Background High phosphorus (P) exposure may have negative effects on kidney function. Nutrient databases provide total P, but bioavailability varies by source. Objective We aimed to assess natural, added and bioavailable P intake, and to relate these to estimated glomerular filtration rate (eGFR) ml/min/1.73m2 in the Jackson Heart Study (JHS). Design 3962 African American participants of the Jackson Heart Study, aged 21-84 y, with urine albumin/creatinine ratio < 30 mg/g, and eGFR ≥ 60 ml/min/1.73 m2, and without self-reported kidney disease, were included. Diet was assessed by food frequency questionnaire. We assigned P in foods as naturally occurring vs. added, and weighted intake by P bioavailability, based on published literature. Relationships between P variables and eGFR were assessed using multivariable regression. Results Mean ± SE intakes were 1178 ± 6.7 and 1168 ± 5.0 mg for total P; 296 ± 2.8 and 291 ± 2.1 mg for bioavailable added P; and 444 ± 2.9 and 443 ± 2.2 mg, for bioavailable natural P, in participants with eGFR 60-89 or ≥ 90 ml/min/1.73m2, 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 intake, including total (β ± SE= -0.32 ± 0.15, P = 0.03), added (-0.73 ± 0.27, P = 0.01), bioavailable total (-0.62 ± 0.23, P = 0.01) and bioavailable added (-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.