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Recommendations Summary

CKD: Macronutrients: Protein Amount (2020)

Click here to see the explanation of recommendation ratings (Strong, Fair, Weak, Consensus, Insufficient Evidence) and labels (Imperative or Conditional). To see more detail on the evidence from which the following recommendations were drawn, use the hyperlinks in the Supporting Evidence Section below.


  • Recommendation(s)

    CKD: Protein Restriction, Non-Dialysis, Non-Diabetic

    In adults with CKD 3-5 who are metabolically stable, we recommend, under close clinical supervision,  protein restriction with or without keto acid analogs,  to reduce risk for ESKD/death (1A) and improve quality of life (2C). 

    • a low protein diet providing 0.55 to 0.60 g dietary protein/kg body weight/day , OR
    • a very-low protein diet providing 0.28 to 0.43 g dietary protein/kg body weight/day with additional keto acid/amino acid analogs to meet protein requirements (0.55 to 0.60 g /kg body weight/day)

    Rating: Strong
    Conditional

    CKD: Dietary Protein Intake, Maintenance Hemodialysis, Non-Diabetic

    In adults with CKD 5D on MHD (1C) who are metabolically stable, we recommend prescribing a dietary protein intake of 1.0 -1.2 g /kg body weight per day to maintain a stable nutritional status.

    Rating: Fair
    Conditional

    CKD: Dietary Protein Intake, Peritoneal Dialysis, Non-Diabetic

    In adults with CKD 5D on PD (OPINION) who are metabolically stable, we recommend prescribing a dietary protein intake of 1.0 -1.2 g /kg body weight per day to maintain a stable nutritional status.

    Rating: Consensus
    Conditional

    • Risks/Harms of Implementing This Recommendation

      Compliance to diets should be monitored frequently during the first year of dietary intervention by dietary interviews (3 is optimal) and urine collection for urea output measures. Then yearly follow-up may be recommended until start of maintenance dialysis.

      These diets should be progressively installed to allow a careful dietary counselling and adequate compliance. Although such diets are not associated with wasting in carefully monitored research studies, on a routine basis, attention should be focused on energy intake which may decrease over time and induce wasting.

       

    • Conditions of Application

      Are LPD/VLPD+ ketoanalogues indicated for malnourished CKD patients? This question cannot easily be answered since it may depend on the cause of patient wasting. For example, an acute catabolic state may induce malnutrition even if the nutrient intake is adequate. However, priority should be given to the correction of wasting and protein intake should be increased until the wasting state improves. An LPD/VLPD with KA diet should not be started during a wasting state in CKD patients.

      Do LPD and VLPD with ketoanalogues have impact on the nutritional status? In a post-hoc analysis of the MDRD study, the authors compared the randomized groups (LPD versus VLPD with ketoanalogues) for various outcomes related to nutritional status. Overall, the results demonstrate the safety of dietary protein restriction over two to three years in patients with moderate to advanced CKD. However, there were small but significant changes from baseline in some nutritional indices, and minimal differences between the randomized groups in some of these changes. In both LPD and VLPDwith ketoanalogues, both protein and energy intake declined. Serum albumin rose, while serum transferrin, body weight, percentage of body fat, arm muscle area and urine creatinine excretion declined. In a longitudinal study looking at body composition, a VLPD with ketoanalogues diet induced a small decline in lean body mass on the average of 1.2 kg, with concomitant increase in fat mass, mainly in the first 3 months; these parameters subsequently stabilized and even improve slightly thereafter.  Other short-term studies did not show noticeable effects of LPD and VLPD with ketoanalogues on nutritional parameters. Nevertheless, small anthropometric measurement’s decline observed in some studies are of concern since, in routine practice, LPD and VLPD with  ketoanalogues are used on the long term and because of the adverse effect of protein-energy wasting in patients with end-stage renal disease. This is why physicians who prescribe low-protein diets must regularly monitor patients' protein and energy intake and nutritional status.

      In the context of these recommendations, “metabolically stable” indicates absence of any active inflammatory or infectious diseases; no hospitalization within two weeks; absence of poorly controlled diabetes and consumptive diseases such as cancer; absence of antibiotics or immunosuppressive medications; and absence of significant short-term loss of body weight.

      Implementation considerations

      • Increase the training and number of specialized renal dietitians worldwide who could effectively and safely implement low and very low protein diets;
      • Promote low protein products to simplify dietary counseling and help achieving low protein diet;
      • Be more aggressive with the dietary interventions to improve symptoms when chronic dialysis is not a treatment option or need to be postponed (vascular access maturation, organizing preemptive renal transplant);   
      • The need for food information is important to obtain a good compliance to the restricted protein intake. However, therapeutic education can help patients to improve personal motivation, and can even become a personal goal to achieve. Getting more interested in food harvesting, preparation, and cooking may improve quality of life. In addition, postponing initiation of dialysis undoubtedly maintains a better quality of life rather than undergoing chronic dialysis (Neumann et al 2018).

    • Potential Costs Associated with Application

      Although costs of MNT sessions and reimbursements vary, MNT sessions are essential for improving outcomes.  In international settings where ketoacid analogs are available, the cost of ketoacid analogs should be considered before recommending to a patient.

    • Recommendation Narrative

      Protein metabolism in the body is responsible for adequate growth in children and maintenance of body protein mass such as muscle mass in adults. Every day, approximately 250 g of protein are catabolized, leading to protein catabolic products, such as urea and many other known or unidentified compounds. Most of these degradation products are normally cleared by the kidneys and excreted in urine. When kidney function impairs, there will be an accumulation of these by-products into the blood, which will progressively impair organ function (Kalantar- Zadeh et al 2017). This has been clearly identified for compounds such as P-cresylsulphate, indoxyl-sulphate, trimethyl aminoxide, fibroblast-growth factor 23, which are now considered as uremic toxins. Secondly, protein intake is responsible for a major fraction of renal workload, and many experimental and clinical research have confirmed the renal effects of a protein load and a deleterious role of the renal hyperfiltration response associated with protein intake. Therefore, in a situation of nephron reduction, such as CKD, reducing protein intake will reduce hyperfiltration, with an additive effect to those of angiotensin-reducing drugs (Kalantar-Zadeh et al 2017). As a consequence of both actions, reducing uremia on one hand and improving renal hemodynamics on the other hand, a reduction in protein intake may reduce the body poisoning and postpone the need to start maintenance dialysis treatment.

      Detailed Justification
      Reducing protein intake may impair nutritional status. However, it is a well-known fact that adults in western countries eat too much protein (1.35 g protein/kg/d) as compared with their optimal daily needs, estimated to be 0.8 g protein/kg/day. Further, metabolic balances in healthy adults and CKD patients have confirmed that, provided a sufficient energy intake (e.g., above 30 kcal/kg/d), the protein intake level can be safely decreased to 0.55-0.6 g protein/kg/d. A further reduction in protein intake to 0.3-0.4 g protein/kg/d can be achieved with the addition of pills of keto acid analogs to ensure a sufficient balance of the essential amino acids (EAAs) normally brought by animal proteins, which are essentially absent in these low protein vegan-like diets.

      Protien Restriction Alone
      In adults with CKD/kidney transplant, thirteen RCTs reported the effect of protein restriction only (no supplementation) on outcomes of interest (Cianciaruso et al , Cianciaruso et al, D'Amico et al 2004, Hansen 2002, Jesudason et al 2013, Kloppenburg et al 2004, Kuhlmann et al 1999, Locatelli et al 1989,   Rosman et al 1989, Rosman et al 1985, Rosman et al 1989b, Sanchez et al 2010, Williams et al 1991). Duration of the follow-up in the included studies ranged from 3 months to 48 months.

      Survival/Renal Death
      Research reports a beneficial effect of protein restriction (0.55-0.6 g/kg/d) on ESRD/death in adults with CKD. In adults with CKD, 5 RCTs reported findings on effect of protein restriction on survival/deaths. Three studies clearly indicated a beneficial effect of moderate restriction in dietary protein on the development of ESRD/death (Hansen 2002,  Rosman et al 1985,  Locatelli et al 1989). Rosman et al indicated people consuming 0.6 g/kg/d of protein had better survival (55%) compared to patients consuming free protein intake (40%). Hansen et al 2002 also indicated that death or ESRD was significantly lower in low protein intake group (0.6g/kg/d) (10%) compared to usual protein intake (27%).  Locatelli et al also indicated that low protein diet (LPD) (0.6 g/kg/d) had fewer events (27/192) compared to usual protein intake (1g/kg/d) (42/188), borderline significant (p<0.06).  Whereas, Cianciaruso et al indicated that cumulative incidences of death and dialysis therapy start were unaffected by the diet regimen, and low protein intake group (0.55 g/kg/d) does not seem to confer a survival advantage compared with a moderate protein intake group (0.80 g/kg/d) but may be explained by a relatively small sample size.  Pooled together, results from the secondary analysis on the number of events of death/ESRD combined from the three studies indicated a beneficial effect of protein restriction on death /ESRD (OR 0.621 CI: 0.391, 0.985). 

      Quality of Life
      Research reports an improved quality of life of a protein restricted diet in one study. In adults with CKD, one RCT examined the effect of protein restriction on quality of life (Sanchez et al 2010).  QoL scores at the end of the study indicated that the protein restricted group had significantly higher scores for general health (MD 4.0, 95% CI: 3.1, 4.86) and physical status (MD 10.0, 95% CI: 9.1, 10.9) compared to the control group (0.6 g/kg/d vs 46.3g protein/day; p<0.05).

      There is seldom information on quality of life of patients with CKD undergoing a dietary protein restriction. The need for food information is important to obtain a good compliance to the restricted protein intake. However, therapeutic education can help patients to improve personal motivation, and can even become a personal goal to achieve. Getting more interested to food harvesting, preparation, cooking may improve quality of life. In addition, postponing dialysis start undoubtedly maintains a better quality of life rather than undergoing chronic dialysis (Neumann et al 2018).

      Glomerular Filtration Rate
      In adults with CKD, 5 RCT’s reported on effect of protein-restricted diet on GFR. Results from the all the studies indicated that LPD (0.55-0.6 g/kg body weight) had no significant effect on GFR compared to the control group (0.8 g/kg protein). Hanson et al indicated that at a 6-month follow-up time, there was a comparable and significant decline in GFR in both groups (Hansen et al 2002). However, the difference between groups was insignificant (p=0.87). Sanchez et al indicated that GFR rates decreased by 17.2% in the control group compared to only 6.9% in low protein group (NS between groups) (Sanchez et al 2010). Cianciaruso et al 2009 indicated no effect of diet assignments was noted on eGFR and proteinuria (0.55g/kg/d vs 0.80 g/kg/d). Juesudason et al reported that dietary treatment had no effect on changes in eGFR.  Meloni et al 2002 (stage 3) also indicated no effect of protein restriction on GFR decline (0.6 g/kg/d).  Decline in GFR was reported by three studies, a pooled analysis of these studies indicated no clear effect of protein restriction without supplementation on GFR (SMD -0.002, CI: -0.192, 0.188).

      Electrolyte Levels
      In adults with CKD, two RCT’s reported mixed results regarding the effect of protein restriction on serum phosphate levels (Cianciaruso et al 2008, Rosman et al 1989). Rosman et al indicated that patients in the protein restriction group had significantly lower S. phosphate levels (used less phosphate binders) (0.4-0.6 vs 0.8 g) (p<0.05). Whereas, Cianciaruso et al 2008, indicated that phosphate levels were similar in the two groups throughout the entire period of follow-up (0.55 g protein/kg/d group vs 0.8 g protein/kg/d).

      Dietary Intake
      Seven randomized controlled studies (D'Amico et al 1994, Hansen et al 2002,  Jesudason et al 2013,  Kloppenburg et al 2004,  Sanchez et al 2010,  Williams et al 1991,  Meloni et al 2002) and 1 NRCT (Kuhlmann et al 1999) reported on dietary intake. These studies indicated that protein intake was lower in groups assigned to low-protein diet (0.6 g/kg/d) compared to control or standard groups (0.8-1.3 g/kg/d).  Dietary intake was used as a compliance measure in most of the studies. In one study, the average protein intake during the entire duration of follow-up was higher than expected in both the groups (CPD=1.03 ± 0.18, LPD=0.78 ± 0.17 g protein/kg/d) (D'Amico et al 1994). Follow-up of at least 1.5 years indicated that compliance to diet did not change in time in either group. Hansen et al (2002) reported an estimated dietary protein intake at 4 years significantly lower in LPD compared to usual PD group (p=0.005) (Hansen et al 2002).  Jesudason et al (2013) showed that the moderate protein intake group increased their protein intake (NS) and standard protein group decreased their protein intake. In the study by Kloppenburg et al the protein intake during the high protein diet was higher than during the regular protein diet. Kuhlmann et al reported that protein intake was not significantly different among the groups. However, total energy intake significantly differed among each other. In the Meloni et al study, patients in the low protein group were maintaining their intake at 0.68 g protein/kg/d level which was significantly lower than the free protein diet group. Phosphate intake was also significantly lower in the LPD group. Sanchez et al showed that protein intake in the LPD group decreased significantly from baseline to end of the study (p<0.05). Energy intake tended to decrease during the study duration in both the groups but it was non-significant. In Williams et al study, compared to control, only dietary protein and phosphate restriction group had significantly lower protein intake level.  Finally, Cianciaruso et al reported that the 2 groups (LPD vs MPD) maintained significantly different protein intakes (p<0.05), with a difference between the 2 groups of 0.17 ±0.05 g/d, which lasted from month 6 until the study end. Dietary intake can be used as a compliance index to the diet.

      Nutritional Status
      Research findings indicated that protein restriction did not affect serum albumin levels of anthropometrics in adult CKD patients. In adults with CKD, 2 RCTs reported no effect of protein restriction (0.55-0.9 g protein/kg/d) on serum albumin levels compared to control group (0.8-1.3 g protein/kg/d) (Cianciaruso et al 2009, Kloppenburg et al 2004).  In adults with CKD, one RCT reported no effect of protein restriction (55-70 g/d) on anthropometrics compared to control group (90-120 g/d) (Jesudason et al 2013).

      Blood Pressure
      Two RCT’s reported no effect of protein-restriction (0.6 g/kg bd wt vs usual) on BP values (Hansen et al 2002, Jesudason et al 2013). Hansen et al reported that BP changes were comparable in the two groups during follow-up period.  BP was equally and significantly reduced during the study compared to baseline in both groups. Jesudason et al reported no overall changes in BP for both the groups. However, there was a time-by-treatment interaction (p<0.05) for diastolic BP. Diastolic BP was lower throughout the follow-up period in the moderate protein intake group.

      Lipid Profile
      Research reported an improvement in serum lipid profile during a low protein diet. Coggins  et al intervention diet (Diet J/K) showed significant decreases in total cholesterol, HDL, and LDL between baseline and 6-month follow-up (p<0.05). Diet L reported trends for decreases in total and LDL-C between baseline and 6-month follow-up (p<0.10). Cianciaruso et al 2009 showed a significant decrease in LDL values in the low protein diet group, but not in the moderate protein intake group.

      Protein Restriction plus Ketoacid Analogs Supplement
      In international settings where ketoacid analogs are available, a very-low protein-controlled diet may be considered. For adults with CKD without diabetes,  not on dialysis, with an eGFR below 20ml per minute per 1.73m2, a very-low protein diet (VLPD) providing 0.28g to 0.43g protein/kg/d with addition of keto acid analogs to meet protein requirements may be recommended. 

      In adults with CKD/kidney transplant, fourteen studies reported the effect of protein restriction with KA supplementation on outcomes of interest.  One non-randomized controlled trial (NRCT) (Bellizzi et al 2007),  and 13 RCTs were included (Coggins et al 1994, Feiten et al 2005,  Herselman et al 1995, Jian et al 2009, Junger et al 1987, Klahr et al 1994, Kopple et al 1997, Levey et al 1996, Li et al 2011, Malvy et al 1999, Menon et al 2005,  Mircescu et al 2007, Prakash et al 2004).

      Survival/Renal Death
      Dietary Protein restriction with KA supplementation probably reduces RRT/renal survival in adults with CKD stages 3 to 5. In adults with CKD, 4 RCTs reported mixed effect of protein- restricted diet with KA on renal survival/RRT (Levey et al 1996,  Malvy et al 1999, Mircescu et al 2007, Garneata et al 2016). Garneata and Mircescu et al indicated a significantly lower percentage of patients in the VLPD with KA group required RRT initiation throughout the therapeutic intervention.  Whereas, Levey and Malvy et al indicated no effect, but Malvy study was unpowered. Pooled analysis of two studies that reported RRT incidence indicated that protein restricted diet with KA has a lower risk ratio for incidence of RRT (RR 0.412, CI: 0.219, 0.773). Levey et al indicated that after controlling for protein intake from food and supplement from the studies evaluated, assignment to the VLPD did not have a significant effect on renal failure/death risk.  Malvy et al also indicated no effect of protein restriction +KA on renal survival.  Whereas, Mircescu et al indicated a significantly lower percentage of patients in the VLPD+KA group required RRT initiation throughout the therapeutic intervention (4% vs. 27%); and Garneata et al also indicated a delay in dialysis initiation.  Both Garneata and Mircescu are newer studies and shorter in duration (12 to 15 months) compared to Levey and Malvy (Levey-2.2 years). When pooled together, there is probably an overall benefit of dietary protein restriction + KA supplementation on RRT/renal survival in CKD stage 3 to 5 patients (RR 0.65, CI 0.49 to 0.85 , p<0.001).

      eGFR
      A VLPD supplemented with keto-analogues (0.28-0.4 g protein/kg/d) could help preserve renal function in stage 3 to 5 CKD patients. One study was conducted in PD patients, and GFR was preserved. In adults with CKD, 1 NRCT (Bellizzi et al 2007)  and 4 randomized controlled trial (Klahr et al 1994, Levey et al 1996,  Mircescu et al 2007, Prakash et al 2004, Garneata et al 2016) reported on effect of protein-restricted diet+ KAA (0.28 - 0.4g/kg body weight) on estimated GFR. Results from the all the 6 studies indicated that VLPD +KAA (0.3-0.4 g/kg body weight) supplementation helped preserve eGFR, whereas, subjects assigned to low protein diet only (0.58-0.68 g/kg protein) did indicate decline in GFR. All studies were conducted in subjects in stages 3 to 5. Pooled analysis for all five studies was not possible to conduct.

      Bellizi reported that GFR significantly decreased in the control group. Garneata et al indicated that the decrease in eGFR was less in keto-supplemented group compared with LPD. Klahr et al indicated that compared with usual protein group, the low-protein group had a more rapid GFR decline in the first four months (p=0.004) but slower decline from the first four months to the end (p=0.009). Among patients with GFR of 13-24 ml/min/1.73m2 (study 2), there was a trend for slower GFR decline in the VLPD group when compared with the low-protein group (p=0.07). Levey et al (post-hoc analysis of MDRD) indicated that at a fixed level of protein intake from food only, assignment to a VLPD was associated with a decrease (trend) in the steepness of the mean GFR slope of 1.19 mL/min/yr (p=0.063). Similarly, after controlling for protein intake from food and supplement, assignment to the VLPD did not improve the rate of decline in GFR (p=0.71).  Mircescu et al indicated that estimated GFR did not change significantly in patients receiving VLPD+KA but significantly decreased in the LPD group (p<0.05), suggesting renal protection for VLPD+KA. Prakesh et al also indicated that GFR stayed unchanged in the KA supplemented group, however, it significantly decreased in the placebo group (p=0.015).  Keto-supplemented diet over the 9-month period helped preserve the GFR.

      Electrolyte Levels
      Research reports that a VLPD supplemented with keto-analogues (0.28-0.4 g protein/kg/d) could decrease serum phosphate and improve some markers of bone metabolism (calcium, parathyroid hormone). Four randomized controlled studies (stages 4-5)(Rosman et al 1989, Feiten et al 2005, Malvy et al 1999, Mircescu et al 2007) indicated a decrease in serum phosphate levels at the end of intervention among LPD+ KAA groups. One study with MHD patients also demonstrated a decrease in serum phosphate in the LPD +KAA group (Li et al 2011). Feiten et al indicated that serum phosphate did not change in the LPD group but tended to decrease in the VLPD + KA group (within VLPD, p=0.07).  Serum PTH concentration did not significantly change in the VLPD with KA group; however, it increased significantly in the LPD group (p=0.01). Li et al in MHD patients indicated that in the LPD with KA group, no significant changes in serum calcium were observed, however, mean serum phosphate levels significantly fell at the end of the study (p<0.001) compared to the NPD group.  Mirescu et al in stages 4 and patients indicated that in the VLPD+KAA group a significant increase was seen in serum calcium levels post intervention (p<0.05); serum phosphate levels decreased (p<0.05); whereas no statistical changes were observed in the LPD group. In Rosman et al study, patients in the low protein diet group showed significantly lower serum phosphate levels  and used less phosphate binders (p<0.05). In a recent meta-analysis, it was reported that serum phosphate levels were lower in patients supplemented very low protein intake in two randomized studies from china (Jiang et al 2018). 

      Dietary Intake
      Research findings indicate that a VLPD supplemented with keto-analogues (0.28-0.40 g protein/kg/d) can effectively be achieved. Dietary intake can be used as a compliance index to the diet. Five randomized controlled studies and 1 NRCT (4 studies with CKD stage 3-5 patients and 1 with PD patients) reported on dietary intake. These studies indicated that protein intake was lower in groups assigned to low-protein diet or very-low-protein diet groups compared to control or standard groups. Dietary intake was used as a compliance measure in most of the studies.

      In Bellizi (stage 4 and 5), at 6 months, protein intake and salt intake were significantly lower in VLPD than LPD (p<0.0001). Feiten et al (stage 4), reported a reduction in protein intake in the VLPD supplemented group; energy intake did not change in both groups during the whole study, and was low (approximately 23 kcal/lg/d). Phosphorus intake decreased significantly only in the VLPD with KA group. Calcium intake was low and did not change during the intervention period for both groups. In Herselma et al study, protein intake during intervention was significantly reduced from baseline in both groups. In the study of Jian et al in PD, dietary protein intake between groups LP and HP was different in the 6th and 10th month (p<0.05). Kopple et al looked at both protein and energy intake (stage 3, 4), compared to usual protein diet, low-protein diet had significantly lower dietary protein intake in study A (p≤0.001). Compared to low protein diet, VLPD had significantly lower dietary protein intake in study B (p≤0.001). Dietary energy intake in low-protein diet was significantly lower in study A (p≤0.001) compared to usual protein diet, however, there was no significant difference between LPD and VLPD in study B (p>0.05). Mircescu et al (Stages 4 and 5) results indicated that compliance with prescribed diet was good throughout the study in both arms.

      Nutritional Status
      Research reports that a VLPD supplemented with keto-analogues (0.28-0.4 g protein/kg/d) had no significant effect on albumin levels and nutritional status as measured by SGA, and effects on anthropometry were inconclusive. In adults with CKD, 6 RCTs (Feiten et al 2005, Jiang et al 2009, Kopple et al 1997,  Mircescu et al 2007, Prakash et al 2004, Garneata et al 2016) and 1 NRCT (Bellizzi et al 2007) reported no effect of protein + ketoanalogues intervention on serum albumin level. No significant effect of protein restriction with ketoanalogues supplementation was noticed in any of these studies on albumin levels. Jian et al and Garneata et al were the only studies that studied effect of protein restriction with ketoanalogues supplementation on SGA and no statistically significant effect was noticed. Both the studies indicated that nutritional status was maintained.

      In the study by Kopple et al., (study B, stages 3 and 4), no significant differences in anthropometrics measurements were observed between groups (p>0.05).  Malvy et al reported that for the patients in the VLPD group, a significant weight loss was observed at the end of the study (p<0.01) and lean and FM were reduced in this group at the end of study. Moderate protein group indicated no difference for weight variables. Garneata, in a larger and more recent study, reported no differences throughout the study period in both groups for BMI, MAMC, and TSF.

      Blood Pressure
      Research reports that the effects of a VLPD supplemented with keto-analogues (0.28-0.40 g protein/kg/d) on blood pressure are inconclusive. In adults with CKD, 1 NRCT (Bellizzi et al 2007) and 2 RCTs (Herselman et al 1995,  Mircescu et al 2007) reported mixed effect of a protein-restricted diet (0.3-0.4 g/kg/d) + ketoanalogues supplements on BP. Only one study showed a significant reduction in systolic BP and diastolic BP (Bellizzi et al 2007). In this study, the VLPD had antihypertensive effect in response to the reduction of sodium intake, type of protein intake and ketoanalogue supplements, independent of actual protein intake. The other two studies reported no effect of protein-restricted diet with ketoanalogues on BP (Herselman et al 1995,  Mircescu et al 2007).

      Lipid Profile
      Research indicates that a VLPD supplemented with ketoanalogues (0.28-0.40 g protein/kg/d) could improve serum lipid profile of CKD patients. In adults with CKD, 1 NRCT (Bellizzi et al 2007) and 4 RCTs reported on the effects of a protein-restricted diet (0.3-0.4 g/kg/d) + ketoanalogues on serum lipid profile (Coggins et al 1994, Feiten et al 2005, Malvy et al 1999, Garneata et al 2016). Feiten et al and Malvy et al reported no effect of VLPD + ketoanalogues on serum lipid profile,  whereas, Bellizi et al indicated a decrease in TC and TG only in the VLPD group. Coggins et al indicated a significant decrease in TC, HDL, LDL in the VLPD group. Garneata et al showed that cholesterol levels remained stable during the entire duration of the study however patients were taking statins/fibrates as standard therapy.

    • Recommendation Strength Rationale

      The evidence supporting the recommendation on protein restriction for pre-dialysis is based on Grade I/Grade A evidence. The evidence supporting the recommendation on protein restriction for MHD is based on Grade III/Grade C evidence. The evidence supporting the recommendation for PD is based on Consensus/expert opinion.

    • Minority Opinions

      Consensus reached.