Dietary Phosphorus Intake and Mortality in Moderate CKD
Background. Dietary phosphorus intake is usually restricted in dialysis patients but the associations of dietary phosphorus intake with mortality in moderate chronic kidney disease (CKD) are unknown. Therefore, we examined these associations in National Health and Nutrition Examination Survey III.
Methods. Dietary phosphorus intake was estimated from 24-h dietary recalls administered by trained personnel. CKD was defined as estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m. Time to mortality was examined by Cox regression models taking into account the complex survey design.
Results. 1105 adults with CKD were studied. Phosphorus intake was 1033 ± 482 mg/day (mean ± SD), eGFR was 49.3 ± 9.5 mL/min/1.73 m and serum phosphorus was 3.5 ± 0.5 mg/dL. Compared to those in the lowest tertile of phosphorus intake (mean 532 ± 161 mg/day), those in the highest third (1478 ± 378 mg/day) had similar serum phosphorus levels (3.6 ± 0.5 versus 3.5 ± 0.6 mg/dL, P = 0.113) and modestly higher eGFR (50.0 ± 8.1 versus 47.5 ± 12.0 mL/min/1.73 m, P = 0.014). After adjustment for demographics, comorbidity, eGFR, physical activity, energy intake and nutritional variables, phosphorus intake was not associated with mortality [hazard ratio (HR) 0.98 per 100 mg/dL increase, 0.93–1.03].
Conclusions. High dietary phosphorus intake is not associated with increased mortality in moderate CKD, presumably because serum phosphorus levels are maintained in the normal range at this level of GFR. Interventional trials are needed to define optimal phosphorus intake in moderate CKD.
Phosphorus is a critically important mineral, playing a vital role in energy metabolism, cellular signaling, nucleic acid metabolism, platelet aggregation and bone mineralization. An average adult contains <1 kg of phosphorus in the body. About 85% of that is present in bones and teeth in the form of apatitie, and the most of the remainder is inside cells in soft tissues. Only ~0.1% of body phosphate circulates in the blood. A well-fed healthy adult consumes ~1.5 g of phosphorus/day and about two-thirds of that is excreted in the urine and the rest in the feces.
The serum phosphorus level is influenced by dietary intake, gastrointestinal absorption, distribution across the body compartments including uptake into bone and excretion. Regulation of serum phosphorus levels involves vitamin D, parathyroid hormone and fibroblast-derived growth factor-23 (FGF-23). Increased serum phosphorus concentrations are associated with vascular calcification and mortality in dialysis patients [3–6]. Reduction in dietary phosphorus intake by avoiding foods high in phosphorus such as colas or dairy products is considered critical in controlling serum phosphorus in dialysis population. Thus, the national guidelines recommend reduction in dietary phosphorus intake in dialysis patients.
As glomerular filtration rate (GFR) declines to about 40–45 mL/min/1.73 m, urinary excretion of phosphorus decreases and serum levels of phosphorus begin to increase. More recently, in non-dialysis-dependent chronic kidney disease (CKD) patients, higher serum phosphorus levels have been shown to be associated with increased mortality. These data raise the possibility that higher dietary phosphorus intake might be associated with increased mortality in non-dialysis CKD. To our knowledge, there are no prior studies on the associations of dietary phosphorus with mortality in moderate CKD. Therefore, we examined these associations in the moderate CKD population in the National Health and Nutrition Examination Survey (NHANES) III data.
Abstract and Introduction
Abstract
Background. Dietary phosphorus intake is usually restricted in dialysis patients but the associations of dietary phosphorus intake with mortality in moderate chronic kidney disease (CKD) are unknown. Therefore, we examined these associations in National Health and Nutrition Examination Survey III.
Methods. Dietary phosphorus intake was estimated from 24-h dietary recalls administered by trained personnel. CKD was defined as estimated glomerular filtration rate (eGFR) <60 mL/min/1.73 m. Time to mortality was examined by Cox regression models taking into account the complex survey design.
Results. 1105 adults with CKD were studied. Phosphorus intake was 1033 ± 482 mg/day (mean ± SD), eGFR was 49.3 ± 9.5 mL/min/1.73 m and serum phosphorus was 3.5 ± 0.5 mg/dL. Compared to those in the lowest tertile of phosphorus intake (mean 532 ± 161 mg/day), those in the highest third (1478 ± 378 mg/day) had similar serum phosphorus levels (3.6 ± 0.5 versus 3.5 ± 0.6 mg/dL, P = 0.113) and modestly higher eGFR (50.0 ± 8.1 versus 47.5 ± 12.0 mL/min/1.73 m, P = 0.014). After adjustment for demographics, comorbidity, eGFR, physical activity, energy intake and nutritional variables, phosphorus intake was not associated with mortality [hazard ratio (HR) 0.98 per 100 mg/dL increase, 0.93–1.03].
Conclusions. High dietary phosphorus intake is not associated with increased mortality in moderate CKD, presumably because serum phosphorus levels are maintained in the normal range at this level of GFR. Interventional trials are needed to define optimal phosphorus intake in moderate CKD.
Introduction
Phosphorus is a critically important mineral, playing a vital role in energy metabolism, cellular signaling, nucleic acid metabolism, platelet aggregation and bone mineralization. An average adult contains <1 kg of phosphorus in the body. About 85% of that is present in bones and teeth in the form of apatitie, and the most of the remainder is inside cells in soft tissues. Only ~0.1% of body phosphate circulates in the blood. A well-fed healthy adult consumes ~1.5 g of phosphorus/day and about two-thirds of that is excreted in the urine and the rest in the feces.
The serum phosphorus level is influenced by dietary intake, gastrointestinal absorption, distribution across the body compartments including uptake into bone and excretion. Regulation of serum phosphorus levels involves vitamin D, parathyroid hormone and fibroblast-derived growth factor-23 (FGF-23). Increased serum phosphorus concentrations are associated with vascular calcification and mortality in dialysis patients [3–6]. Reduction in dietary phosphorus intake by avoiding foods high in phosphorus such as colas or dairy products is considered critical in controlling serum phosphorus in dialysis population. Thus, the national guidelines recommend reduction in dietary phosphorus intake in dialysis patients.
As glomerular filtration rate (GFR) declines to about 40–45 mL/min/1.73 m, urinary excretion of phosphorus decreases and serum levels of phosphorus begin to increase. More recently, in non-dialysis-dependent chronic kidney disease (CKD) patients, higher serum phosphorus levels have been shown to be associated with increased mortality. These data raise the possibility that higher dietary phosphorus intake might be associated with increased mortality in non-dialysis CKD. To our knowledge, there are no prior studies on the associations of dietary phosphorus with mortality in moderate CKD. Therefore, we examined these associations in the moderate CKD population in the National Health and Nutrition Examination Survey (NHANES) III data.
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