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Objectives Circulating placental growth factor (PlGF) is a potential biomarker for preeclampsia. Prior studies show its limited precision in predicting or diagnosing preeclampsia, underscoring a common problem in biomarker data analyses in general – that large studies are needed to overcome clinical heterogeneity and to provide sufficient statistical power. Attaining such sample sizes often requires aggregation of cohorts. Different studies may use disparate platforms for laboratory analyses, complicating data merging. Here, we assessed whether PlGF concentrations could be merged across studies using inter-platform standardization. Methods Of 16516 pregnancies from 23 cohorts, 12,804 had at least one PlGF concentration (gestational age >20 weeks), analyzed using one of four platforms: R&D Systems, Alere-Triage, Roche-Elecsys or Abbott-Architect. Two merging algorithms, using Z -Score or Multiple of Median (MOM) transformations, were applied. A single Best Reference Curve (BRC), based on merged non-case PlGF concentrations, was constructed. Case-identification performance of the BRC for PlGF was compared to platform-specific curves. Results PlGF concentrations from different analytical platforms were merged ( Z -scores marginally better than MOMs) and, overall, BRC case-identification rates out-performed platform-specific curves. Conclusions Laboratory measurements from different platforms can be standardised and merged to give reference curves from aggregated PlGF datasets. This method allows for analysis of PlGF as a diagnostic marker for preeclampsia and is generalisable to other medical questions, thereby extending the scope of individual studies to answer a variety of important medical questions. Disclosures O. Burke: None. S. Benton: None. P. Szafranski: None. P. von Dadelszen: None. C. Buhimschi: None. I. Cetin: None. L. Chapell: None. F. Figueras: None. A. Galindo: None. I. Herraiz: None. C. Holzman: None. C. Hubel: None. U. Knudsen: None. C. Kronborg: None. H. Laivuori: None. T. McElrath: None. M. Moertl: None. J. Meyers: None. R.B. Ness: None. L. Oliviera: None. G. Olson: None. L. Poston: None. C. Ris-Stalphers: None. J.M. Roberts: None. E. Schistermann: None. E. Steegers: None. H. Stepan: None. O. Lapaire: None. D. Schlembach: None. S. Timmermans: None. V. Tsatsaris: None. J.A. van der Post: None. S. Verlohren: Consultant, Research Support Recipient, Commercial Interest: Roche Diagnostics, ThermoFisher, Novartis. P.M. Villa: None. D. Williams: None. H. Zeisler: None. C. Zhang: None. C.W. Redman: None. A. Staff: None.

Objectives Several studies have demonstrated an association between preeclampsia and premature development of cardiovascular disease (CVD) later in life. Although the association is incompletely understood, it probably includes pre-existing common risk factors. However, preeclampsia may also induce permanent vascular and metabolic alterations that could affect the systemic arterial elastic properties. In this regard, arterial stiffening could represent a link between the systemic effects of preeclampsia and CVD risk. We aimed to evaluate the effect of preeclampsia on markers of arterial stiffness and subclinical atherosclerosis in women with a history of preeclampsia. Methods A 10-year follow-up study comparing 19 exposed women (previous pre-eclamptic pregnancies) and 19 unexposed women (previous normotensive pregnancies) matched on age and time since delivery. Markers of arterial stiffness (aortic pulse wave velocity and augmentation index) and of atherosclerosis (carotid intima-media thickness and atheromatous plaques presence) – as well as traditional CVD risk factors - were compared between the two groups. Results Paired analysis showed a higher aortic pulse wave velocity in women with a history of preeclampsia than in unexposed women (7.96 ± 1.45 vs. 7.16 ± 0.66 m/s, respectively, P = 0.055). However, the difference fell marginally short of statistical significance. Waist-Hip ratio ( P = 0.04) and percentage with hypertension (defined as elevated systolic and/or diastolic blood pressure and/or antihypertensive drug treatment ( P = 0.03)) were significantly higher in previous preeclamptic women. No difference was observed in augmentation index, intima-media thickness or plaque presence. Conclusions Women with preeclamptic pregnancies 10 years earlier tended to have higher pulse wave velocity compared to women with previous normotensive pregnancies. To the best of our knowledge, this is the first comparative assessment of arterial stiffness 10 years after pregnancies complicated by preeclampsia. Disclosures M. Christensen: None. C.J. Kronborg: None. U.B. Knudsen: None.

T13.6 – Table 2. Comparison table Normal Chronic hypertension Superimposed hypertension Pre-eclampsia Gestational hypertension Normal – P = 0.377 P = 0.031 P< 0.0001 P = 0.002 Chronic hypertension P = 0.377 – P = 0.107 P = 0.003 P = 0.021 Superimposed hypertension P = 0.031 P = 0.107 – P = 0.218 P = 0.673 Pre-eclampsia P< 0.0001 P = 0.003 P = 0.218 – P = 0.201 Gestational hypertension P = 0.002 P = 0.021 P = 0.673 P = 0.201 – sensitivity and specificity increased to 100% and 92%, respectively. Combined, a positive PlGF test was able to diagnosis early onset pre-eclampsia or nIUGR with 94% sensitivity and 93% specificity. Conclusion: This evidence suggests that PlGF can be used to confirm diagnosis of early onset pre-eclampsia and identify nIUGR of placental origin from mimics. Funding: Biosite, CIHR, MSFHR, CFRI T13.6 Urinary placental growth factor differentiates the hypertensive disorders of pregnancy Neil Campbell1, Robert Ogle1, Annemarie Hennessy2, Charlene Thornton1. 1Royal Prince Alfred Hospital, Sydney, Australia; 2University of Western Sydney and Heart Research Institute, Australia Objective: The objective of this study is to establish whether urinary placental growth factor (uPlGF) is capable of discriminating between the different types of hypertensive disease in pregnancy in the third trimester. Design: This is a prospective descriptive case control study. Setting: Royal Prince Alfred Hospital, Urban tertiary referral hospital in Sydney, Australia. The Canterbury Hospital, district general hospital, Sydney, Australia Patients: Women in the third trimester of pregnancy who were currently inpatients on the antenatal ward or patients attending the antenatal outpatients department. Interventions: Patients in the third trimester of pregnancy were selected from the above settings, reviewed for eligibility and demographic data extracted. Patients were then asked to provide a urine specimen some of which was analysed for protein and creatinine and the rest stored and then later analysed for urine PlGF level. These levels after correction for creatinine concentration were then used in the final analysis. Measurements & main results: We have identified 36 women in the hypertensive group (preeclampsia (n=15), Gestational hypertension (n=13), Chronic hypertension (n=8), Preeclampsia superimposed on chronic hypertension (n=5)) and 47 women in the normal control group. There is a statistically significant difference in PlGF levels between the preeclamptic group and the normotensive controls (P