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对于阶段1-3慢性肾脏病的饮食危险因素的管理

时间:2016-04-20 13:52:08来源: 作者:www.liuxuelw.com 点击:0
身体健康的人理所当然地认为食品其烹饪,而不是它的生化值。
Figure 1. GFR Decline in Patients of Usual and Low Protein Group During 36 Months (n=585). Estimated mean (±SEM) GFR declines from baseline (B) to select follow-up times (F) are shown.10(Journal of the American Society of Nephrology J Am Soc Nephrol 10: 2426–2439, 1999)
Protein intake in the low protein diets in the MDRD Study is approximately 0.6 g/kg per day. This level of protein intake is below the average protein intake in the United States of 90-100g/d11,12, but is similar to the Recommended Dietary Allowances (RDA) of the Food and Nutrition Board of 0.8g/kg per day13. Protein intake of 0.6 g/kg per day, together with adequate energy intake, appears sufficient to maintain nitrogen balance in chronic renal disease patients14,15. Walser studies also document the safety of several years’ duration of dietary protein intake restriction16,17.
Within the nutritional schedule, dietary phosphorus also plays a special role in the conservative management of chronic renal disease patients18.There is a study conducted by Barsotti G etc. indicate this. The progression rate of renal failure has been evaluated in two homogenous groups of chronic renal patients with early insufficiency. In two groups the diet given the same energy (approximately 35 Kcal/Kg/day) and the protein intake equally restricted (approximately 0.6g/Kg/day). The phosphorus intake of Group 1 was lower (6.5mg/Kg/day) than in Group 2 (12mg/Kg/day). The rate of decline of creatinine clearance in both groups decreased when patients changed to the protein and phosphorus controlled diets (they are on free mixed diet before), but in Group 1 (lower phosphorus intake) the decrease was more remarkable than in Group 2. Group 1 patients had normal mean levels of serum phosphate and of intact parathyroid hormone (IPTH) while group 2 had elecated mean levels of serum IPTH19. 
In the year 2002, the remnant kidney model in the rat has marked the critical role of dietary phosphorus intake for the protection of progressive renal damage20.In this study, by treating normal cow’s milk with boehmite, only phosphate ions could be reduced in food without affecting calories and the amount of calcium and protein.Low phosphate milk contains about 470ppm while normal milk contains about 900ppm. Other ingredients were almost the same. Twenty-six rats weighing 344-428g were divided into six groups. Groups1-3 were controls(n=3,n=4,n=4). Groups4-6(n=5 for each) consisted of rats with renal failure. Groups 1 and 4 rats were fed a regular diet; groups 2 and 5 were fed normal milk alone; groups 3 and 6 were low phosphate milk alone. 2ml bold samples were collected weekly from the hearts of rats, then measured the serum concentration of inorganic phosphorus, calcium, creatinine and blood urine nitrogen.
Figure 2. Changes in body weights of the rats. Values are expressed as mean±SD. p<0.05, compared with other groups except group4. ∆Group1,□Group2, ○Group3, ▲Group4, ■Group5, ●Group6.20 (T. Koizumi et al. / Biochemical and Biophysical Research Communications 295 (2002) 917–921)
Figure 3. Serumlevels of creatinine (A) and blood urine nitrogen (B). Valuesare expressed as mean±SD. P < 0:05, P < 0:01, compared with group 1 and *P < 0:05, **P < 0:01,compared with group 6. ∆Group1, □Group2, ○Group3, ▲Group4, ■Group5, ●Group6.20 (T. Koizumi et al. / Biochemical and Biophysical Research Communications 295 (2002) 917–921)
The difference between normal milk diet rats and low phosphorus milk diet rats in phosphorus content suggests that restriction of dietary phosphate delays the progression of renal failure20.Phosphorus restriction was more effective for delaying chronic renal failure progression than was protein restriction20. The implementation of a low phosphorus dietary regimen is to slow the decrease of residual kidney function and to prevent or improve calcium-phosphate metabolism abnormalities18. Restrict of dietary phosphorus protected the residual nephron by preventing damage caused by adaptive hyperfiltration which linked to renal mass reduction. That would induce precipitation and deposition of calcium phosphate crystals in the tubular lumen, peritubular space, capillaries and interstitum20. The inflammatory reaction will finally results in interstitial fibrosis and tubular atrophy21. There are also many other studies have suggested that phosphate accelerates the progression of renal failure22,23,24.
In patients with chronic kidney disease, near to 70% of patients in the early stages of the diseasehave at least mild coronary artery calcification, this risky population might benefit from vitamin K- a local regulator of vascular calcification25. At the end of the 7-week study of adenine-induced chronic kidney disease, animals on the adenine diet had lost 10 ± 5%, 15 ± 3% of their initial body weight in the high dietary vitamin K group (n=8), low dietary vitamin K group (n=16), respectively4. The high vitamin K group rats (n=6) lost significantly less weight than the low vitamin K group (n=12). The control groups rats (normal dietary intake) gained 12 ± 2% (high dietary vitamin K) and 9 ± 5% (low dietary vitamin K). In conclusion, this study supports the hypothesis that vitamin K status has a critical role in the management of chronic kidney disease.