Rule-in and rule-out of pre-eclampsia using DELFIA Xpress PlGF 1-2-3 and sFlt-1: PlGF ratio.

OBJECTIVES: The objective of this study was to explore and validate thresholds for Placental growth factor (PlGF) and soluble fms-like tyrosine-kinase 1 (s-Flt-1) (as s-Flt-1: PlGF ratio), to rule-in and rule-out disease in women with suspected pre-eclampsia, using DELFIA® Xpress PlGF1-2-3 and sFlt-1 assays. STUDY DESIGN: 369 samples from women with suspected or confirmed pre-eclampsia were analysed from a prospective cohort study. MAIN OUTCOME MEASURES: Serum PlGF and sFlt-1: PlGF were quantified using DELFIA® Xpress PlGF1-2-3 and DELFIA® Xpress sFlt-1 tests. Performances were evaluated at established and exploratory thresholds. Low PlGF concentration and sFlt-1: PlGF AUROC were compared. RESULTS: PlGF 1-2-3 concentration thresholds were confirmed to have high performance for rule-in (<50 pg/ml) and rule-out (≥150 pg/ml) pre-eclampsia within seven days (20-33+6 Weeks <50 pg/ml: Negative predictive value (NPV) 90.7% (95% CI 83.9, 95.3); ≥150 pg/ml: NPV 94.8% (95% CI 88.4, 98.3)) and 28 days (20-33+6 Weeks <50 pg/ml: Negative predictive value (NPV) 83.9% (95% CI 76.0, 90.0); ≥150 pg/ml: NPV 92.8% (95% CI 85.7, 97.0)). Optimal sFlt-1: PlGF thresholds for rule-in were ≥ 70 before 34 weeks and ≥ 90 after 34 weeks, and <50 to rule-out pre-eclampsia. Low PlGF alone had comparable performance to sFlt-1: PlGF, but test performance for both was reduced in women with Kidney Disease. CONCLUSIONS: DELFIA® Xpress PlGF1-2-3 and sFlt-1 assays for pre-eclampsia rule-in and rule-out have comparable performance to other established assays, and could be an alternative for clinical use. Performance was not enhanced by use of sFlt-1: PlGF ratio, suggesting that PlGF alone could provide a cheaper alternative to dual biomarker testing.

Renal biopsy findings during and after pregnancy.

BACKGROUND: Chronic kidney disease is estimated to affect up to 6% of women of reproductive age. Maternity care represents an opportunity for early diagnosis but there is limited understanding of chronic kidney disease aetiology occurring in or revealed by pregnancy. METHODS: A retrospective evaluation of renal biopsies during and after pregnancy between 2000 and 2015 was undertaken. A large academic health centre pathology database was searched for free text pregnancy-related terms, restricted to typology code 71000 (kidney). Indications and findings of postpartum renal biopsies were reviewed. RESULTS: Sixty-three renal biopsy reports were identified. Of 45 biopsies performed postpartum, 34 (75.6%) investigated persistent postpartum proteinuria. 20/34 (70.6%) of these biopsies yielded a primary renal disease, and 6/34 (17.6%) women had progressed to end stage renal disease at latest follow-up. CONCLUSION: Renal biopsy findings of women investigated for persistent postpartum proteinuria revealed a high incidence of histological diagnosis of de novo renal disease.

Acute kidney injury in pregnancy including renal disease diagnosed in pregnancy.

Pregnancy-related acute kidney injury (AKI) is a rare but serious complication in high-income settings and remains an important cause of maternal and foetal morbidity and mortality in low- and middle-income settings. Hypertensive disorders of pregnancy are the leading cause of pregnancy-related AKI worldwide. In this article, we outline the epidemiology, aetiology, recognition, investigation and management of pregnancy-related AKI. Difficulties in the definition of AKI, approaches to determine the cause of AKI in diagnostically challenging circumstances and diagnosis of new renal disease in pregnancy are discussed.