Plant Protein Intake is Associated With Fibroblast Growth Factor 23 and Serum Bicarbonate Levels in Patients With Chronic Kidney Disease: The Chronic Renal Insufficiency Cohort Study
ABSTRACT Protein from plant, as opposed to animal, sources may be preferred in chronic kidney disease (CKD) because of the lower bioavailability of phosphate and lower nonvolatile acid load.
Observational cross-sectional study.
A total of 2,938 participants with CKD and information on their dietary intake at the baseline visit in the Chronic Renal Insufficiency Cohort Study.
Percentage of total protein intake from plant sources (percent plant protein) was determined by scoring individual food items using the National Cancer Institute Diet History Questionnaire (DHQ).
Metabolic parameters, including serum phosphate, bicarbonate (HCO₃), potassium, and albumin, plasma fibroblast growth factor 23 (FGF-23), and parathyroid hormone (PTH), and hemoglobin levels.
We modeled the association between percent plant protein and metabolic parameters using linear regression. Models were adjusted for age, sex, race, diabetes status, body mass index, estimated glomerular filtration rate, income, smoking status, total energy intake, total protein intake, 24-hour urinary sodium concentration, use of angiotensin-converting enzyme inhibitors/angiotensin receptor blockers, and use of diuretics.
Higher percent plant protein was associated with lower FGF-23 (P = .05) and higher HCO₃ (P = .01) levels, but not with serum phosphate or parathyroid hormone concentrations (P = .9 and P = .5, respectively). Higher percent plant protein was not associated with higher serum potassium (P = .2), lower serum albumin (P = .2), or lower hemoglobin (P = .3) levels. The associations of percent plant protein with FGF-23 and HCO₃ levels did not differ by diabetes status, sex, race, CKD stage (2/3 vs. 4/5), or total protein intake (≤0.8 g/kg/day vs. >0.8 g/kg/day; P-interaction >.10 for each).
This is a cross-sectional study; determination of percent plant protein using the Diet History Questionnaire has not been validated.
Consumption of a higher percentage of protein from plant sources may lower FGF-23 and raise HCO₃ levels in patients with CKD.
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- "Also, 24-h urinary phosphate excretion was 29% lower on the quasi-vegan dietdbearing out its lower phosphate bioavailability. Moreover, in a recent cross-sectional study focusing on patients with CKD, the proportion of dietary protein derived from plant sources correlated inversely with serum FGF23 . Increasing the proportion of plant products in a diet appears to be a practical and health-compatible way to moderate dietary phosphate absorption. "
ABSTRACT: Increased fasting serum phosphate within the normal physiological range has been linked to increased cardiovascular risk in prospective epidemiology; increased production of fibroblast growth factor 23 (FGF23), and direct vascular effects of phosphate, may mediate this risk. Although dietary phosphate intake does not clearly influence fasting serum phosphate in those with normal renal function, increased phosphate intake can provoke an increase in FGF23, and in diurnal phosphate levels, and hence may adversely influence vascular health. Dietary phosphate absorption can be moderated by emphasizing plant-based dietary choices (which provide phosphate in less-bioavailable forms), avoidance of processed foods containing inorganic phosphate food additives, and by ingestion of phosphate-binder drugs, magnesium supplements, or niacin, which precipitate phosphate or suppress its gastrointestinal absorption. The propensity of dietary phosphate to promote vascular calcification may be opposed by optimal intakes of magnesium, vitamin K, and vitamin D; the latter should also counter the tendency of phosphate to elevate parathyroid hormone.Nutrition 01/2013; 30(7-8). DOI:10.1016/j.nut.2013.12.010 · 3.05 Impact Factor
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ABSTRACT: High serum phosphorus is linked to poor health outcome and mortality in chronic kidney disease (CKD) patients before or after the initiation of dialysis. Dietary intake of phosphorus, a major determinant of serum phosphorus, seems to be systematically underestimated using the available software tools and generalized nutrient content databases. Several sources of dietary phosphorus including the addition of phosphorus ingredients in food processing, and phosphorus content of vitamin and mineral supplements and commonly used over-the-counter or prescription medications are not fully accounted for by the nutrient content databases and software programs in current clinical use or used in large population studies. In this review, we explore the many unknown sources of phosphorus in the food supply to identify all possible contributors to total phosphorus intake of Americans that have escaped inclusion in past intake estimates. Our goal is to help delineate areas for future interventions that will enable tighter control of dietary phosphorus intake, a critical factor to maintaining health and quality of life in CKD and dialysis patients.Seminars in Dialysis 12/2012; 26(1). DOI:10.1111/sdi.12042 · 2.07 Impact Factor
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ABSTRACT: Nonvolatile acid is produced from the metabolism of organic sulfur in dietary protein and the production of organic anions during the combustion of neutral foods. Organic anion salts that are found primarily in plant foods are directly absorbed in the gastrointestinal tract and yield bicarbonate. The difference between endogenously produced nonvolatile acid and absorbed alkali precursors yields the dietary acid load, technically known as the net endogenous acid production, and must be excreted by the kidney to maintain acid-base balance. Although typically 1 mEq/kg/day, dietary acid load is lower with greater intake of fruits and vegetables. In the setting of CKD, a high dietary acid load invokes adaptive mechanisms to increase acid excretion despite reduced nephron number, such as increased per nephron ammoniagenesis and augmented distal acid excretion mediated by the renin-angiotensin system and endothelin-1. These adaptations may promote kidney injury. Additionally, high dietary acid loads produce low-grade, subclinical acidosis that may result in bone and muscle loss. Early studies suggest that lowering the dietary acid load can improve subclinical acidosis, preserve bone and muscle, and slow the decline of glomerular filtration rate in animal models and humans. Studies focusing on hard clinical outcomes are needed.Advances in chronic kidney disease 03/2013; 20(2):141-9. DOI:10.1053/j.ackd.2012.11.001 · 1.94 Impact Factor