Skip to main content

Main menu

  • Home
  • Content
    • Published Ahead of Print
    • Current Issue
    • JASN Podcasts
    • Article Collections
    • Archives
    • ASN Meeting Abstracts
    • Saved Searches
  • Authors
    • Submit a Manuscript
    • Author Resources
  • Editorial Team
  • Editorial Fellowship
    • Editorial Fellowship Team
    • Editorial Fellowship Application Process
  • More
    • About JASN
    • Advertising
    • Alerts
    • Feedback
    • Impact Factor
    • Reprints
    • Subscriptions
  • ASN Kidney News
  • Other
    • CJASN
    • Kidney360
    • Kidney News Online
    • American Society of Nephrology

User menu

  • Subscribe
  • My alerts
  • Log in
  • My Cart

Search

  • Advanced search
American Society of Nephrology
  • Other
    • CJASN
    • Kidney360
    • Kidney News Online
    • American Society of Nephrology
  • Subscribe
  • My alerts
  • Log in
  • My Cart
Advertisement
American Society of Nephrology

Advanced Search

  • Home
  • Content
    • Published Ahead of Print
    • Current Issue
    • JASN Podcasts
    • Article Collections
    • Archives
    • ASN Meeting Abstracts
    • Saved Searches
  • Authors
    • Submit a Manuscript
    • Author Resources
  • Editorial Team
  • Editorial Fellowship
    • Editorial Fellowship Team
    • Editorial Fellowship Application Process
  • More
    • About JASN
    • Advertising
    • Alerts
    • Feedback
    • Impact Factor
    • Reprints
    • Subscriptions
  • ASN Kidney News
  • Follow JASN on Twitter
  • Visit ASN on Facebook
  • Follow JASN on RSS
  • Community Forum
Clinical Nephrology
You have accessRestricted Access

Adaptive Response to a Low-Protein Diet in Predialysis Chronic Renal Failure Patients

JACQUES BERNHARD, BERNARD BEAUFRÈRE, MAURICE LAVILLE and DENIS FOUQUE
JASN June 2001, 12 (6) 1249-1254;
JACQUES BERNHARD
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
BERNARD BEAUFRÈRE
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
MAURICE LAVILLE
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
DENIS FOUQUE
  • Find this author on Google Scholar
  • Find this author on PubMed
  • Search for this author on this site
  • Article
  • Figures & Data Supps
  • Info & Metrics
  • View PDF
Loading

Abstract

Abstract. A randomized, controlled study of 12 patients with mild chronic renal failure was designed to assess the metabolic effects of a low-protein diet supplemented (n = 6) or not (n = 6) with ketoanalogs of amino acids. The protein intake was prescribed so that both groups were isonitrogenous. The dietary survey each month included a 3-d food record and a 24-h urine collection for urea measurement. After a 4- to 6-wk equilibrium period (standard occidental diet, 1.11 g of protein and 32 kcal/kg per d), patients reduced their protein intake to reach 0.71 g of protein/kg per d during the third month. Energy intake was kept constant (31 kcal/kg per d) during the 3-mo period. Compliance to the diet was achieved after 2 mo of training. Leucine turnover measurement was performed before and at the end of the 3-mo low-protein period. There was no clinical change, whereas total body flux decreased by 8% (P < 0.05) and leucine oxidation by 18% (P < 0.05). No difference could be attributed to the ketoanalogs themselves. Thus, under sufficient energy intake, a low-protein diet is nutritionally and metabolically safe during chronic renal failure. The nitrogen-sparing effect of a low-protein diet is still present during mild chronic renal insufficiency.

Many studies have addressed the safety of a moderate restriction in protein intake on the nutritional status during chronic renal failure (CRF). Whereas it is well established that in healthy individuals, low-protein diets result in a reduction of whole-body protein turnover and amino acid oxidation (1,2), there have been some discrepancies about this adaptive response in CRF (3). In addition, the metabolic effects of the ketoanalogs of amino acids have been evaluated only in CRF patients during more restricted protein diets (4,5). To clarify these adaptations during a short period, we designed a randomized, controlled study and administered a moderately lowprotein diet supplemented or not with ketoanalogs of amino acids during 3 mo in 12 patients who presented with mild CRF.

Materials and Methods

Patients

Twelve patients with CRF (10 men and 2 women, aged 44.3 ± 4.6 [SEM] yr) were studied before and 3 mo after a reduction in their protein intake (Table 1). None of these patients was known to have any malignant or inflammatory illness. Three mo before inclusion, serum creatinine was measured to ensure that renal failure was not progressive (difference between serum creatinine at inclusion being <50 μmol/L). Patients did not experience any catabolic event or treatment during this study. All patients received a conservative treatment including calcium carbonate, vitamin-D supplement, sodium bicarbonate, and antihypertensive medication if needed. None received erythropoietin or vaccination against hepatitis B virus. No vascular shunt procedure was realized during the study.

View this table:
  • View inline
  • View popup
Table 1.

Patient characteristics before and after a 3-mo low-protein dieta

Dietary Assessment

Patients were selected from our regular dietary program, which has been run in our unit since 1974. A trained dietitian conducted two interviews with each patient before inclusion. Patients were interviewed at the early diagnosis of renal failure and before any former diet. They were asked not to modify their diet and were selected if their dietary protein intake was between 1 and 1.5 g/kg per d and their energy intake was >30 kcal/kg per d. Estimation of the baseline diet was performed with a 3-d dietary record and a 24-h urea collection. Patients who were willing to lose weight or who had insulin or noninsulin diabetes mellitus or progressive renal failure were not included. After 4 to 6 wk of their usual diet, the patients were admitted to the metabolic ward for 4 d for the baseline study. Patients were then randomized to receive a low-protein diet (0.6 g of protein/kg per d with at least half of the protein being of high biologic value), with or without ketoanalogs of amino acids. Energy intake was kept constant (31 kcal/kg per d) during the 3-mo period. The dietary survey each month included a 3-d food record and a 24-h urine collection for urea measurement.

Ketoanalogs of Amino Acids

After random allocation, six patients were asked to take a supplement of ketoacids (Cetolog; Clintec Corp., Velizy, France), 1 tablet/5 kg body wt per d. Compliance was assessed by pill count; the overall dose per patient was 0.167 ± 0.007 tablets/kg body wt per d for the 3-mo period, i.e., 84% of prescribed dose. Each 900-mg tablet contained 76 mg of ketoisoleucine, 97 mg of ketoleucine, 68 mg of ketovaline, 26 mg of hydroxymethionine, 118 mg of L-ornithine, 129 mg of L-lysine, 26 mg of L-histidine, 75 mg of L-threonine, 152 mg of L-tyrosine, and 3.4 mg of calcium. The daily dosage, i.e., 10 to 15 pills, was divided into two to three doses and taken during meals. No side effect from the ketoanalog supplement was reported.

Protocol Design

The leucine turnover procedure was carried out on the fourth day of the metabolic assessment in the Center d'Explorations Métaboliques. Patients fasted from 8:00 p.m. the day before the test until 12:00 a.m. the following morning. At 8:00 a.m., a 3.5-h intravenous infusion of L[1-13C] leucine (Tracer Technologies, Inc., Woburn, MA) was started. Blood and expired air samples were taken at -15 and -5 min to determine the basal 13C enrichment of plasma α-ketoisocaproate (KIC) and CO2. Two boluses of [1-13C] leucine (1 mg/kg) and 13C-sodium bicarbonate (5 mg) were followed by a constant intravenous [1-13C] leucine infusion of 0.08 μmol/kg per min over the next 3.5 h. Four times during the last hour of infusion, blood and gas were collected and CO2 production rate (VCO2) was measured by indirect calorimetry (Deltatrac MBM-100; Datex Instrumentation, Helsinki, Finland).

Analytical Methods and Calculation of Protein Turnover

13CO2 was determined by isotope ratio mass spectrometry, and plasma KIC enrichment was determined by gas chromatography mass spectrometry (6). Leucine fluxes were calculated with the use of the plasma KIC enrichment (7). Endogenous leucine rate of appearance, an index of protein breakdown, is then equal to total leucine flux minus the tracer infusion rate. Leucine oxidation was calculated from the appearance of 13CO2 in the expired gas divided by the plasma 13C KIC times 0.90 to correct for retention of CO2 in the bicarbonate pool. Nonoxidative leucine disposal, an index of whole-body protein synthesis, was calculated from the difference between the flux and oxidation of leucine. In the fasting state, total leucine flux can be assimilated to the leucine appearance from protein mobilization.

Amino Acid Determination

Plasma was drawn at 7:45 a.m. on the fourth day of the metabolic study, after an overnight fast. Plasma amino acids were determined with a Jeol automat (Jeol Corp., Tokyo, Japan) in the research laboratory at Edouard Herriot Hospital, with the use of a standard liquid chromatography.

Statistical Analyses

Values are reported as mean ± SD. Comparisons between baseline and the follow-up admission were analyzed with the use of the paired t test. Comparisons between subgroups at a given period were performed with the Wilcoxon test on Statview statistical software (Abacus Concept, Berkeley, CA). Differences were considered significant at P < 0.05.

Results

As shown in Table 1, patients were not malnourished. The degree of renal failure was mild, corresponding to a GFR of approximately 30 ml/min per 1.73 m2. Renal failure was not progressing rapidly, as evidenced by the fact that patients' serum creatinine did not increase by more than 50 μmol/L within the last 3 mo. None of them experienced nephrotic syndrome or massive proteinuria (Table 1). Patients did not present metabolic acidosis or advanced renal osteodystrophy.

Compliance to the diet was obtained after training with our specialized renal dietitian. Patients were asked not to reduce their energy intake; this was accomplished by increasing slightly the marmalade in breakfast and by increasing to satisfactory levels the daily oil intake mainly in salad dressing. As shown in Table 2 and based on dietary interviews, the energy intake of patients, although not excessive, was kept within acceptable values, e.g., >30 kcal/kg per d. Protein intake was assessed by two different methods. We determined protein nitrogen appearance (PNA) from urinary urea output (Table 2), according to Maroni's formula (8). We also monitored protein intake from the 3-d home dietary records obtained monthly (Table 2). The protein equivalent of the nitrogen content in the ketoanalogs was not included in the estimated dietary protein intake (DPI) and averaged 0.08 ± 0.004 g of protein/kg per d, partly explaining a greater PNA than the DPI (Table 2). Overall, patients gradually reduced their daily protein intake by approximately 40% (diet records), 44% (24-h urinary urea), and 50% (Maroni's estimation; Table 2). Patients did not present body weight or body mass index changes over 3 mo (Table 1).

View this table:
  • View inline
  • View popup
Table 2.

Monthly compliance with the low-protein dieta

Effect of Overall Reduction in Protein Intake on Leucine Turnover

Because there was no difference between the two groups, results are presented for all 12 patients (Table 3). The reduction in protein intake induced a decrease in leucine oxidation by approximately 18% (P < 0.05), associated with a parallel 8% reduction (P < 0.05) in leucine rate of appearance, an estimation of protein degradation. There was no change in the nonoxidative leucine disposal during the low-protein diet period (Table 3).

View this table:
  • View inline
  • View popup
Table 3.

Effects of reducing protein intake with or without KA supplementation on protein metabolism as assessed by whole-body leucine turnovera

Effects of Ketoanalogs on Leucine Turnover

The effect of ketoanalogs on leucine turnover was estimated from the comparison of the variation in leucine kinetics from baseline (Table 3). Although there was a trend for a reduction for all measurements and these variations seemed to be more pronounced in the nonketoanalog group, no statistical difference could be observed between group that received a ketoanalog supplement and group that did not.

Plasma Amino Acid Pattern

Plasma amino acids were obtained on the fourth day of the metabolic study, after an overnight fast. There were almost no change from baseline (Table 4), with the exception for arginine, which decreased in the nonsupplemented group from 177 ± 37 to 105 ± 33 μmol/L (P < 0.05). In the ketoanalog-supplemented group of patients, the only significant change was a 14% reduction in plasma tyrosine from baseline (P < 0.05; Table 4). When we compared the changes from baseline between groups to test the effects of ketoanalog supplement, there was no significant difference for any single amino acid, ratio, or total amino acids. Particularly, plasma branched-chain amino acids (leucine, isoleucine, and valine) did not change significantly between the start and the end of the study and between the two groups of patients.

View this table:
  • View inline
  • View popup
Table 4.

Absolute variation in fasting plasma amino acids before and after a 3-mo LPD supplemented with KA or nota

Discussion

The present study shows that compliance with a low-protein diet can be obtained by intensive dietitian interviews and that a moderately low-protein diet can be prescribed safely with an adequate energy intake. In addition, we provide further data that show clearly an adequate metabolic response when patients with mild CRF consume a moderately low-protein diet for an extended period.

Compliance with any diet is the key to success. Renal diets often are complicated by superimposed diseases, chronic medications, spontaneous anorexia, or inappropriate counseling. Furthermore, there is a regular spontaneous reduction in protein and energy intakes after renal function deterioration (9). In the present study, we assessed energy intake by food records and protein intake using a combined food record and urinary nitrogen measurement (8). Table 2 shows the decrease in daily protein intake as estimated by two independent means, i.e., food records and urinary urea nitrogen. The baseline protein intake was 1.13 g/kg per d, slightly lower than the mean protein intake in the French adult population (approximately 1.3 g/kg per d). After the protein restriction was initiated, both protein intake from records and urinary urea decreased to attain statistical significance from baseline at month 3 (Table 2). It is interesting to note that the difference between these two techniques in evaluating actual protein intake is approximately 0.20 to 0.30 g/kg per d during the first two diet interviews but drops to 0.15 g/kg per d after 3 mo of patient training and diet adjustment by the dietitian. These differences likely are explained by the fact that we did not recorded as “protein” the amount of nitrogen in the ketoanalog supplement (approximately 6 g of protein equivalent/d for 6 of the 12 patients), thus explaining a greater nitrogen output than recorded on the diet report (Table 2). In addition, a PNA higher than DPI could be explained by an underestimation of intakes by home diet records because this difference seemed to diminish over time after the number of dietitian interviews was increased (0.19 g of protein/kg per d at month 1, 0.29 at month 2, and 0.15 at month 3; Table 2), whereas patients did not change their ketoanalogs intake during the study. Although none of these differences was statistically significant, we believe that the quality of diet reports can be improved after repeated interviews between patient (and spouse if available) and the specialized renal dietitian. Other reasons for observing a PNA greater than the DPI include acute inflammatory or septic episodes, steroid treatments, or chronic acidosis. None of these conditions occurred during the study, and mean serum bicarbonate was 22.3 and 23.7 mmol/L at baseline and at the end of study, respectively (Table 1).

To avoid a well-described energy limitation associated with the reduction in protein intake (4,10,11), energy intake was monitoring carefully during diet interviews and kept constant during the study. There was no change in actual energy intake of patients during the 3-mo period (Table 2), and this level of energy intake can be considered adequate (12). Generally, energy intake and energy need are less reported than protein intake because it is more difficult to monitor energy needs than to collect urine for urea or nitrogen output measurement. Indeed, sophisticated research techniques, such as direct calorimetry performed in a metabolic chamber or double-labeled water, should be used to assess energy metabolism reliably. A study of 29 women reported that a 7-d diet record underestimated by approximately 20% the true energy needs as estimated by double-labeled water (13). If this were true for patients with CRF, then it may explain partly why such low energy intakes, i.e., 20 to 22 kcal/kg per d, are sometimes reported without concomitant severe malnutrition and/or impaired outcome (14). Another study comparing diet records and weighting food trays at the same time concluded that a diet record underestimated energy intake by <2% (15). In any event, the present energy intake of patients could be considered to be adequate, thus allowing a valid interpretation of the metabolic study (12).

Protein metabolism was assessed by the leucine turnover measurement. This technique has been used extensively in healthy humans. Adaptation to a reduction in protein intake is associated with a decrease in amino acid oxidation during fasting and postprandial states in healthy volunteers (16,17,18,19) and in patients with renal disease and/or renal failure (3,4,5,20,21,22). Table 3 indicates the values obtained before and after 3 mo on a low-protein diet. The fasting leucine rate of appearance (Table 3) and fasting leucine oxidation (Table 3 and Figure 1) decreased by 8% and 18%, respectively (P < 0.05) after reducing protein intake. These facts indicate that a proteinsparing mechanism occurred in response to the reduction of protein intake. The metabolic adaptation, hence, is present in patients with mild CRF, and the magnitude of the amino acid oxidation decrease we observed after 3 mo of protein reduction (- 18%, Table 3 and Figure 1) is suggestive of an important and sustained protein-sparing mechanism.

Figure 1.
  • Download figure
  • Open in new tab
  • Download powerpoint
Figure 1.

The individual leucine oxidation value before and after a 3-mo low-protein diet. The low-protein diet was supplemented with ketoanalogs of amino acids (○) or not ([UNK]); *, P < 0.05 from baseline for all patients (paired t test); no difference between groups at baseline or at the end of study.

Other studies have reported similar findings in CRF patients who were undergoing different types of diet intervention but mostly during shorter studies. Goodship et al. (3) studied six patients with moderate CRF during a short-term (1 wk) regular (1 g of protein/kg per d) or reduced protein intake (0.6 g of protein/kg per d) and energy intakes of 32.5 kcal/kg per d. Fasting leucine oxidation did not change significantly during the lower protein intake, whereas postprandial leucine oxidation decreased by approximately 25% (P < 0.05). Extending a comparable diet up to 3 mo in the present study induced a significant and sustained reduction in fasting leucine oxidation (Table 3). Altogether, these data show that patients with moderate CRF can adapt their protein metabolism during acute and chronic protein intake reductions by reducing amino acid oxidation during both postprandial and fasting states.

More profound protein restrictions reduce amino acid oxidation to a greater magnitude. Masud et al. (5) showed in six predialysis patients that a diet that provided 0.35 g of protein/kg per d supplemented with either ketoacids or essential amino acids for 25 d allowed for maintaining neutral nitrogen balances and body composition. These diets were associated with very low leucine oxidation values, which were not different whether patients were supplemented with ketoanalogs or essential amino acids (5). In a long-term follow-up of these patients (16 mo), the fasting leucine oxidation remained at a low level of 10.0 ± 2.2 μmol/kg per h (4). As compared with the present study (baseline, 16.8 ± 4.2; low-protein diet, 13.8 ± 2.4 μmol/kg per h; Table 3), these amino acid oxidation values seem to be even lower in response to a lower protein intake, thus suggesting a potential “functional reserve” for protein sparing in CRF patients.

The addition of ketoacid supplements to the low-protein diet did not modify the protein metabolism as assessed by leucine turnover measurement (Table 3). Although there was a trend to a greater decrease in turnover values in the nonsupplemented group, none of these changes was significant. It could be argued that the protein restriction that we studied here was not restricted enough to observe the nitrogen-sparing effect of ketoacid administration. Indeed, in other diet intervention studies in uremia, the protein intake was reduced to a greater extent and generally averaged 0.3 to 0.5 g of protein/kg per d (4,5,23).

Amino acids were measured before and after the protein intake reduction (Table 4). Overall, there was almost no change in plasma essential, nonessential, and total amino acids. Branched chain amino acids did not vary between periods and within groups, whether patients received ketoacids or not, as reported by Masud et al. (5). In the ketoanalog-supplemented group, plasma tyrosine decreased by 15% (P < 0.05; Table 4) although tyrosine was included in the ketoanalog supplement (153 mg/pill, corresponding to an intake of 1.2 to 2 g/d). In the low-protein group that was not supplemented with ketoanalogs, arginine decreased by 34% (P < 0.05). More important, the essential/nonessential amino acid ratio (EAA/NEAA) decreased by 23% from 0.47 ± 0.07 to 0.36 ± 0.04 (P < 0.05) as a result of an increase in nonessential amino acids. These values are in agreement with those published by Kopple et al. (11,14). The absence of a comparable decrease of EAA/NEAA in the ketoanalog-supplemented group may be compatible with a better nutritional response. However, the absence of significant essential amino acid decrease in both groups during the study also is an important fact to consider (Table 4).

Finally, another indirect index for an adequate protein metabolism response is that serum insulin-like growth factor-1, a sensitive marker of body protein status (24,25), did not decrease during the 3-mo diet in each group (all patients: baseline, 278 ± 20 μg/L; end, 257 ± 20 μg/L) (26), thus indicating a well-preserved body protein compartment.

In summary, this is the first report of a 3-mo moderate reduction in protein intake in mild CRF patients that shows an adequate metabolic and body composition response. This suggests that under an energy intake >31 kcal/kg per d, a protein intake of 0.7 g/kg per d is metabolically and nutritionally safe. According to the current evidence for prescribing a low-protein diet to patients with mild CRF (27,28,29), this study confirms that such a diet therapy is worth being proposed to patients. Whether patients eventually will accept it certainly may rely more on physicians' beliefs and enthusiasm.

Acknowledgments

This work was supported in part by a grant from the INSERM nutrition network.

We thank Patricia Raton, RD, for patient counseling and diet report analysis; Joelle Goudable, PharmD, for nitrogen measurements; and Georges Richard, PharmD, for amino acid determinations. We are particularly indebted to the nurses of the Renal Unit, Pavillon P, for excellent patient care and technical assistance.

  • © 2001 American Society of Nephrology

References

  1. ↵
    Garlick PJ, McNurlan MA, Ballmer PE: Influence of dietary protein intake on whole-body protein turnover in humans. Diabetes Care 14:1189 -1198, 1991
    OpenUrlAbstract/FREE Full Text
  2. ↵
    Price GM, Halliday D, Pacy PJ, Quevedo MR, Millward DJ: Nitrogen homeostasis in man: Influence of protein intake on the amplitude of diurnal cycling of body nitrogen. Clin Sci86 : 91-102,1994
    OpenUrlCrossRefPubMed
  3. ↵
    Goodship TH, Mitch WE, Hoerr RA, Wagner DA, Steinman TI, Young VR: Adaptation to low-protein diets in renal failure: Leucine turnover and nitrogen balance. J Am Soc Nephrol1 : 66-75,1990
    OpenUrlAbstract/FREE Full Text
  4. ↵
    Tom K, Young VR, Chapman T, Masud T, Akpele L, Maroni BJ: Long-term adaptive responses to dietary protein restriction in chronic renal failure. Am J Physiol 268:E668 -E677, 1995
    OpenUrlPubMed
  5. ↵
    Masud T, Young VR, Chapman T, Maroni BJ: Adaptive responses to very low protein diets: The first comparison of ketoacids to essential amino acids. Kidney Int 45:1182 -1192, 1994
    OpenUrlCrossRefPubMed
  6. ↵
    Schwenk WF, Berg PJ, Beaufrere B, Miles JM, Haymond MW: Use of t-butyldimethylsilylation in the gas chromatographic/mass spectrometric analysis of physiologic compounds found in plasma using electron-impact ionization. Anal Biochem 141:101 -109, 1984
    OpenUrlCrossRefPubMed
  7. ↵
    Schwenk WF, Beaufrere B, Haymond MW: Use of reciprocal pool specific activities to model leucine metabolism in humans. Am J Physiol 249:E646 -E650, 1985
    OpenUrlPubMed
  8. ↵
    Maroni BJ, Steinman TI, Mitch WE: A method for estimating nitrogen intake of patients with chronic renal failure. Kidney Int 27: 58-65,1985
    OpenUrlCrossRefPubMed
  9. ↵
    Ikizler TA, Greene JH, Wingard RL, Parker RA, Hakim RM: Spontaneous dietary protein intake during progression of chronic renal failure. J Am Soc Nephrol 6:1386 -1391, 1995
    OpenUrlAbstract/FREE Full Text
  10. ↵
    Fouque D, Joly MO, Laville M, Beaufrere B, Goudable J, Pozet N, Chatelain P, Zech P: Increase of circulating insulin-like growth factor-I in chronic renal failure is reduced by low-protein diet. Miner Electrolyte Metab 18:276 -279, 1992
    OpenUrlPubMed
  11. ↵
    Kopple JD, Berg R, Houser H, Steinman TI, Teschan P: Nutritional status of patients with different levels of chronic renal insufficiency. Modification of Diet in Renal Disease (MDRD) Study Group. Kidney Int Suppl 27:S184 -S194, 1989
    OpenUrlPubMed
  12. ↵
    Kopple JD, Monteon FJ, Shaib JK: Effect of energy intake on nitrogen metabolism in nondialyzed patients with chronic renal failure. Kidney Int 29:734 -742, 1986
    OpenUrlPubMed
  13. ↵
    Martin LJ, Su W, Jones PJ, Lockwood GA, Tritchler DL, Boyd NF: Comparison of energy intakes determined by food records and doubly labeled water in women participating in a dietary-intervention trial. Am J Clin Nutr 63:483 -490, 1996
    OpenUrlAbstract/FREE Full Text
  14. ↵
    Kopple JD, Levey AS, Greene T, Chumlea WC, Gassman JJ, Hollinger DL, Maroni BJ, Merrill D, Scherch LK, Schulman G, Wang SR, Zimmer GS: Effect of dietary protein restriction on nutritional status in the Modification of Diet in Renal Disease Study. Kidney Int52 : 778-791,1997
    OpenUrlPubMed
  15. ↵
    Karvetti RL, Knuts LR: Validity of the estimated food diary: Comparison of 2-day recorded and observed food and nutrient intakes. J Am Diet Assoc 92:580 -584, 1992
    OpenUrlPubMed
  16. ↵
    Young VR: 1987 McCollum award lecture. Kinetics of human amino acid metabolism: Nutritional implications and some lessons. Am J Clin Nutr 46: 709-725,1987
    OpenUrlAbstract/FREE Full Text
  17. ↵
    Motil KJ, Matthews DE, Bier DM, Burke JF, Munro HN, Young VR: Whole-body leucine and lysine metabolism: Response to dietary protein intake in young men. Am J Physiol 240:E712 -E721, 1981
    OpenUrlPubMed
  18. ↵
    Quevedo MR, Price GM, Halliday D, Pacy PJ, Millward DJ: Nitrogen homoeostasis in man: Diurnal changes in nitrogen excretion, leucine oxidation and whole body leucine kinetics during a reduction from a high to a moderate protein intake. Clin Sci 86:185 -193, 1994
    OpenUrlCrossRefPubMed
  19. ↵
    Reaich D, Channon SM, Scrimgeour CM, Goodship TH: Ammonium chloride-induced acidosis increases protein breakdown and amino acid oxidation in humans. Am J Physiol 263:E735 -E739, 1992
    OpenUrlPubMed
  20. ↵
    Reaich D, Channon SM, Scrimgeour CM, Daley SE, Wilkinson R, Goodship TH: Correction of acidosis in humans with CRF decreases protein degradation and amino acid oxidation. Am J Physiol265 : E230-E235,1993
    OpenUrlPubMed
  21. ↵
    Graham KA, Reaich D, Channon SM, Downie S, Goodship TH: Correction of acidosis in hemodialysis decreases whole-body protein degradation. J Am Soc Nephrol 8:632 -637, 1997
    OpenUrlAbstract
  22. ↵
    Graham KA, Reaich D, Channon SM, Downie S, Gilmour E, Passlick-Deetjen J, Goodship TH: Correction of acidosis in CAPD decreases whole body protein degradation. Kidney Int49 : 1396-1400,1996
    OpenUrlCrossRefPubMed
  23. ↵
    Klahr S, Levey AS, Beck GJ, Caggiula AW, Hunsicker L, Kusek JW, Striker G: The effects of dietary protein restriction and blood-pressure control on the progression of chronic renal disease. Modification of Diet in Renal Disease Study Group. N Engl J Med330 : 877-884,1994
    OpenUrlCrossRefPubMed
  24. ↵
    Isley WL, Underwood LE, Clemmons DR: Changes in plasma somatomedin-C in response to ingestion of diets with variable protein and energy content. J Parenter Enteral Nutr8 : 407-411,1984
    OpenUrlCrossRefPubMed
  25. ↵
    Clemmons DR, Underwood LE, Dickerson RN, Brown RO, Hak LJ, MacPhee RD, Heizer WD: Use of plasma somatomedin-C/insulin-like growth factor I measurements to monitor the response to nutritional repletion in malnourished patients. Am J Clin Nutr 41:191 -198, 1985
    OpenUrlAbstract/FREE Full Text
  26. ↵
    Fouque D, Le Bouc Y, Laville M, Combarnous F, Joly MO, Raton P, Zech P: Insulin-like growth factor-1 and its binding proteins during a low-protein diet in chronic renal failure. J Am Soc Nephrol 6:1427 -1433, 1995
    OpenUrlAbstract/FREE Full Text
  27. ↵
    Pedrini MT, Levey AS, Lau J, Chalmers TC, Wang PH: The effect of dietary protein restriction on the progression of diabetic and nondiabetic renal diseases: A meta-analysis. Ann Intern Med124 : 627-632,1996
    OpenUrlCrossRefPubMed
  28. ↵
    Fouque D, Wang P, Laville M, Boissel JP: Low protein diets delay end-stage renal disease in non-diabetic adults with chronic renal failure. Nephrol Dial Transplant 15:1986 -1992, 2000
    OpenUrlCrossRefPubMed
  29. ↵
    Clinical practice guidelines for nutrition in chronic renal failure. Am J Kidney Dis35 [Suppl 2]: S1-S140,2000
    OpenUrlPubMed
PreviousNext
Back to top

In this issue

Journal of the American Society of Nephrology: 12 (6)
Journal of the American Society of Nephrology
Vol. 12, Issue 6
1 Jun 2001
  • Table of Contents
  • Index by author
View Selected Citations (0)
Print
Download PDF
Sign up for Alerts
Email Article
Thank you for your help in sharing the high-quality science in JASN.
Enter multiple addresses on separate lines or separate them with commas.
Adaptive Response to a Low-Protein Diet in Predialysis Chronic Renal Failure Patients
(Your Name) has sent you a message from American Society of Nephrology
(Your Name) thought you would like to see the American Society of Nephrology web site.
CAPTCHA
This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.
Citation Tools
Adaptive Response to a Low-Protein Diet in Predialysis Chronic Renal Failure Patients
JACQUES BERNHARD, BERNARD BEAUFRÈRE, MAURICE LAVILLE, DENIS FOUQUE
JASN Jun 2001, 12 (6) 1249-1254;

Citation Manager Formats

  • BibTeX
  • Bookends
  • EasyBib
  • EndNote (tagged)
  • EndNote 8 (xml)
  • Medlars
  • Mendeley
  • Papers
  • RefWorks Tagged
  • Ref Manager
  • RIS
  • Zotero
Request Permissions
Share
Adaptive Response to a Low-Protein Diet in Predialysis Chronic Renal Failure Patients
JACQUES BERNHARD, BERNARD BEAUFRÈRE, MAURICE LAVILLE, DENIS FOUQUE
JASN Jun 2001, 12 (6) 1249-1254;
del.icio.us logo Digg logo Reddit logo Twitter logo CiteULike logo Facebook logo Google logo Mendeley logo
  • Tweet Widget
  • Facebook Like

Jump to section

  • Article
    • Abstract
    • Materials and Methods
    • Results
    • Discussion
    • Acknowledgments
    • References
  • Figures & Data Supps
  • Info & Metrics
  • View PDF

More in this TOC Section

  • A Randomized, Controlled Trial of Steroids and Cyclophosphamide in Adults with Nephrotic Syndrome Caused by Idiopathic Membranous Nephropathy
  • Lower Progression Rate of End-Stage Renal Disease in Patients with Peripheral Arterial Disease Using Statins or Angiotensin-Converting Enzyme Inhibitors
  • IgACE: A Placebo-Controlled, Randomized Trial of Angiotensin-Converting Enzyme Inhibitors in Children and Young People with IgA Nephropathy and Moderate Proteinuria
Show more Clinical Nephrology

Cited By...

  • Low-protein diet for diabetic nephropathy: a meta-analysis of randomized controlled trials
  • Effect of Dietary Protein Intake on Serum Total CO2 Concentration in Chronic Kidney Disease: Modification of Diet in Renal Disease Study Findings
  • Application of Branched-Chain Amino Acids in Human Pathological States: Renal Failure
  • Google Scholar

Similar Articles

Related Articles

  • No related articles found.
  • PubMed
  • Google Scholar

Articles

  • Current Issue
  • Early Access
  • Subject Collections
  • Article Archive
  • ASN Annual Meeting Abstracts

Information for Authors

  • Submit a Manuscript
  • Author Resources
  • Editorial Fellowship Program
  • ASN Journal Policies
  • Reuse/Reprint Policy

About

  • JASN
  • ASN
  • ASN Journals
  • ASN Kidney News

Journal Information

  • About JASN
  • JASN Email Alerts
  • JASN Key Impact Information
  • JASN Podcasts
  • JASN RSS Feeds
  • Editorial Board

More Information

  • Advertise
  • ASN Podcasts
  • ASN Publications
  • Become an ASN Member
  • Feedback
  • Follow on Twitter
  • Password/Email Address Changes
  • Subscribe to ASN Journals

© 2021 American Society of Nephrology

Print ISSN - 1046-6673 Online ISSN - 1533-3450

Powered by HighWire