肾病患者饮食治疗(MDRD)限蛋白对肌酐及尿酸的影响
作者：Britt Newsome, Joachim H. Ix, Gerald J. Beck 来源：AJKD 日期：2013-02-19
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MDRD
Effect of Protein Restriction on Serum and Urine Phosphate in the Modification of Diet in Renal Disease (MDRD) Study
Increased serum phosphate levels are associated with chronic kidney disease (CKD), cardiovascular events, and mortality.1, 2, 3 Practice guidelines recommend dietary phosphorus restriction to treat elevated serum phosphate levels.4 However, there are few data establishing the efficacy of this intervention. We conducted a post hoc analysis of the MDRD Study5 to assess the effect of dietary protein restriction—the major source of dietary phosphorus—on serum and urine phosphate levels.
The MDRD Study randomly assigned patients to receive a usual-protein (UP) or low-protein (LP) diet in study A (n = 585; glomerular filtration rate [GFR], 25-55 mL/min/1.73 m2) or an LP or very LP (VLP) with ketoacids diet in study B (n = 255; GFR, 13-24 mL/min/1.73 m2) with 3 years' follow-up. For the UP, LP, and VLP diets, the prescribed phosphorus content was 16-20, 5-10, and 4-9 mg/kg/d, respectively (corresponding to 1,120-1,400, 350-700, and 280-630 mg/d for a 70-kg participant).
Differences between diet groups were tested using unpaired t test. Serum samples generally were collected in the morning after overnight fasting. Models included random-effects intercept and slope terms with a knot at 4 months and a diet-group-and-time interaction term. Least squares means (with 95% CI) for serum and urine phosphate levels over time were calculated for each diet group.
Mean age was 52 ± 12 (SD) years, GFR was 39 ± 9 mL/min/1.73 m2 in study A and 19 ± 3 mL/min/1.73 m2 in study B. The mean difference in urine phosphate levels (in mg) between months 0 and 4 was −55 (95% CI, −76 to −34) for study A UP, −244 (95% CI, −265 to −223) for study A LP, −151 (95% CI, −181 to −121) for study B LP, and −233 (95% CI, −264 to −202) for study B VLP diet (Fig 1). Decreases in urine phosphate levels were sustained in each diet group throughout the study. Mean serum phosphate level change (in mg/dL) from 0 to 4 months was 0.01 (95% CI, −0.05 to 0.06) for study A UP, −0.05 (95% CI, −0.10 to 0.01) for study A LP, −0.17 (95% CI, −0.29 to −0.04) for study B LP, and −0.25 (95% CI, −0.38 to −0.12) for study B VLP diet.
Our results show that dietary protein restriction is effective in reducing urinary phosphate levels and was associated with a very modest but sustained decrease in serum phosphate levels. It is known that fasting morning serum phosphate level represents the nadir of 24-hour serum phosphate and may not adequately discriminate meaningful differences between treatment groups.6 Although differences in serum phosphate levels between the randomly assigned groups were modest, those with mild CKD achieved stable serum phosphate levels over 3 years. There are few long-term data for whether these differences may translate into reductions in clinically important outcomes.
These findings are consistent with a recent randomized controlled trial in which high doses of phosphate binders decreased urinary phosphate excretion but had a modest effect on serum phosphate levels.7 In aggregate, these results raise questions about the effectiveness of dietary phosphate restriction or prescription of phosphate binders as monotherapy to reduce serum phosphate levels in patients with CKD. Achieving substantive reductions may require multiple interventions, including decreasing dietary phosphate intake, prescribing phosphate binders, and inhibiting active intestinal phosphate transport.8
The clinical benefits of reducing dietary phosphorus may be independent from any effect on serum phosphate level. The phosphate-regulating hormone FGF-23 has been reported to directly cause left ventricular hypertrophy. Yamamoto et al9 have shown that higher dietary phosphate is associated with higher left ventricular mass. Short-term studies have shown that dietary phosphate reduction effectively decreases FGF-23 levels.9, 10 Long-term trials with multiple interventions are required to understand the effect of reducing dietary phosphate and serum phosphate level on adverse clinical outcomes.
http://www.ajkd.org/article/S0272-6386(13)00034-6/fulltext
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