Food deserts (FD), low-income areas with low-access to healthful foods, are associated with higher burden of cardiovascular risk factors. Few studies have examined the impact of FD on clinical outcomes in heart failure (HF). FD status was assessed in 457 HF patients (mean age 55.9 ± 12.5 years; 50.3% Black) using the Food Desert Research Atlas. The Andersen-Gill extension of Cox model was used to examine the association of living in a FD with risk of repeat hospitalization (all-cause and HF-specific). Patients living in a FD were younger (P=0.01), more likely to be Black (P<0.0001), less educated (P=0.003), and less likely to have commercial insurance (P=0.003). During a median follow-up of 827 (506, 1379) days, death occurred in 60 (13.1%) subjects, and hospitalizations occurred in 262 (57.3%) subjects. There was no difference in the risk of death based on FD status. The overall frequency of all-cause (94.1 vs. 63.6 per 100 patient-years) and HF-specific (59.6 vs. 30.5 per 100 patient-years) hospitalizations was higher in subjects who lived in a FD. After adjustment for covariates, living in a FD was associated with an increased risk of repeat all-cause (hazard ratio [HR] 1.39, 95% confidence interval [Cl] 1.19-1.63; P=0.03) and HF-specific (HR 1.30, 95% Cl 1.02-1.65; P=0.03) hospitalizations. In conclusion, patients living in a FD have a higher risk of repeat all-cause and HF-specific hospitalization.

Background and objectivesMitochondrial DNA copy number is a biomarker of mitochondrial function, which has been hypothesized to contribute to pathogenesis of CKD through podocyte injury, tubular epithelial cell damage, and endothelial dysfunction. The prospective association of mitochondrial DNA copy number with CKD progression has not been previously evaluated.Design, setting, participants, & measurementsChronic Renal Insufficiency Cohort study participants had serum levels of mitochondrial DNA copy number calculated from probe intensities of mitochondrial single nucleotide polymorphisms genotyped on the Illumina HumanOmni 1-Quad Array. CKD progression was defined as kidney failure or halving of eGFR from baseline. Cox proportional hazards models were used to calculate hazard ratios for mitochondrial DNA copy number and risk of CKD progression.ResultsAmong 2943 participants, mean age was 58 years, 45% were women, and 48% self-identified as Black. There were 1077 patients who experienced CKD progression over a median follow-up of 6.5 years. The incidence rate of CKD progression was highest for those in the lowest tertile of mitochondrial DNA copy number (tertile 1, 58.1; tertile 2, 50.8; tertile 3, 46.3 per 1000 person-years). Risk for CKD progression was higher for participants with lower levels of mitochondrial DNA copy number after adjustment for established risk factors (for tertile 1 versus 3, hazard ratio, 1.28 [95% confidence interval, 1.10 to 1.50]; for tertile 2 versus 3, hazard ratio, 0.99 [95% confidence interval, 0.85 to 1.16]; trend P=0.002). Similar results were seen among those with albuminuria (for tertile 1 versus 3, hazard ratio, 1.24; 95% confidence interval, 1.05 to 1.47), but there were no statistically significant associations among individuals without albuminuria (for tertile 1 versus 3, hazard ratio, 1.04; 95% confidence interval, 0.70 to 1.53; interaction P<0.001).ConclusionsThese findings suggest lower mitochondrial DNA copy number is associated with higher risk of CKD progression, independent of established risk factors among patients with CKD.