Background Teaching methods in most residency and fellowship programs have not yet addressed the challenges of rapid dissemination of new scientific information. Our Northwell nephrology fellowship program used the smartphone application WhatsApp® to facilitate nephrology education. A qualitative study was conducted to explore perceptions of nephrology fellows and faculty using WhatsApp® as a teaching tool. Methods A WhatsApp® messenger group called ‘Northwell Renal Forum’ was created in 2018, which included all eight fellows and seven selected faculty members. Multiple choice questions on various nephrology topics were posted, about one to two per week. Fellows responded at their leisure. After 7 months, data were analyzed following two 1-h focus groups (one for faculty and one for fellows). Focus groups were moderated by two qualitative researchers, unknown to the participants, who asked open-ended questions about the WhatsApp® learning approach. Results Faculty feedback was generally positive. Three major themes arose: control over learning material, comfort being fostered between faculty and fellows and faculty perceptions of fellows. The fellows also reported an overall positive experience. Control and comfort were themes again identified in this focus group. Fellows reported feeling control over which faculty member was in the group and when to respond to questions. Fellows also felt comfort from learning without pressure. Variety was the third theme that arose. Conclusion Focus group evaluations elucidated the strengths of using WhatsApp®, and the overall positive experience of both faculty and fellows. This inexpensive and easy-to-use tool can augment the learning of nephrology during fellowship.

Parathyroid hormone (PTH) regulates calcium metabolism and bone strength. Chronic kidney disease (CKD) leads to secondary hyperparathyroidism (SHP) which increases morbidity and mortality. High PTH expression in SHP is due to increased PTH mRNA stability mediated by changes in PTH mRNA interaction with stabilizing AUF1 and destabilizing KSRP. Pin1 isomerizes target proteins, including mRNA binding proteins. In SHP, Pin1 isomerase activity is decreased and phosphorylated KSRP fails to bind PTH mRNA, resulting in high PTH mRNA stability and levels. The molecular mechanisms underlying Pin1 regulation and their effect to increase PTH expression are unknown. We show by mass-spectrometry (MS) the CKD induced changes in rat parathyroid proteome and phosphoproteome profiles. Parathyroid Pin1 Ser16 and Ser71 phosphorylation, that disrupts Pin1 activity, is enhanced in acute and chronic kidney failure rats. Accordingly, pharmacologic Pin1 inhibition increases PTH expression in parathyroid organ cultures and transfected cells, through the PTH mRNA protein binding cis element and KSRP phosphorylation. Therefore, CKD leads to parathyroid loss of Pin1 activity by inducing Pin1 phosphorylation. This predisposes parathyroids to increase PTH production through modified PTH mRNA-KSRP interaction that is dependent on KSRP phosphorylation. CKD induced Pin1 and KSRP phosphorylation and the Pin1-KSRP-PTH mRNA axis thus drive secondary hyperparathyroidism.

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