Abstract
BACKGROUND: High phosphorus (P) exposure may have negative effects on kidney function. Nutrient databases provide total P, but bioavailability varies by source. OBJECTIVES: We aimed to assess natural, added, and bioavailable P intake, and to relate these to estimated glomerular filtration rate (eGFR) in the Jackson Heart Study (JHS). METHODS: A total of 3962 African-American participants of the JHS, aged 21-84 y, with urine albumin:creatinine ratio < 30 mg/g, and eGFR ≥ 60 mL · min-1 · 1.73 m-2, and without self-reported kidney disease, were included. Diet was assessed by FFQ. We assigned P in foods as naturally occurring or added, and weighted intake by P bioavailability, based on published literature. Relations between P variables and eGFR were assessed using multivariable regression. RESULTS: Mean ± SE intakes were 1178 ± 6.7 mg and 1168 ± 5.0 mg for total P, 296 ± 2.8 mg and 291 ± 2.1 mg for bioavailable added P, and 444 ± 2.9 mg and 443 ± 2.2 mg for bioavailable natural P, in participants with eGFR = 60-89 and ≥90 mL · min-1 · 1.73 m-2, respectively. Major sources of total P included fish, milk, beef, eggs, cheese, and poultry; and of added P, fish, beef, processed meat, soft drinks, and poultry. After adjustment for confounders, P intakes, including total (β ± SE: -0.32 ± 0.15; P = 0.03), added (β ± SE: -0.73 ± 0.27; P = 0.01), bioavailable total (β ± SE: -0.62 ± 0.23; P = 0.01), and bioavailable added (β ± SE: -0.77 ± 0.29; P = 0.01), were significantly associated with lower eGFR. However, neither total nor bioavailable P from natural sources were associated with eGFR. CONCLUSIONS: Added, but not natural, P was negatively associated with kidney function, raising concern about P additives in the food supply. Further studies are needed to improve estimation of dietary P exposure and to clarify the role of added P as a risk factor for kidney disease.