Abstract: SA-PO362
Plasma 25-Hydroxyvitamin D Levels and Renal Function Decline in African Americans
Session Information
- CKD: Risk Factors for Incidence and Progression - III
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Chronic Kidney Disease (Non-Dialysis)
- 301 CKD: Risk Factors for Incidence and Progression
Authors
- Lunyera, Joseph, Duke University School of Medicine, Durham, North Carolina, United States
- Davenport, Clemontina A., Duke University School of Medicine, Durham, North Carolina, United States
- Diamantidis, Clarissa Jonas, Duke University School of Medicine, Durham, North Carolina, United States
- Bhavsar, Nrupen Anjan, Duke University School of Medicine, Durham, North Carolina, United States
- Sims, Mario, University of Mississippi Medical Center, Jackson, Mississippi, United States
- Wolf, Myles S., Duke University School of Medicine, Durham, North Carolina, United States
- Pendergast, Jane F., Duke University School of Medicine, Durham, North Carolina, United States
- Boulware, L. Ebony, Duke University School of Medicine, Durham, North Carolina, United States
- Scialla, Julia J., Duke University School of Medicine, Durham, North Carolina, United States
Background
25-hydroxyvitamin D [25(OH)D] deficiency is highly prevalent among African Americans and may contribute to their disproportionate risk of adverse chronic kidney disease (CKD) outcomes. We examined the association between plasma 25(OH)D levels and adverse CKD outcomes in the Jackson Heart Study (JHS).
Methods
We adjusted plasma 25(OH)D3 levels measured at baseline for monthly variation in sunlight exposure by using the residuals from the regression of 25(OH)D3 on the month of blood draw plus the overall mean. We examined the associations between baseline adjusted 25(OH)D3 and (a) annual estimated glomerular filtration rate (eGFR) decline and (b) incident CKD during follow-up using generalized linear models adjusted for demographics, behavioral factors, and comorbidity. Incident CKD was defined as either eGFR <60 mL/min/1.73m2and a 25% decline in eGFR between baseline and follow-up, or albumin-to-creatinine ratio ≥30 mg/g at follow up among those without CKD at baseline.
Results
Among 5164 participants with non-missing 25(OH)D3 (97% of JHS cohort), the median [IQR] adjusted 25(OH)D3 was 12.0 [8.71-16.56] ng/mL, and mean ±SD eGFR was 94.11 ±21.98 mL/min/1.73m2 at baseline. Over a median of 8 years, the mean ±SD annual eGFR decline was 1.27 ±1.96 mL/min/1.73m2 per year, and 249 participants (12% of those whose CKD status could be determined) developed incident CKD. After adjusting for demographics, behavioral factors and comorbidity, each 10 ng/mL lower adjusted 25(OH)D3 was associated with 0.19 (95% CI 0.05-0.33) mL/min/1.73m2 per year faster eGFR decline. However, the association did not persist after additional adjustment for baseline eGFR (p=0.146). 25(OH)D3 was not associated with incident CKD (OR [95% CI] per 10 ng/mL lower 25(OH)D3 1.12 [0.85,1.47]).
Conclusion
Plasma 25(OH)D3 was not associated with risk of kidney function decline in African Americans after adjustment for baseline eGFR and other covariates. Despite low levels at baseline, our data do not support a role of supplementation in preventing or slowing CKD in African Americans
Funding
- NIDDK Support