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Introduction: The COVID-19 pandemic has expanded the use of telemedicine to patient populations that were previously constrained to in-person visits. Few studies have investigated the role that telemedicine plays in shaping the care of these patient populations. This project explores the impact of telemedicine for one such population: patients and parents of gender-diverse individuals seeking gender-affirming surgery. Methods: A 10-question survey using previously validated questions was completed by 34 patients and 9 parents of patients (aged 15-31) who received virtual care at the Center for Gender Surgery at Boston Children's Hospital between March 2020 and April 2021. The survey was divided into two parts. The first section collected demographic information. The second assessed participant perspectives on remote surgical gender care through a series of Likert-type and open-ended questions. Results: A total of 100% of the respondents felt that their telemedicine visit was convenient; 60% (18) of the patients and 87% (7) of the parents stated that they look forward to future use of this modality. Free responses highlighted common perspectives on remote surgical gender care, including the increased accessibility of gender-affirming care through telehealth, the limitations of telehealth for addressing physical and relational aspects of gender care, patients' desire for autonomy and privacy during telehealth visits, and parents' desire to be involved throughout their children's gender journey. Conclusion: These results demonstrate the unique ability of telemedicine, if implemented thoughtfully, to enhance outcomes for patients seeking surgical gender affirmation.
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BACKGROUND: Hypertension is a complex trait with an ill-defined genetic predisposition, in which renal mechanisms seem to be involved even at the early stages. Renal kallikrein excretion is diminished in patients with hypertension, and perhaps even in the early, prehypertensive phases of the syndrome. African Americans, a group at increased risk of developing hypertension, have especially diminished kallikrein expression, coupled with decreased renal excretion of K(+), a known stimulant of kallikrein expression, suggesting an environmental mechanism for their kallikrein deficit. We, therefore, tested whether short-term indirect (K(+)) or direct (fludrocortisone) stimulation of mineralocorticoid activity might be capable of restoring kallikrein excretion in African Americans. METHODS: Nineteen healthy normotensive young men (n = 10 white, n = 9 African Americans) were treated with the following sequence of four oral medications, each for 1 week: placebo, KCl (120 mEq/day), placebo, and the mineralocorticoid fludrocortisone (0.4 mg/day). At each stage, we measured vital signs, excretion of kallikrein, aldosterone and electrolytes, and serum renin. Results were evaluated by two-way, repeated measures ANOVA. RESULTS: African Americans had diminished urinary excretion of not only kallikrein (P =.007), but also K(+) (P <.001) and aldosterone (P =.015). Kallikrein responses to mineralocorticoid stimulation were substantially blunted in African Americans, whether achieved indirectly (by supplemental K(+); P =.019) or directly (by the exogenous mineralocorticoid fludrocortisone; P =.027), despite achievement of substantial increments in K(+) excretion after KCl (P =.002), and multiple other mineralocorticoid effects after fludrocortisone (P =.005). The kallikrein increment after KCl was best predicted by renin activity (P =.001) rather than ethnicity. Potassium chloride did not lower blood pressure (BP) in either group (P >.4). CONCLUSIONS: Restoration of K(+) and aldosterone secretion to levels found in whites does not normalize kallikrein excretion or lower BP in African Americans, at least in the short term. Nor does exogenous mineralocorticoid stimulation fully restore kallikrein expression in African Americans. Therefore, the diminution of kallikrein biosynthesis in African Americans seems to involve mechanisms at or distal to the aldosterone receptor, and perhaps at the level of the kallikrein gene itself.