Research Statement

      Normal pregnancy is associated with alterations in renal electrolyte handling. Activation of the renin-angiotensin-aldosterone system stimulates renal sodium reabsorption which drives maternal plasma volume expansion (~40%). This volume expansion is critical to the development of the growing uterus and fetus as inadequate volume expansion is associated with fetal growth restriction. Fetal growth restriction occurs in about 10-15% of all pregnancies and, despite advances in obstetric care, remains a serious long term health problem for the offspring. Fetal growth restriction is associated not only with increased perinatal morbidity and mortality, but also long-term complications such as adult onset hypertension, metabolic syndrome, and reduced nephron number leading to renal disease. The major focus of my research has been on the mechanisms permitting the avid sodium reabsorption of pregnancy. We have found that the epithelial sodium channel (ENaC) is increased in pregnancy and is critical for sodium reabsorption, blood pressure maintenance, and ultimately fetal growth. Our recent work supports activation of an alternative sodium retaining pathway in the distal nephron, the thiazide sensitive pendrin/ Na+ driven Cl-/HCO3- exchanger-mediated mechanism. Further investigation into the regulation of this mechanism is one of the aims of my current research.