in PE. Preeclampsia (PE) is a multisystem disorder of pregnancy in which renal damage has a significant contribution. A set level of proteinuria has been used to predict high-risk groups and define treatment for PE. In terms of physiopathology, proteinuria emerges due to processes that disturb the glomerular filtration barrier. Besides the classical mechanisms of glomerular damage such as endotheliosis and loss of podocytes 1,2 , an evidence for tubular injury have also been reported. Markers of proximal tubule injury such as kidney injury molecule-1 (KIM-1), neutrophil gelatinase-associated lipocalin (NGAL), and retinol-binding protein (RBP) were higher in the urine of PE patients than in urine of healthy pregnancies 3 In addition, urinary lysosomal enzyme excretion is elevated in patients with PE compared to a pregnant woman with chronic hypertension 4. Burwick et al. demonstrated that pregnancies affected by severe PE have high amounts of KIM-1 in the urine, which was closely correlated with urinary complement activation products, suggesting that tubular injury in PE is intensified by inflammation-activated complement 5. Direct effects of proteinuria on tubular cell damage have been ...