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.
"Although there is concern that high protein intake and phosphorus intake may promote renal damage by chronically increasing glomerular pressure and hyperfiltration
[33-35], we did not find a significant association between them. This is not surprising in that Remer et al.
[1,2], Goraya et al.
[8,32], and Scialla et al.
 show that the more important determinant of the effect of dietary protein on nephropathy progression is the quality of the ingested protein (i.e., whether it induces acid-production [like most animal protein] or base production [like most fruit and vegetable protein]) when ingested rather than the quantity of protein ingested. It is important to note that our results suggested a higher risk of albuminuria in adults with greater DAL than that suggested by the amount of either protein or phosphorus intake alone. "
[Show abstract][Hide abstract] ABSTRACT: Background
Diet can markedly affect acid-base status and it significantly influences chronic kidney disease (CKD) and its progression. The relationship of dietary acid load (DAL) and CKD has not been assessed on a population level. We examined the association of estimated net acid excretion (NAEes) with CKD; and socio-demographic and clinical correlates of NAEes.
Among 12,293 U.S. adult participants aged >20 years in the National Health and Nutrition Examination Survey 1999–2004, we assessed dietary acid by estimating NAEes from nutrient intake and body surface area; kidney damage by albuminuria; and kidney dysfunction by eGFR < 60 ml/min/1.73m2 using the MDRD equation. We tested the association of NAEes with participant characteristics using median regression; while for albuminuria, eGFR, and stages of CKD we used logistic regression.
Median regression results (β per quintile) indicated that adults aged 40–60 years (β [95% CI] = 3.1 [0.3–5.8]), poverty (β [95% CI] = 7.1 [4.01–10.22]), black race (β [95% CI] = 13.8 [10.8–16.8]), and male sex (β [95% CI] = 3.0 [0.7- 5.2]) were significantly associated with an increasing level of NAEes. Higher levels of NAEes compared with lower levels were associated with greater odds of albuminuria (OR [95% CI] = 1.57 [1.20–2.05]). We observed a trend toward greater NAEes being associated with higher risk of low eGFR, which persisted after adjustment for confounders.
Higher NAEes is associated with albuminuria and low eGFR, and socio-demographic risk factors for CKD are associated with higher levels of NAEes. DAL may be an important target for future interventions in populations at high risk for CKD.
"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. "
[Show abstract][Hide abstract] 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.
[Show abstract][Hide abstract] 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 · 1.75 Impact Factor
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