A qualitative assessment of factors contributing to Spanish-speaking federally qualified health center patients' chronic pain experiences.

People of Hispanic or Latino ethnicity (Latinx people) experience pain diagnosis, treatment, and care disparities relative to non-Latinx Whites. Those whose preferred language is Spanish may experience additional disparities when receiving care in a language-discordant environment. In order to better understand medically underserved Spanish-speaking Latinx patients' pain care experience in primary care, we conducted semi-structured qualitative interviews with federally qualified health center staff members (n = 9) and Spanish-speaking adult Latinx patients with chronic pain (n = 12) to capture data on their perspectives. Interview data were mapped to the individual (microsystem), interpersonal (mesosystem), organizational (exosystem), and environmental (macrosystem) levels of Bronfenbrenner's Ecological Systems Theory and analyzed using thematic content analysis informed by the Framework Method. Findings suggest that Spanish-speaking patients and English-speaking care team members may interpret information about pain state and severity differently, may have misaligned expectations about care, treatment methodologies, and treatment goals, and may experience difficulty forming a mutual understanding during health care encounters due to cross-linguistic and cross-cultural miscommunication. Patients preferred to describe their pain in words rather than with numbers or standardized scales, and both patients and frontline care team members expressed frustration with medical interpretation services, which added time and complexity to visits. Patients and health center staff emphasized the diversity of experiences among Spanish-speaking Latinx people, and the need to account for both linguistic and cultural differences during care encounters. Both groups supported hiring more Spanish-speaking, Latinx healthcare personnel who better resemble the patient population, which has the potential to improve linguistic and cultural concordance and competence, with the aim of improving care outcomes and patient satisfaction. Further study is warranted to examine how linguistic and cultural communication barriers impact pain assessment and treatment in primary care, the extent to which patients feel understood by their care teams, and their confidence in their ability to understand and interpret treatment recommendations.

The diabetic microenvironment causes mitochondrial oxidative stress in glomerular endothelial cells and pathological crosstalk with podocytes.

BACKGROUND: In the setting of diabetes mellitus, mitochondrial dysfunction and oxidative stress are important pathogenic mechanisms causing end organ damage, including diabetic kidney disease (DKD), but mechanistic understanding at a cellular level remains obscure. In mouse models of DKD, glomerular endothelial cell (GEC) dysfunction precedes albuminuria and contributes to neighboring podocyte dysfunction, implicating GECs in breakdown of the glomerular filtration barrier. In the following studies we wished to explore the cellular mechanisms by which GECs become dysfunctional in the diabetic milieu, and the impact to neighboring podocytes. METHODS: Mouse GECs were exposed to high glucose media (HG) or 2.5% v/v serum from diabetic mice or serum from non-diabetic controls, and evaluated for mitochondrial function (oxygen consumption), structure (electron microscopy), morphology (mitotracker), mitochondrial superoxide (mitoSOX), as well as accumulation of oxidized products (DNA lesion frequency (8-oxoG, endo-G), double strand breaks (γ-H2AX), endothelial function (NOS activity), autophagy (LC3) and apoptotic cell death (Annexin/PI; caspase 3). Supernatant transfer experiments from GECs to podocytes were performed to establish the effects on podocyte survival and transwell experiments were performed to determine the effects in co-culture. RESULTS: Diabetic serum specifically causes mitochondrial dysfunction and mitochondrial superoxide release in GECs. There is a rapid oxidation of mitochondrial DNA and loss of mitochondrial biogenesis without cell death. Many of these effects are blocked by mitoTEMPO a selective mitochondrial anti-oxidant. Secreted factors from dysfunctional GECs were sufficient to cause podocyte apoptosis in supernatant transfer experiments, or in co-culture but this did not occur when GECs had been previously treated with mitoTEMPO. CONCLUSION: Dissecting the impact of the diabetic environment on individual cell-types from the kidney glomerulus indicates that GECs become dysfunctional and pathological to neighboring podocytes by increased levels of mitochondrial superoxide in GEC. These studies indicate that GEC-signaling to podocytes contributes to the loss of the glomerular filtration barrier in DKD. Video abstract.