title: Understanding sources of dietary phosphorus in the treatment of patients with chronic kidney disease.
abstract: In individuals with chronic kidney disease, high dietary phosphorus (P) burden may worsen hyperparathyroidism and renal osteodystrophy, promote vascular calcification and cardiovascular events, and increase mortality. In addition to the absolute amount of dietary P, its type (organic versus inorganic), source (animal versus plant derived), and ratio to dietary protein may be important. Organic P in such plant foods as seeds and legumes is less bioavailable because of limited gastrointestinal absorption of phytate-based P. Inorganic P is more readily absorbed by intestine, and its presence in processed, preserved, or enhanced foods or soft drinks that contain additives may be underreported and not distinguished from the less readily absorbed organic P in nutrient databases. Hence, P burden from food additives is disproportionately high relative to its dietary content as compared with natural sources that are derived from organic (animal and vegetable) food proteins. Observational and metabolic studies indicate nutritional and longevity benefits of higher protein intake in dialysis patients. This presents challenges to providing appropriate nutrition because protein and P intakes are closely correlated. During dietary counseling of patients with chronic kidney disease, the absolute dietary P content as well as the P-to-protein ratio in foods should be addressed. Foods with the least amount of inorganic P, low P-to-protein ratios, and adequate protein content that are consistent with acceptable palatability and enjoyment to the individual patient should be recommended along with appropriate prescription of P binders. Provision of in-center and monitored meals during hemodialysis treatment sessions in the dialysis clinic may facilitate the achievement of these goals.
authors.affiliation: Harold Simmons Center for Chronic Disease Research and Epidemiology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, 1124 West Carson Street, C1-Annex, Torrance, CA 90509-2910, USA. kamkal@ucla.edu
authors.forename: Kamyar
authors.initials: K
authors.lastname: Kalantar-Zadeh
authors.forename: Lisa
authors.initials: L
authors.lastname: Gutekunst
authors.forename: Rajnish
authors.initials: R
authors.lastname: Mehrotra
authors.forename: Csaba P
authors.initials: CP
authors.lastname: Kovesdy
authors.forename: Rachelle
authors.initials: R
authors.lastname: Bross
authors.forename: Christian S
authors.initials: CS
authors.lastname: Shinaberger
authors.forename: Nazanin
authors.initials: N
authors.lastname: Noori
authors.forename: Raimund
authors.initials: R
authors.lastname: Hirschberg
authors.forename: Debbie
authors.initials: D
authors.lastname: Benner
authors.forename: Allen R
authors.initials: AR
authors.lastname: Nissenson
authors.forename: Joel D
authors.initials: JD
authors.lastname: Kopple
mesh_terms: D002614:Chelating Agents / Q000627:therapeutic use*; D002908:Chronic Disease; D003131:Combined Modality Therapy; D003376:Counseling; D004044:Dietary Proteins / Q000009:adverse effects / Q000378:metabolism; D005503:Food Additives / Q000009:adverse effects; D006801:Humans; D054559:Hyperphosphatemia / Q000209:etiology / Q000378:metabolism / Q000628:therapy*; D007674:Kidney Diseases / Q000150:complications / Q000378:metabolism / Q000628:therapy*; D009752:Nutritional Status; D016226:Phosphorus, Dietary / Q000008:administration & dosage / Q000009:adverse effects* / Q000378:metabolism; D006435:Renal Dialysis; D018570:Risk Assessment; D012307:Risk Factors; D016896:Treatment Outcome
chemical_list: D002614:Chelating Agents; D004044:Dietary Proteins; D005503:Food Additives; D016226:Phosphorus, Dietary