Association of Acute Kidney Injury and Cardiovascular Disease Following Percutaneous Coronary Intervention: Assessment of Interactions by Race, Diabetes, and Kidney Function.

RATIONALE & OBJECTIVE: Black patients and those with diabetes or reduced kidney function experience a disproportionate burden of acute kidney injury (AKI) and cardiovascular events. However, whether these factors modify the association between AKI and cardiovascular events after percutaneous coronary intervention (PCI) is unknown and was the focus of this study. STUDY DESIGN: Observational cohort. SETTING & PARTICIPANTS: Patients who underwent PCI at Duke between January 1, 2003, and December 31, 2013, with data available in the Duke Databank for Cardiovascular Disease. EXPOSURE: AKI, defined as ≥1.5-fold relative elevation in serum creatinine within 7 days from a reference value ascertained 30 days before PCI, or a 0.3 mg/dL increase from the reference value within 48 hours. OUTCOME: A composite of all-cause death, myocardial infarction, stroke, or revascularization during the first year after PCI. ANALYTICAL APPROACH: Cox regression models adjusted for potential confounders and with interaction terms between AKI and race, diabetes, or baseline estimated glomerular filtration rate (eGFR). RESULTS: Among 9,422 patients, 9% (n = 865) developed AKI, and the primary composite outcome occurred in 21% (n = 2,017). AKI was associated with a nearly 2-fold higher risk of the primary outcome (adjusted HR, 1.94 [95% CI, 1.71-2.20]). The association between AKI and cardiovascular risk did not significantly differ by race (P interaction, 0.4), diabetes, (P interaction, 0.06), or eGFR (P interaction, 0.2). However, Black race and severely reduced eGFR, but not diabetes, each had a cumulative impact with AKI on risk for the primary outcome. Compared with White patients with no AKI as the reference, the risk for the outcome was highest in Black patients with AKI (HR, 2.27 [95% CI, 1.83-2.82]), followed by White patients with AKI (HR, 1.87 [95% CI, 1.58-2.21]), and was least in patients of other races with AKI (HR, 1.48 [95% CI, 0.88-2.48]). LIMITATIONS: Residual confounding, including the impact of clinical care following PCI on cardiovascular outcomes of AKI. CONCLUSIONS: Neither race, diabetes, nor reduced eGFR potentiated the association of AKI with cardiovascular risk, but Black patients with AKI had a qualitatively greater risk than White patients with AKI or patients of other races with AKI. PLAIN-LANGUAGE SUMMARY: This study examined differences by race, diabetes, or kidney function in the well-known association of AKI with increased risk for cardiovascular outcomes among patients undergoing percutaneous coronary intervention. The authors found that AKI was associated with a greater risk for cardiovascular outcomes, but this risk did not differ by patients' race, diabetes status, or level of kidney function before the procedure. That said, the risk for cardiovascular outcomes was numerically highest among Black patients compared with White patients or those of other races. These study findings suggest that future efforts to prevent AKI among patients undergoing the procedure could reduce racial disparities in risk for unfavorable cardiovascular outcomes afterward.

Trends in Mineral Metabolism Treatment Strategies in Patients Receiving Hemodialysis in the United States.

BACKGROUND AND OBJECTIVES: With multiple medications indicated for mineral metabolism, dialysis providers can apply various strategies to achieve target phosphate and parathyroid hormone (PTH) levels. We describe common prescribing patterns and practice variation in mineral metabolism treatment strategies over the last decade. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: In a cohort of adults initiating hemodialysis at Dialysis Clinic, Inc. facilities, we assessed prescriptions of vitamin D sterols, phosphate binders, and cinacalcet longitudinally. To identify the influence of secular trends in clinical practice, we stratified the cohort by dialysis initiation year (2006-2008, 2009-2011, and 2012-2015). To measure practice variation, we estimated the median odds ratio for prescribing different mineral metabolism treatment strategies at 12 months post-dialysis initiation across facilities using mixed effects multinomial logistic regression. Sensitivity analyses evaluated strategies used after detection of first elevated PTH. RESULTS: Among 23,549 incident patients on hemodialysis, there was a decline in vitamin D sterol-based strategies and a corresponding increase in strategies without PTH-modifying agents (i.e., phosphate binders alone or no mineral metabolism medications) and cinacalcet-containing treatment strategies between 2006 and 2015. The proportion with active vitamin D sterol-based strategies at dialysis initiation decreased across cohorts: 15% (2006-2008) to 5% (2012-2015). The proportion with active vitamin D sterol-based strategies after 18 months of dialysis decreased across cohorts: 52% (2006-2008) to 34% (2012-2015). The odds of using individual strategies compared with reference (active vitamin D sterol with phosphate binder) varied from 1.5- to two-fold across facilities in 2006-2008 and 2009-2011 cohorts, and increased to two- to three-fold in the 2012-2015 cohort. Findings were similar in sensitivity analyses starting from first elevated PTH measurement. CONCLUSIONS: Over time, mineral metabolism management involved less use of vitamin D sterol-based strategies, greater use of both more conservative and cinacalcet-containing strategies, and increased practice variation, suggesting growing equipoise.

Life Course Socioeconomic Status, Allostatic Load, and Kidney Health in Black Americans.

BACKGROUND AND OBJECTIVES: Low socioeconomic status confers unfavorable health, but the degree and mechanisms by which life course socioeconomic status affects kidney health is unclear. DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS: We examined the association between cumulative lifetime socioeconomic status and CKD in black Americans in the Jackson Heart Study. We used conditional process analysis to evaluate allostatic load as a potential mediator of this relation. Cumulative lifetime socioeconomic status was an age-standardized z-score, which has 1-SD units by definition, and derived from self-reported childhood socioeconomic status, education, and income at baseline. Allostatic load encompassed 11 baseline biomarkers subsuming neuroendocrine, metabolic, autonomic, and immune physiologic systems. CKD outcomes included prevalent CKD at baseline and eGFR decline and incident CKD over follow-up. RESULTS: Among 3421 participants at baseline (mean age 55 years [SD 13]; 63% female), cumulative lifetime socioeconomic status ranged from -3.3 to 2.3, and 673 (20%) had prevalent CKD. After multivariable adjustment, lower cumulative lifetime socioeconomic status was associated with greater prevalence of CKD both directly (odds ratio [OR], 1.18; 95% confidence interval [95% CI], 1.04 to 1.33 per 1 SD and OR, 1.45; 95% CI, 1.15 to 1.83 in lowest versus highest tertile) and via higher allostatic load (OR, 1.09; 95% CI, 1.06 to 1.12 per 1 SD and OR, 1.17; 95% CI, 1.11 to 1.24 in lowest versus highest tertile). After a median follow-up of 8 years (interquartile range, 7-8 years), mean annual eGFR decline was 1 ml/min per 1.73 m2 (SD 2), and 254 out of 2043 (12%) participants developed incident CKD. Lower cumulative lifetime socioeconomic status was only indirectly associated with greater CKD incidence (OR, 1.04; 95% CI, 1.01 to 1.07 per 1 SD and OR, 1.08; 95% CI, 1.02 to 1.14 in lowest versus highest tertile) and modestly faster annual eGFR decline, in milliliters per minute (OR, 0.01; 95% CI, 0.00 to 0.02 per 1 SD and OR, 0.02; 95% CI, 0.00 to 0.04 in lowest versus highest tertile), via higher baseline allostatic load. CONCLUSIONS: Lower cumulative lifetime socioeconomic status was substantially associated with CKD prevalence but modestly with CKD incidence and eGFR decline via baseline allostatic load.

Low socioeconomic status associates with higher serum phosphate irrespective of race.

Hyperphosphatemia, which associates with adverse outcomes in CKD, is more common among blacks than whites for unclear reasons. Low socioeconomic status may explain this association because poverty both disproportionately affects racial and ethnic minorities and promotes excess intake of relatively inexpensive processed and fast foods enriched with highly absorbable phosphorus additives. We performed a cross-sectional analysis of race, socioeconomic status, and serum phosphate among 2879 participants in the Chronic Renal Insufficiency Cohort Study. Participants with the lowest incomes or who were unemployed had higher serum phosphate concentrations than participants with the highest incomes or who were employed (P < 0.001). Although we also observed differences in serum phosphate levels by race, income modified this relationship: Blacks had 0.11 to 0.13 mg/dl higher serum phosphate than whites in the highest income groups but there was no difference by race in the lowest income group. In addition, compared with whites with the highest income, both blacks and whites with the lowest incomes had more than twice the likelihood of hyperphosphatemia in multivariable-adjusted analysis. In conclusion, low socioeconomic status associates with higher serum phosphate concentrations irrespective of race. Given the association between higher levels of serum phosphate and cardiovascular disease, further studies will need to determine whether excess serum phosphate may explain disparities in kidney disease outcomes among minority populations and the poor.