Comparison of Breastfeeding Practices in Mothers With Chronic Kidney Disease With or Without Kidney Transplantation.

Introduction: Existing literature on pregnant patients with chronic kidney disease (CKD) with or without kidney transplantation focuses mainly on their pregnancy outcomes, but there are scant data on their lactation outcomes. Our objective was to characterize the lactation outcomes of patients with CKD with or without kidney transplantation. Methods: This is a single-institution retrospective cohort study of female-identifying patients with CKD with or without kidney transplantation who had a birth hospitalization at a tertiary health system between 2010 and 2020. Maternal and pediatric data on medical history, pregnancy, delivery, neonatal, and lactation outcomes, medications, and care team involved were collected. Primary outcome measures were breastfeeding initiation within 24-hour postpartum, breastfeeding 8 or more times per day during hospitalization, and any breastfeeding beyond 1 month. Health professionals' comments related to lactation and medications were extracted for qualitative data analysis. Results: Patients with and without kidney transplantation had similar comorbidities, pregnancy, delivery, and neonatal outcomes, and hospital length of stay (p > 0.05). Patients without kidney transplantation were more likely to initiate breastfeeding in the first 24 hours (p = 0.03) after delivery and continue breastfeeding beyond 1 month postpartum. There was a lack of consistency between specialties regarding medication compatibility with lactation. Patients on immunosuppression were more likely to exclusively formula feed (p = 0.02) or to initiate breastfeeding and then switch to formula (p = 0.0004) because of their immunosuppressive medications versus patients on any other medication. Conclusion: Patients with CKD but without a kidney transplantation were more likely to initiate breastfeeding or provide breast milk to their infant within 24 hours of delivery, breastfeed >8 times per day during their hospital stay, and breastfeed beyond a month postpartum than those with a transplanted kidney. Lactation support and pharmacology should be incorporated into graduate medical education.

Impaired proteostasis in senescent vascular endothelial cells: a perspective on estrogen and oxidative stress in the aging vasculature.

The heat shock response is an important cytoprotective mechanism for protein homeostasis and is an essential protective response to cellular stress and injury. Studies on changes in the heat shock response with aging have been mixed with regard to whether it is inhibited, and this, at least in part, reflects different tissues and different models. Cellular senescence is a key feature in aging, but work on the heat shock response in cultured senescent (SEN) cells has largely been limited to fibroblasts. Given the prevalence of oxidative injury in the aging cardiovascular system, we investigated whether SEN primary human coronary artery endothelial cells have a diminished heat shock response and impaired proteostasis. In addition, we tested whether this downregulation of heat shock response can be mitigated by 17ß-estradiol (E2), which has a critical cardioprotective role in women, as we have previously reported that E2 improves the heat shock response in endothelial cells (Hamilton KL, Mbai FN, Gupta S, Knowlton AA. Arterioscler Thromb Vasc Biol 24: 1628-1633, 2004). We found that SEN endothelial cells, despite their unexpectedly increased proteasome activity, had a diminished heat shock response and had more protein aggregation than early passage cells. SEN cells had increased oxidative stress, which promoted protein aggregation. E2 treatment did not decrease protein aggregation or improve the heat shock response in either early passage or SEN cells. In summary, cellular senescence in adult human endothelial cells is accompanied by increased oxidative stress and a blunting of proteostasis, and E2 did not mitigate these changes. NEW & NOTEWORTHY Senescent human endothelial cells have a diminished heat shock response and increased protein aggregates. Senescent human endothelial cells have increased basal oxidative stress, which increases protein aggregates. Physiological level of 17ß-estradiol did not improve proteostasis in endothelial cells.