Abstract
We have determined the sequence and extent of maternal renal and uterine adaptation to pregnancy and examined the role of hormonal factors in their regulation. Renal bipolar diameter (RBD), renal artery resistance index (RARI), uterine artery pulsatility index (UAPI), and plasma relaxin, human chorionic gonadotropin (hCG), progesterone, estradiol, urea, and creatinine were measured longitudinally in women with normal spontaneous singleton pregnancies, in vitro fertilization (IVF) singleton pregnancies, ovum donation (OD) singleton pregnancies, and multiple pregnancies from prepregnancy to postpartum. There was a progressive increase in the RBD and the RARI and a decrease in the UAPI during pregnancy. These changes reversed toward prepregnancy levels by 6 weeks post delivery. There was no difference in the rate of change of RBD, RARI, and UAPI between spontaneous singleton, IVF singleton, OD singleton, and multiple pregnancies (p < 0.05), but relaxin was directly correlated to the RARI (r = 0.654, p = 0.015), and progesterone was inversely correlated to uterine artery PI (r = 0.554, p = 0.049). These data show that renal size and resistance to blood flow increase with advancing gestation, whereas the uterine artery resistance declined with gestation. These changes may be influenced by relaxin and progesterone.
ACKNOWLEDGMENTS
We are most grateful to the Charing Cross and Westminster Trustees for financial support to perform some hormonal assays. We would like to thank Professor Philip Steer in particular and Imperial College School of Medicine in general for giving us the opportunity and facilities to carry out this study. Dr. E.M. Wright, Medical Statistician at Imperial College (Hammersmith Hospital), gave us statistical advice. We are extremely grateful to her. Finally, We should like to acknowledge the huge contribution made by all the people who volunteered to take part in this study. Without them this work would not have been possible.
Declaration of Interest
The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.