Current Practices in Operationalizing and Addressing Racial Equity in the Provision of Type 1 Diabetes Care: Insights from the Type 1 Diabetes Exchange Quality Improvement Collaborative Health Equity Advancement Lab.

OBJECTIVE: Medical racism contributes to adverse health outcomes. Type 1 Diabetes Exchange Quality Improvement Collaborative (T1DX-QI) is a large population-based cohort engaged in data sharing and quality improvement to drive system changes in T1D care. The annual T1DX-QI survey included questions to evaluate racial equity in diabetes care and practices to promote equity. METHODS: The annual T1DX-QI survey was administered to participating clinics in fall 2022 and had a 93% response rate. There were 50 responses (pediatric: 66% and adult: 34%). Questions, in part, evaluated clinical resources and racial equity. Response data were aggregated, summarized, and stratified by pediatric/adult institutions. RESULTS: Only 21% pediatric and 35% adult institutions felt that all their team members can articulate how medical racism contributes to adverse diabetes outcomes. Pediatric institutions reported more strategies to address medical racism than adult (3.6 vs 3.1). Organizational strategies to decrease racial discrimination included employee trainings, equity offices/committees, patient resources, and hiring practices. Patient resources included interpreter services, transportation, insurance navigation, and housing and food assistance. Hiring practices included changing prior protocols, hiring from the community, and diversifying workforces. Most institutions have offered antiracism training in the last year (pediatric: 85% and adult: 72%) and annually (pediatric: 64% and adult: 56%). Pediatric teams felt that their antiracism training was effective more often (pediatric: 60% and adult: 45%) and more commonly, they were provided resources (pediatric: 67% and adult: 47%) to help address inequities. CONCLUSION: Despite increased antiracism training, insufficient institutional support and perceived subeffective training still represent obstacles, especially in adult institutions. Sharing effective strategies to address medical racism will help institutions take steps to mitigate inequities.

Cardiac damage prevention by eplerenone: comparison with low sodium diet or potassium loading.

To determine the extent to which dietary sodium modulates aldosterone-induced cardiovascular damage, and to determine whether increased dietary potassium can prevent this damage, we used the Nomega-nitro-L-arginine methyl ester (L-NAME)/angiotensin II (Ang II) rat model of cardiac injury. This model is dependent on the presence of aldosterone for the occurrence of myocardial damage. Two sets of experiments were performed. In the first set, the following groups were studied: (1) 1% NaCl to drink (control group); (2) L-NAME/Ang II with water to drink (low salt group); (3) L-NAME/Ang II/1% NaCl (high salt group); (4) L-NAME/Ang II/1% NaCl/eplerenone (eplerenone group). Systolic blood pressure increased similarly in all groups compared with controls. Compared with the controls, the high salt group, but not the low salt or eplerenone groups, developed significant myocardial damage. In the second set of experiments three groups of animals were studied: (1) L-NAME/Ang II/1%NaCl (high salt group) (2) L-NAME/Ang II/1%NaCl/eplerenone (eplerenone group), and (3) L-NAME/Ang II/1%NaCl with an extra 1% KCl in food (high dietary potassium group). Eplerenone, but not dietary potassium supplementation, prevented the development of cardiac damage. Thus, mineralocorticoid receptor antagonist treatment and low sodium diet were effective in preventing cardiac damage, which suggests that a minimal level of aldosterone and a moderately high sodium diet are both required for the development of the cardiovascular damage in the L-NAME/Ang II model. The inability of potassium supplementation to reduce myocardial damage suggests that eplerenone's protective effect is not due to its potassium-sparing ability, but is rather related to some other feature of its selective aldosterone antagonism.