American Journal of Obstetrics and Gynecology
ResearchImagingFetal renal artery impedance as assessed by Doppler ultrasound in pregnancies complicated by intraamniotic inflammation and preterm birth
Section snippets
Study population and research design
We evaluated fetal renal artery blood flow hemodynamics in 70 fetuses. A flow diagram of our study population is presented in Figure 1. Fifty-six fetuses (study group) were delivered by mothers who had a clinically indicated amniocentesis to rule out intraamniotic infection/inflammation. Gestational age renal artery blood flow velocity reference ranges were generated based on fetuses with uncomplicated pregnancies (n = 14) (control group). All our control fetuses were carried by asymptomatic
Results
Of the 56 women who presented with clinical signs or symptoms of preterm labor or PPROM (study group), 19 (34%) had AF proteomic profiles characteristic of intraamniotic inflammation. All 19 women had a clinically indicated preterm delivery (Figure 1). In 37 women (66%), AF infection/inflammation was excluded based on the amniocentesis results. Of these, 30 still delivered preterm. Only 5 women in the study group (14%) delivered fetuses at term. In the absence of intraamniotic
Comment
We found that a systemic fetal inflammatory response, defined as an increased cord blood IL-6 level, is not associated with detectable changes of the renal artery blood flow impedance, in utero. Thus, our original hypothesis that the fetal renal artery impedance is significantly altered in the context of intraamniotic infection/inflammation is rejected. Furthermore, we show that the process of intraamniotic inflammation is linked to elevated neonatal serum BUN levels in the first day of life.
In
Acknowledgments
We are indebted to the nurses, fellows, and residents at Department of Obstetrics, Gynecology and Reproductive Sciences, Yale New Haven Hospital, and to all patients who participated in the study. The funding source had no involvement in study design, interpretation of data, writing of the report, or decision to submit the paper for publication.
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2020, Seminars in Fetal and Neonatal MedicineCitation Excerpt :However, it is possible that fetal urine production is altered in FIRS, and this can result from redistribution of blood flow away from the kidneys to ensure adequate blood flow to critical organs and increase efficiency of oxygen utilization [185,186]. It is interesting that neonates delivered to mothers with intra-amniotic inflammation have higher serum blood urea nitrogen concentrations and that such concentrations correlate with amniotic fluid IL-6 [187]. In a murine model, maternal intraperitoneal endotoxin injection induced fetal leukocyte activation, recruitment, and infiltration of the fetal renal parenchyma [188].
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Cite this article as: Azpurua H, Dulay AT, Buhimschi IA, et al. Fetal renal artery impedance as assessed by Doppler ultrasound in pregnancies complicated by intraamniotic inflammation and preterm birth. Am J Obstet Gynecol 2009;200:203.e1-203.e11.
This study was supported by National Institutes of Health (NIH)/Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) Grant R01 HD 047321 (to I.A.B.). C.S.B. was supported by the NIH/NICHD Grant R03 HD 50249, and K12 HD 1027766 (C.J.L.).