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ContextPatients with advanced cancer often involve family caregivers in health-related decision-making from diagnosis to end-of-life; however, few interventions have been developed to enhance caregiver decision support skills.ObjectivesAssess the feasibility, acceptability, and potential efficacy of individual intervention components of CASCADE (CAre Supporters Coached to be Adept DEcision Partners), an early telehealth, palliative care coach-led decision support training intervention for caregivers.MethodsPilot factorial trial using the multiphase optimization strategy (October 2019-October 2020). Family caregivers and their care recipients with newly-diagnosed advanced cancer (n = 46 dyads) were randomized to1 of 8 experimental conditions that included a combination of one of the following three CASCADE components: 1) effective decision support psychoeducation; 2) decision support communication training; and 3) Ottawa Decision Guide training. Feasibility was assessed by completion of sessions and questionnaires (predefined as ≥80%). Acceptability was determined through postintervention interviews and participants' ratings of their likelihood to recommend. Measures of effective decision support and caregiver and patient distress were collected at Twelve and Twenty four weeks.ResultsCaregiver participants completed 78% of intervention sessions and 81% of questionnaires; patients completed 80% of questionnaires. Across conditions, average caregiver ratings for recommending the program to others was 9.9 on a scale from 1-Not at all likely to 10-Extremely likely. Individual CASCADE components were observed to have potential benefit for effective decision support and caregiver distress.ConclusionWe successfully piloted a factorial trial design to examine components of a novel intervention to enhance the decision support skills of advanced cancer family caregivers. A fully-powered factorial trial is warranted.Key messageWe pilot tested components of CASCADE, an early palliative care decision support training intervention for family caregivers of patients with advanced cancer. CASCADE components were acceptable and the trial design feasible, providing promising future directions for palliative care intervention development and testing. Pilot results will inform a fully-powered trial.

BackgroundApproval of living kidney donors (LKD) with end-stage kidney disease (ESKD) risk factors, such as obesity, has increased. While lifetime ESKD development data are lacking, the study of intermediate outcomes such as diabetes is critical for LKD safety. Donation-attributable diabetes risk among persons with obesity remains unknown. The purpose of this study was to evaluate 10-year diabetes-free survival among LKDs and non-donors with obesity.MethodsThis longitudinal cohort study identified adult, LKDs (1976-2020) from 42 US transplant centers and non-donors from the Coronary Artery Risk Development in Young Adults (1985-1986) and the Atherosclerosis Risk in Communities (1987-1989) studies with body mass index ≥30 kg/m2. LKDs were matched to non-donors on baseline characteristics (age, sex, race, body mass index, systolic and diastolic blood pressure) plus diabetes-specific risk factors (family history of diabetes, impaired fasting glucose, smoking history). Accelerated failure time models were utilized to evaluate 10-year diabetes-free survival.FindingsAmong 3464 participants, 1119 (32%) were LKDs and 2345 (68%) were non-donors. After matching on baseline characteristics plus diabetes-specific risk factors, 4% (7/165) LKDs and 9% (15/165) non-donors developed diabetes (median follow-up time 8.5 (IQR: 5.6-10.0) and 9.1 (IQR: 5.9-10.0) years, respectively). While not significant, LKDs were estimated to live diabetes-free 2 times longer than non-donors (estimate 1.91; 95% CI: 0.79-4.64, p = 0.15).ConclusionsLKDs with obesity trended toward living longer diabetes-free than non-donors with obesity, suggesting within the decade following donation there was no increased diabetes risk among LKDs. Further work is needed to evaluate donation-attributable diabetes risk long-term.

BACKGROUND: Live donor kidney transplantation has been popularized to help mitigate the organ shortage crisis. At the time of living donor nephrectomy, living donors lose 50% of their kidney function or glomerular filtration rate (GFR). Studies have shown that in healthy living donors, the remaining kidney is able to adapt and recover 10% to 25% of postdonation lost GFR. GFR recovery is critical to long-term kidney health, particularly for Black Americans who disproportionately suffer from kidney disease with an incidence 2.5 times White Americans. To date, no study has examined whether health inequities in renal recovery postdonation exist. STUDY DESIGN: We retrospectively analyzed 100,121 living kidney donors reported to the Scientific Registry of Transplant Recipients between 1999 and 2021. We estimated GFR (eGFR) using the Chronic Kidney Disease Epidemiology Collaboration 2021 equation and predicted the likelihood (logistic regression) and time (Cox regression) to recovery of 60% and 75% predonation eGFR. Models adjusted for age, sex, race, BMI, and predonation eGFR. RESULTS: Black patients were 47% (adjusted odds ratio 0.53, 95% CI 0.50 to 0.56, p < 0.001) and 43% (adjusted odds ratio 0.57, 95% CI 0.54 to 0.60, p < 0.001) less likely to recover 60% and 75% of predonation eGFR, respectively, compared with their White counterparts. The hazard ratio for time to renal recovery of 60% and 75% of predonation eGFR was 22% (adjusted hazard ratio 0.78, 95% CI 0.76 to 0.80, p < 0.001) and 38% (adjusted hazard ratio 0.62, 95% CI 0.60 to 0.65, p < 0.001) lower, respectively, than White patients. CONCLUSIONS: Black living kidney donors were less likely to recover predonation eGFR, and time to renal recovery was significantly longer than their White counterparts. These data highlight the need for enhanced living kidney donor follow-up, particularly for Black living kidney donors who are at greatest future risk of end-stage kidney disease. [ABSTRACT FROM AUTHOR]

Background Hyperparathyroidism (HPT) and malignancy are the most common causes of hypercalcemia. Among kidney transplant (KT) recipients, hypercalcemia is mostly caused by tertiary HPT. Persistent tertiary HPT after KT is associated with allograft failure. Previous studies on managing tHPT were subjected to survivor treatment selection bias; as such, the impact of tertiary HPT treatment on allograft function remained unclear. We aim to assess the association between hypercalcemic tertiary HPT treatment and kidney allograft survival. Materials and Methods We identified 280 KT recipients (2015-2019) with elevated post-KT adjusted serum calcium and parathyroid hormone (PTH). KT recipients were characterized by treatment: cinacalcet, parathyroidectomy, or no treatment. Time-varying Cox regression with delayed entry at the time of first elevated post-KT calcium was conducted, and death-censored and all-cause allograft failure were compared by treatment groups. Results Of the 280 recipients with tHPT, 49 underwent PTx, and 98 received cinacalcet. The median time from KT to first elevated calcium was 1 month (IQR: 0-4). The median time from first elevated calcium to receiving cinacalcet and parathyroidectomy was 0(IQR: 0-3) and 13(IQR: 8-23) months, respectively. KT recipients with no treatment had shorter dialysis vintage (P  = .017) and lower PTH at KT (P  = .002), later onset of hypercalcemia post-KT (P  < .001). Treatment with PTx (adjusted hazard ratio (aHR) = 0.18, 95%CI 0.04-0.76, P  = .02) or cinacalcet (aHR = 0.14, 95%CI 0.004-0.47, P  = .002) was associated with lower risk of death-censored allograft failure. Moreover, receipt of PTx (aHR = 0.28, 95%CI 0.12-0.66, P  < .001) or cinacalcet (aHR = 0.38, 95%CI 0.22-0.66, P  < .001) was associated with lower risk of all-cause allograft failure. Conclusions This study demonstrates that treatment of hypercalcemic tertiary HPT post-KT is associated with improved allograft survival. Although these findings are not specific to hypercalcemia of malignancy, they do demonstrate the negative impact of hypercalcemic tertiary HPT on kidney function. Hypercalcemic HPT should be screened and aggressively treated post-KT. [ABSTRACT FROM AUTHOR]