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Q) Some of my CKD patients are malnourished; in fact, some of those on dialysis do not eat well and have low albumin levels. Previously in this column, it was stated that higher albumin levels (> 4 g/dL) confer survival benefits to dialysis patients. Should I consider prescribing megestrol acetate to improve appetite? If I do prescribe it, what dose is safe for CKD and dialysis patients?

Malnutrition affects one-third of dialysis patients,¹ and malnutrition-inflammation complex syn­drome (MICS) is common in those with stage 5 CKD. Albumin is used as an indicator of MICS in dialysis patients; however, since other factors (stress, infection, inflammation, comorbidities) affect nutritional status,² serum albumin alone may not be sufficient to assess it.

In fact, a recent consensus statement on malnutrition from the Academy of Nutrition and Dietetics and the American Society for Parenteral and Enteral Nutrition excluded serum albumin as a diagnostic characteristic; the criteria included percentage of energy requirement, percentage of weight loss and time frame, loss of body fat and muscle mass, presence of edema, and reduced grip strength.³ These may be better measures of malnutrition in dialysis patients and could be used as criteria for determining when to prescribe an appetite stimulant, such as megestrol acetate.

In recent years, megestrol acetate (an antineoplastic drug) has been used to improve appetite, weight, albumin levels, and MICS in patients receiving maintenance dialysis.^1,4-6 Rammohan et al found significant increases in weight, BMI, body fat, triceps skinfold thickness, protein/energy intake, and serum albumin in 10 dialysis patients who took megestrol acetate (400 mg/d) for 16 weeks.⁴

Continue for megestrol acetate's effects >>

In a 20-week randomized, double-blind, placebo-controlled trial, Yeh et al found significant increases in weight, body fat, and fat-free mass in elderly hemodialysis patients receiving megestrol acetate (800 mg/d). The treatment group also demonstrated greater improvement in ability to exercise.⁵

Monfared and colleagues looked specifically at megestrol acetate’s effect on serum albumin levels in dialysis patients.¹ Using a much lower dose (40 mg bid for two months), they found a significant increase in serum albumin in the treatment group. Although an increase in appetite was noted, the researchers did not observe any significant change in total weight following treatment.¹

In a letter to the editor of the Journal of Renal Nutrition, Golebiewska et al reported their use of megestrol acetate in maintenance hemodialysis and peritoneal dialysis patients.⁶ Hypoalbuminemic patients were given megestrol acetate (160 mg/d). Significant increases in weight, BMI, subjective global assessment scores (a measure of nutritional status based on clinical indices such as weight, appetite, muscle, and fat mass), and serum albumin levels were seen. Only 12 of the 32 patients completed the study; the others dropped out due to adverse effects, including high intradialytic weight gain (the amount of fluid gained between dialysis sessions), dyspnea, diarrhea, and nausea.⁶

Currently, there is no consensus in the literature regarding the most effective dosage of megestrol acetate. Furthermore, evidence is lacking as to whether megestrol acetate–induced increases in appetite, oral intake, weight, and serum albumin level bestow any survival benefit or affect outcomes in dialysis patients.⁴ However, the increased sense of well-being a patient experiences when appetite returns and weight is restored may be worth the effort.

Luanne DiGuglielmo, MS, RD, CSR
DaVita Summit Renal Center
Mountainside, New Jersey

REFERENCES
1. Monfared A, Heidarzadeh A, Ghaffari M, Akbarpour M. Effect of megestrol acetate on serum albumin level in malnourished dialysis patients. J Renal Nutr. 2009;19(2):167-171.
2. Byham-Gray L, Stover J, Wiesen K. A clinical guide to nutrition care in kidney disease. Acad Nutr Diet. 2013.
3. White JV, Guenter P, Jensen G, Malone A, Schofield M; Academy of Nutrition and Dietetics Malnutrition Work Group; ASPEN Malnutrition Task Force; ASPEN Board of Directors. Consensus statement of the Academy of Nutrition and Dietetics/American Society for Parenteral and Enteral Nutrition: characteristics recommended for the identification and documentation of adult malnutrition (undernutrition)  [erratum appears in J Acad Nutr Diet. 2012 Nov;112(11):1899].
J Acad Nutr Diet. 2012;112(5):730-738.
4. Rammohan M, Kalantar-Zedeh K, Liang A, Ghossein C. Megestrol acetate in a moderate dose for the treatment of malnutrition-inflammation complex in maintenance dialysis patients. J Ren Nutr. 2005;15(3):345-355.
5. Yeh S, Marandi M, Thode H Jr, et al. Report of a pilot, double blind, placebo-controlled study of megestrol acetate in elderly dialysis patients with cachexia. J Ren Nutr. 2010; 20(1):52-62.
6. Golebiewska JE, Lichodziejewska-Niemierko M, Aleksandrowicz-Wrona E, et al. Megestrol acetate use in hypoalbuminemic dialysis patients [comment]. J Ren Nutr. 2011;21(2): 200-202.
7. Bendik I, Friedel A, Roos FF, et al. Vitamin D: a critical and necessary micronutrient for human health. Front Physiol. 2014;5:248.
8. Cabone F, Mach F, Vuilleumier N, Montecucco F. Potential pathophysiological role for the vitamin D deficiency in essential hypertension. World J Cardiol. 2014;6(5):260-276. 
9. Sypniewska G, Pollak J, Strozecki P, et al. 25-hydroxyvitamin D, biomarkers of endothelial dysfunction and subclinical organ damage in adults with hypertension. Am J Hypertens. 2014;27(1):114-121. 
10. Vimaleswaran KS, Cavadino A, Berry DJ, et al. Association of vitamin D status with arterial blood pressure and hypertension risk:  a mendelian randomisation study. Lancet Diabetes Endocrinol. 2014;2(9):719-729.

Q) Some of my CKD patients are malnourished; in fact, some of those on dialysis do not eat well and have low albumin levels. Previously in this column, it was stated that higher albumin levels (> 4 g/dL) confer survival benefits to dialysis patients. Should I consider prescribing megestrol acetate to improve appetite? If I do prescribe it, what dose is safe for CKD and dialysis patients?

Malnutrition affects one-third of dialysis patients,¹ and malnutrition-inflammation complex syn­drome (MICS) is common in those with stage 5 CKD. Albumin is used as an indicator of MICS in dialysis patients; however, since other factors (stress, infection, inflammation, comorbidities) affect nutritional status,² serum albumin alone may not be sufficient to assess it.

In fact, a recent consensus statement on malnutrition from the Academy of Nutrition and Dietetics and the American Society for Parenteral and Enteral Nutrition excluded serum albumin as a diagnostic characteristic; the criteria included percentage of energy requirement, percentage of weight loss and time frame, loss of body fat and muscle mass, presence of edema, and reduced grip strength.³ These may be better measures of malnutrition in dialysis patients and could be used as criteria for determining when to prescribe an appetite stimulant, such as megestrol acetate.

In recent years, megestrol acetate (an antineoplastic drug) has been used to improve appetite, weight, albumin levels, and MICS in patients receiving maintenance dialysis.^1,4-6 Rammohan et al found significant increases in weight, BMI, body fat, triceps skinfold thickness, protein/energy intake, and serum albumin in 10 dialysis patients who took megestrol acetate (400 mg/d) for 16 weeks.⁴

Continue for megestrol acetate's effects >>

In a 20-week randomized, double-blind, placebo-controlled trial, Yeh et al found significant increases in weight, body fat, and fat-free mass in elderly hemodialysis patients receiving megestrol acetate (800 mg/d). The treatment group also demonstrated greater improvement in ability to exercise.⁵

Monfared and colleagues looked specifically at megestrol acetate’s effect on serum albumin levels in dialysis patients.¹ Using a much lower dose (40 mg bid for two months), they found a significant increase in serum albumin in the treatment group. Although an increase in appetite was noted, the researchers did not observe any significant change in total weight following treatment.¹

In a letter to the editor of the Journal of Renal Nutrition, Golebiewska et al reported their use of megestrol acetate in maintenance hemodialysis and peritoneal dialysis patients.⁶ Hypoalbuminemic patients were given megestrol acetate (160 mg/d). Significant increases in weight, BMI, subjective global assessment scores (a measure of nutritional status based on clinical indices such as weight, appetite, muscle, and fat mass), and serum albumin levels were seen. Only 12 of the 32 patients completed the study; the others dropped out due to adverse effects, including high intradialytic weight gain (the amount of fluid gained between dialysis sessions), dyspnea, diarrhea, and nausea.⁶

Currently, there is no consensus in the literature regarding the most effective dosage of megestrol acetate. Furthermore, evidence is lacking as to whether megestrol acetate–induced increases in appetite, oral intake, weight, and serum albumin level bestow any survival benefit or affect outcomes in dialysis patients.⁴ However, the increased sense of well-being a patient experiences when appetite returns and weight is restored may be worth the effort.

Luanne DiGuglielmo, MS, RD, CSR
DaVita Summit Renal Center
Mountainside, New Jersey

REFERENCES
1. Monfared A, Heidarzadeh A, Ghaffari M, Akbarpour M. Effect of megestrol acetate on serum albumin level in malnourished dialysis patients. J Renal Nutr. 2009;19(2):167-171.
2. Byham-Gray L, Stover J, Wiesen K. A clinical guide to nutrition care in kidney disease. Acad Nutr Diet. 2013.
3. White JV, Guenter P, Jensen G, Malone A, Schofield M; Academy of Nutrition and Dietetics Malnutrition Work Group; ASPEN Malnutrition Task Force; ASPEN Board of Directors. Consensus statement of the Academy of Nutrition and Dietetics/American Society for Parenteral and Enteral Nutrition: characteristics recommended for the identification and documentation of adult malnutrition (undernutrition)  [erratum appears in J Acad Nutr Diet. 2012 Nov;112(11):1899].
J Acad Nutr Diet. 2012;112(5):730-738.
4. Rammohan M, Kalantar-Zedeh K, Liang A, Ghossein C. Megestrol acetate in a moderate dose for the treatment of malnutrition-inflammation complex in maintenance dialysis patients. J Ren Nutr. 2005;15(3):345-355.
5. Yeh S, Marandi M, Thode H Jr, et al. Report of a pilot, double blind, placebo-controlled study of megestrol acetate in elderly dialysis patients with cachexia. J Ren Nutr. 2010; 20(1):52-62.
6. Golebiewska JE, Lichodziejewska-Niemierko M, Aleksandrowicz-Wrona E, et al. Megestrol acetate use in hypoalbuminemic dialysis patients [comment]. J Ren Nutr. 2011;21(2): 200-202.
7. Bendik I, Friedel A, Roos FF, et al. Vitamin D: a critical and necessary micronutrient for human health. Front Physiol. 2014;5:248.
8. Cabone F, Mach F, Vuilleumier N, Montecucco F. Potential pathophysiological role for the vitamin D deficiency in essential hypertension. World J Cardiol. 2014;6(5):260-276. 
9. Sypniewska G, Pollak J, Strozecki P, et al. 25-hydroxyvitamin D, biomarkers of endothelial dysfunction and subclinical organ damage in adults with hypertension. Am J Hypertens. 2014;27(1):114-121. 
10. Vimaleswaran KS, Cavadino A, Berry DJ, et al. Association of vitamin D status with arterial blood pressure and hypertension risk:  a mendelian randomisation study. Lancet Diabetes Endocrinol. 2014;2(9):719-729.

Q) Some of my CKD patients are malnourished; in fact, some of those on dialysis do not eat well and have low albumin levels. Previously in this column, it was stated that higher albumin levels (> 4 g/dL) confer survival benefits to dialysis patients. Should I consider prescribing megestrol acetate to improve appetite? If I do prescribe it, what dose is safe for CKD and dialysis patients?

Malnutrition affects one-third of dialysis patients,¹ and malnutrition-inflammation complex syn­drome (MICS) is common in those with stage 5 CKD. Albumin is used as an indicator of MICS in dialysis patients; however, since other factors (stress, infection, inflammation, comorbidities) affect nutritional status,² serum albumin alone may not be sufficient to assess it.

In fact, a recent consensus statement on malnutrition from the Academy of Nutrition and Dietetics and the American Society for Parenteral and Enteral Nutrition excluded serum albumin as a diagnostic characteristic; the criteria included percentage of energy requirement, percentage of weight loss and time frame, loss of body fat and muscle mass, presence of edema, and reduced grip strength.³ These may be better measures of malnutrition in dialysis patients and could be used as criteria for determining when to prescribe an appetite stimulant, such as megestrol acetate.

In recent years, megestrol acetate (an antineoplastic drug) has been used to improve appetite, weight, albumin levels, and MICS in patients receiving maintenance dialysis.^1,4-6 Rammohan et al found significant increases in weight, BMI, body fat, triceps skinfold thickness, protein/energy intake, and serum albumin in 10 dialysis patients who took megestrol acetate (400 mg/d) for 16 weeks.⁴

Continue for megestrol acetate's effects >>

In a 20-week randomized, double-blind, placebo-controlled trial, Yeh et al found significant increases in weight, body fat, and fat-free mass in elderly hemodialysis patients receiving megestrol acetate (800 mg/d). The treatment group also demonstrated greater improvement in ability to exercise.⁵

Monfared and colleagues looked specifically at megestrol acetate’s effect on serum albumin levels in dialysis patients.¹ Using a much lower dose (40 mg bid for two months), they found a significant increase in serum albumin in the treatment group. Although an increase in appetite was noted, the researchers did not observe any significant change in total weight following treatment.¹

In a letter to the editor of the Journal of Renal Nutrition, Golebiewska et al reported their use of megestrol acetate in maintenance hemodialysis and peritoneal dialysis patients.⁶ Hypoalbuminemic patients were given megestrol acetate (160 mg/d). Significant increases in weight, BMI, subjective global assessment scores (a measure of nutritional status based on clinical indices such as weight, appetite, muscle, and fat mass), and serum albumin levels were seen. Only 12 of the 32 patients completed the study; the others dropped out due to adverse effects, including high intradialytic weight gain (the amount of fluid gained between dialysis sessions), dyspnea, diarrhea, and nausea.⁶

Currently, there is no consensus in the literature regarding the most effective dosage of megestrol acetate. Furthermore, evidence is lacking as to whether megestrol acetate–induced increases in appetite, oral intake, weight, and serum albumin level bestow any survival benefit or affect outcomes in dialysis patients.⁴ However, the increased sense of well-being a patient experiences when appetite returns and weight is restored may be worth the effort.

Luanne DiGuglielmo, MS, RD, CSR
DaVita Summit Renal Center
Mountainside, New Jersey

REFERENCES
1. Monfared A, Heidarzadeh A, Ghaffari M, Akbarpour M. Effect of megestrol acetate on serum albumin level in malnourished dialysis patients. J Renal Nutr. 2009;19(2):167-171.
2. Byham-Gray L, Stover J, Wiesen K. A clinical guide to nutrition care in kidney disease. Acad Nutr Diet. 2013.
3. White JV, Guenter P, Jensen G, Malone A, Schofield M; Academy of Nutrition and Dietetics Malnutrition Work Group; ASPEN Malnutrition Task Force; ASPEN Board of Directors. Consensus statement of the Academy of Nutrition and Dietetics/American Society for Parenteral and Enteral Nutrition: characteristics recommended for the identification and documentation of adult malnutrition (undernutrition)  [erratum appears in J Acad Nutr Diet. 2012 Nov;112(11):1899].
J Acad Nutr Diet. 2012;112(5):730-738.
4. Rammohan M, Kalantar-Zedeh K, Liang A, Ghossein C. Megestrol acetate in a moderate dose for the treatment of malnutrition-inflammation complex in maintenance dialysis patients. J Ren Nutr. 2005;15(3):345-355.
5. Yeh S, Marandi M, Thode H Jr, et al. Report of a pilot, double blind, placebo-controlled study of megestrol acetate in elderly dialysis patients with cachexia. J Ren Nutr. 2010; 20(1):52-62.
6. Golebiewska JE, Lichodziejewska-Niemierko M, Aleksandrowicz-Wrona E, et al. Megestrol acetate use in hypoalbuminemic dialysis patients [comment]. J Ren Nutr. 2011;21(2): 200-202.
7. Bendik I, Friedel A, Roos FF, et al. Vitamin D: a critical and necessary micronutrient for human health. Front Physiol. 2014;5:248.
8. Cabone F, Mach F, Vuilleumier N, Montecucco F. Potential pathophysiological role for the vitamin D deficiency in essential hypertension. World J Cardiol. 2014;6(5):260-276. 
9. Sypniewska G, Pollak J, Strozecki P, et al. 25-hydroxyvitamin D, biomarkers of endothelial dysfunction and subclinical organ damage in adults with hypertension. Am J Hypertens. 2014;27(1):114-121. 
10. Vimaleswaran KS, Cavadino A, Berry DJ, et al. Association of vitamin D status with arterial blood pressure and hypertension risk:  a mendelian randomisation study. Lancet Diabetes Endocrinol. 2014;2(9):719-729.

Q) In my admitting orders for a CKD patient, I wrote for a “renal diet.” However, the nephrology practitioners changed it to a DASH diet. What is the difference? Why would they not want a “renal diet”?

The answer to this question is: It depends—on the patient, his/her comorbidities, and the need for dialysis treatments (and if so, what type he/she is receiving). Renal diet is a general term used to refer to medical nutrition therapy (MNT) given to a patient with CKD. Each of the five stages of CKD has its own specific MNT requirements.

The MNT for CKD patients often involves modification of the following nutrients: protein, sodium, potassium, phosphorus, and sometimes fluid. The complexity of this therapy often confuses health care professionals when a CKD patient is admitted to the hospital. Let’s examine each nutrient modification to understand optimal nutrition for CKD patients.

Protein. As kidneys fail to excrete urea, protein metabolism is compromised. Thus, in CKD stages 1 and 2, the general recommendations for protein intake are 0.8 to 1.4 g/kg/d. As a patient progresses into CKD stages 3 and 4, these recommendations decrease to 0.6 to 0.8 g/kg/d. In addition, the Kidney Disease Outcomes Quality Initiative (KDOQI) and the Academy of Nutrition and Dietetics recommend that at least 50% of that protein intake be of high biological value (eg, foods of animal origin, soy proteins, dairy, legumes, and nuts and nut butters).²

Why the wide range in protein intake? Needs vary depending on the patient’s comorbidities and nutritional status. Patients with greater need (eg, documented malnutrition, infections, or wounds) will require more protein than those without documented catabolic stress. Additionally, protein needs are based on weight, making it crucial to obtain an accurate weight. When managing a very overweight or underweight patient, an appropriate standard body weight must be calculated. This assessment should be done by a registered dietitian (RD).

Also, renal replacement therapies, once introduced, sharply increase protein needs. Hemodialysis (HD) can account for free amino acid losses of 5 to 20 g per treatment. Peritoneal dialysis (PD) can result in albumin losses of 5 to 15 g/d.² As a result, protein needs in HD and PD patients are about 1.2 g/kg/d of standard body weight. It has been reported that 30% to 50% of patients are not consuming these amounts, placing them at risk for malnutrition and a higher incidence of morbidity and mortality.²

Sodium. In CKD stages 1 to 4, dietary sodium intake should be less than 2,400 mg/d. The Dietary Approaches to Stop Hypertension (DASH) diet and a Mediterranean diet have been associated with ­reduced risk for decline in glomerular filtration rate (GFR) and better blood pressure control.³ Both of these diets can be employed, especially in the beginning stages of CKD. But as CKD progresses and urine output declines, recommendations for sodium intake for both HD and PD patients decrease to 2,000 mg/d. In an anuric patient, 2,000 mg/d is the maximum.²

Potassium. As kidney function declines, potassium retention occurs. In CKD stages 1 to 4, potassium restriction is not employed unless the serum level rises above normal.² The addition of an ACE inhibitor or an angiotensin II receptor blocker to the medication regimen necessitates close monitoring of potassium levels. Potassium allowance for HD varies according to the patient’s urine output and can range from 2 to 4 g/d. PD patients generally can tolerate 3 to 4 g/d of potassium without becoming hyperkalemic, as potassium is well cleared with PD.²

Continue for further examinations >>

Phosphorus. Mineral bone abnormalities begin early in the course of CKD and lead to high-turnover bone disease, adynamic bone disease, fractures, and soft-tissue calcification. Careful monitoring of calcium, intact parathyroid hormone, and phosphorus levels is required throughout all stages of CKD, with hyperphosphatemia of particular concern.

In CKD stages 1 and 2, dietary phosphorus should be limited to maintain a normal serum level.² As CKD progresses and phosphorus retention increases, 800 to 1,000 mg/d or 10 to 12 mg of phosphorus per gram of protein should be prescribed.

Even with the limitation of dietary phosphorus, phosphate-binding medications may be ­required to control serum phosphorus in later CKD stages and in HD and PD patients.² Limiting ­dietary phosphorus can be difficult for patients because of inorganic phosphate salt additives widely found in canned and processed foods; they are also added to dark colas and to meats and poultry to act as preservatives and improve flavor and texture. Phosphorus additives are 100% bioavailable and therefore more readily absorbed than organic phosphorus.⁴

Fluid. Lastly, CKD patients need to think about their fluid intake. HD patients with a urine output of > 1,000 mL/24-h period will be allowed up to 2,000 mL/d of fluid. (A 12-oz canned drink is 355 mL.) Those with less than 1,000 mL of urine output will be allowed 1,000 to 1,500 mL/d, with anuric patients capped at 1,000 mL/d. PD patients are allowed 1,000 to 3,000 mL/d depending on urine output and overall status.² Patients should also be reminded that foods such as soup and gelatin are counted in their fluid allowance.

The complexities of the “renal diet” make patient education by an RD critical. However, a recent article suggested that MNT for CKD patients is underutilized, with limited referrals and lack of education for primary care providers and RDs cited as reasons.⁵ This is mystifying considering that Medicare will pay for RD services for CKD patients.

The National Kidney Disease Education Program, in association with the Academy of Nutrition and Dietetics, has developed free professional and patient education materials to address this need; they are available at http://nkdep.nih.gov/.

Luanne DiGuglielmo, MS, RD, CSR
DaVita Summit Renal Center
Mountainside, New Jersey

REFERENCES
1. McMahon GM, Preis SR, Hwang S-J, Fox CS. Mid-adulthood risk factor profiles for CKD. J Am Soc Nephrol. 2014 Jun 26; [Epub ahead of print].
2. Byham-Gray L, Stover J, Wiesen K. A Clinical Guide to Nutrition Care in Kidney Disease. 2nd ed. The Academy of Nutrition and Dietetics; 2013.
3. Crews DC. Chronic kidney disease and access to healthful foods. ASN Kidney News. 2014;6(5):11.
4. Moe SM. Phosphate additives in food: you are what you eat—but shouldn’t you know that? ASN Kidney News. 2014;6(5):8.
5. Narva A, Norton J. Medical nutrition therapy for CKD. ASN Kidney News. 2014;6(5):7.

Q) In my admitting orders for a CKD patient, I wrote for a “renal diet.” However, the nephrology practitioners changed it to a DASH diet. What is the difference? Why would they not want a “renal diet”?

The answer to this question is: It depends—on the patient, his/her comorbidities, and the need for dialysis treatments (and if so, what type he/she is receiving). Renal diet is a general term used to refer to medical nutrition therapy (MNT) given to a patient with CKD. Each of the five stages of CKD has its own specific MNT requirements.

The MNT for CKD patients often involves modification of the following nutrients: protein, sodium, potassium, phosphorus, and sometimes fluid. The complexity of this therapy often confuses health care professionals when a CKD patient is admitted to the hospital. Let’s examine each nutrient modification to understand optimal nutrition for CKD patients.

Protein. As kidneys fail to excrete urea, protein metabolism is compromised. Thus, in CKD stages 1 and 2, the general recommendations for protein intake are 0.8 to 1.4 g/kg/d. As a patient progresses into CKD stages 3 and 4, these recommendations decrease to 0.6 to 0.8 g/kg/d. In addition, the Kidney Disease Outcomes Quality Initiative (KDOQI) and the Academy of Nutrition and Dietetics recommend that at least 50% of that protein intake be of high biological value (eg, foods of animal origin, soy proteins, dairy, legumes, and nuts and nut butters).²

Why the wide range in protein intake? Needs vary depending on the patient’s comorbidities and nutritional status. Patients with greater need (eg, documented malnutrition, infections, or wounds) will require more protein than those without documented catabolic stress. Additionally, protein needs are based on weight, making it crucial to obtain an accurate weight. When managing a very overweight or underweight patient, an appropriate standard body weight must be calculated. This assessment should be done by a registered dietitian (RD).

Also, renal replacement therapies, once introduced, sharply increase protein needs. Hemodialysis (HD) can account for free amino acid losses of 5 to 20 g per treatment. Peritoneal dialysis (PD) can result in albumin losses of 5 to 15 g/d.² As a result, protein needs in HD and PD patients are about 1.2 g/kg/d of standard body weight. It has been reported that 30% to 50% of patients are not consuming these amounts, placing them at risk for malnutrition and a higher incidence of morbidity and mortality.²

Sodium. In CKD stages 1 to 4, dietary sodium intake should be less than 2,400 mg/d. The Dietary Approaches to Stop Hypertension (DASH) diet and a Mediterranean diet have been associated with ­reduced risk for decline in glomerular filtration rate (GFR) and better blood pressure control.³ Both of these diets can be employed, especially in the beginning stages of CKD. But as CKD progresses and urine output declines, recommendations for sodium intake for both HD and PD patients decrease to 2,000 mg/d. In an anuric patient, 2,000 mg/d is the maximum.²

Potassium. As kidney function declines, potassium retention occurs. In CKD stages 1 to 4, potassium restriction is not employed unless the serum level rises above normal.² The addition of an ACE inhibitor or an angiotensin II receptor blocker to the medication regimen necessitates close monitoring of potassium levels. Potassium allowance for HD varies according to the patient’s urine output and can range from 2 to 4 g/d. PD patients generally can tolerate 3 to 4 g/d of potassium without becoming hyperkalemic, as potassium is well cleared with PD.²

Continue for further examinations >>

Phosphorus. Mineral bone abnormalities begin early in the course of CKD and lead to high-turnover bone disease, adynamic bone disease, fractures, and soft-tissue calcification. Careful monitoring of calcium, intact parathyroid hormone, and phosphorus levels is required throughout all stages of CKD, with hyperphosphatemia of particular concern.

In CKD stages 1 and 2, dietary phosphorus should be limited to maintain a normal serum level.² As CKD progresses and phosphorus retention increases, 800 to 1,000 mg/d or 10 to 12 mg of phosphorus per gram of protein should be prescribed.

Even with the limitation of dietary phosphorus, phosphate-binding medications may be ­required to control serum phosphorus in later CKD stages and in HD and PD patients.² Limiting ­dietary phosphorus can be difficult for patients because of inorganic phosphate salt additives widely found in canned and processed foods; they are also added to dark colas and to meats and poultry to act as preservatives and improve flavor and texture. Phosphorus additives are 100% bioavailable and therefore more readily absorbed than organic phosphorus.⁴

Fluid. Lastly, CKD patients need to think about their fluid intake. HD patients with a urine output of > 1,000 mL/24-h period will be allowed up to 2,000 mL/d of fluid. (A 12-oz canned drink is 355 mL.) Those with less than 1,000 mL of urine output will be allowed 1,000 to 1,500 mL/d, with anuric patients capped at 1,000 mL/d. PD patients are allowed 1,000 to 3,000 mL/d depending on urine output and overall status.² Patients should also be reminded that foods such as soup and gelatin are counted in their fluid allowance.

The complexities of the “renal diet” make patient education by an RD critical. However, a recent article suggested that MNT for CKD patients is underutilized, with limited referrals and lack of education for primary care providers and RDs cited as reasons.⁵ This is mystifying considering that Medicare will pay for RD services for CKD patients.

The National Kidney Disease Education Program, in association with the Academy of Nutrition and Dietetics, has developed free professional and patient education materials to address this need; they are available at http://nkdep.nih.gov/.

Luanne DiGuglielmo, MS, RD, CSR
DaVita Summit Renal Center
Mountainside, New Jersey

REFERENCES
1. McMahon GM, Preis SR, Hwang S-J, Fox CS. Mid-adulthood risk factor profiles for CKD. J Am Soc Nephrol. 2014 Jun 26; [Epub ahead of print].
2. Byham-Gray L, Stover J, Wiesen K. A Clinical Guide to Nutrition Care in Kidney Disease. 2nd ed. The Academy of Nutrition and Dietetics; 2013.
3. Crews DC. Chronic kidney disease and access to healthful foods. ASN Kidney News. 2014;6(5):11.
4. Moe SM. Phosphate additives in food: you are what you eat—but shouldn’t you know that? ASN Kidney News. 2014;6(5):8.
5. Narva A, Norton J. Medical nutrition therapy for CKD. ASN Kidney News. 2014;6(5):7.

Q) In my admitting orders for a CKD patient, I wrote for a “renal diet.” However, the nephrology practitioners changed it to a DASH diet. What is the difference? Why would they not want a “renal diet”?

The answer to this question is: It depends—on the patient, his/her comorbidities, and the need for dialysis treatments (and if so, what type he/she is receiving). Renal diet is a general term used to refer to medical nutrition therapy (MNT) given to a patient with CKD. Each of the five stages of CKD has its own specific MNT requirements.

The MNT for CKD patients often involves modification of the following nutrients: protein, sodium, potassium, phosphorus, and sometimes fluid. The complexity of this therapy often confuses health care professionals when a CKD patient is admitted to the hospital. Let’s examine each nutrient modification to understand optimal nutrition for CKD patients.

Protein. As kidneys fail to excrete urea, protein metabolism is compromised. Thus, in CKD stages 1 and 2, the general recommendations for protein intake are 0.8 to 1.4 g/kg/d. As a patient progresses into CKD stages 3 and 4, these recommendations decrease to 0.6 to 0.8 g/kg/d. In addition, the Kidney Disease Outcomes Quality Initiative (KDOQI) and the Academy of Nutrition and Dietetics recommend that at least 50% of that protein intake be of high biological value (eg, foods of animal origin, soy proteins, dairy, legumes, and nuts and nut butters).²

Why the wide range in protein intake? Needs vary depending on the patient’s comorbidities and nutritional status. Patients with greater need (eg, documented malnutrition, infections, or wounds) will require more protein than those without documented catabolic stress. Additionally, protein needs are based on weight, making it crucial to obtain an accurate weight. When managing a very overweight or underweight patient, an appropriate standard body weight must be calculated. This assessment should be done by a registered dietitian (RD).

Also, renal replacement therapies, once introduced, sharply increase protein needs. Hemodialysis (HD) can account for free amino acid losses of 5 to 20 g per treatment. Peritoneal dialysis (PD) can result in albumin losses of 5 to 15 g/d.² As a result, protein needs in HD and PD patients are about 1.2 g/kg/d of standard body weight. It has been reported that 30% to 50% of patients are not consuming these amounts, placing them at risk for malnutrition and a higher incidence of morbidity and mortality.²

Sodium. In CKD stages 1 to 4, dietary sodium intake should be less than 2,400 mg/d. The Dietary Approaches to Stop Hypertension (DASH) diet and a Mediterranean diet have been associated with ­reduced risk for decline in glomerular filtration rate (GFR) and better blood pressure control.³ Both of these diets can be employed, especially in the beginning stages of CKD. But as CKD progresses and urine output declines, recommendations for sodium intake for both HD and PD patients decrease to 2,000 mg/d. In an anuric patient, 2,000 mg/d is the maximum.²

Potassium. As kidney function declines, potassium retention occurs. In CKD stages 1 to 4, potassium restriction is not employed unless the serum level rises above normal.² The addition of an ACE inhibitor or an angiotensin II receptor blocker to the medication regimen necessitates close monitoring of potassium levels. Potassium allowance for HD varies according to the patient’s urine output and can range from 2 to 4 g/d. PD patients generally can tolerate 3 to 4 g/d of potassium without becoming hyperkalemic, as potassium is well cleared with PD.²

Continue for further examinations >>

Phosphorus. Mineral bone abnormalities begin early in the course of CKD and lead to high-turnover bone disease, adynamic bone disease, fractures, and soft-tissue calcification. Careful monitoring of calcium, intact parathyroid hormone, and phosphorus levels is required throughout all stages of CKD, with hyperphosphatemia of particular concern.

In CKD stages 1 and 2, dietary phosphorus should be limited to maintain a normal serum level.² As CKD progresses and phosphorus retention increases, 800 to 1,000 mg/d or 10 to 12 mg of phosphorus per gram of protein should be prescribed.

Even with the limitation of dietary phosphorus, phosphate-binding medications may be ­required to control serum phosphorus in later CKD stages and in HD and PD patients.² Limiting ­dietary phosphorus can be difficult for patients because of inorganic phosphate salt additives widely found in canned and processed foods; they are also added to dark colas and to meats and poultry to act as preservatives and improve flavor and texture. Phosphorus additives are 100% bioavailable and therefore more readily absorbed than organic phosphorus.⁴

Fluid. Lastly, CKD patients need to think about their fluid intake. HD patients with a urine output of > 1,000 mL/24-h period will be allowed up to 2,000 mL/d of fluid. (A 12-oz canned drink is 355 mL.) Those with less than 1,000 mL of urine output will be allowed 1,000 to 1,500 mL/d, with anuric patients capped at 1,000 mL/d. PD patients are allowed 1,000 to 3,000 mL/d depending on urine output and overall status.² Patients should also be reminded that foods such as soup and gelatin are counted in their fluid allowance.

The complexities of the “renal diet” make patient education by an RD critical. However, a recent article suggested that MNT for CKD patients is underutilized, with limited referrals and lack of education for primary care providers and RDs cited as reasons.⁵ This is mystifying considering that Medicare will pay for RD services for CKD patients.

The National Kidney Disease Education Program, in association with the Academy of Nutrition and Dietetics, has developed free professional and patient education materials to address this need; they are available at http://nkdep.nih.gov/.

Luanne DiGuglielmo, MS, RD, CSR
DaVita Summit Renal Center
Mountainside, New Jersey

REFERENCES
1. McMahon GM, Preis SR, Hwang S-J, Fox CS. Mid-adulthood risk factor profiles for CKD. J Am Soc Nephrol. 2014 Jun 26; [Epub ahead of print].
2. Byham-Gray L, Stover J, Wiesen K. A Clinical Guide to Nutrition Care in Kidney Disease. 2nd ed. The Academy of Nutrition and Dietetics; 2013.
3. Crews DC. Chronic kidney disease and access to healthful foods. ASN Kidney News. 2014;6(5):11.
4. Moe SM. Phosphate additives in food: you are what you eat—but shouldn’t you know that? ASN Kidney News. 2014;6(5):8.
5. Narva A, Norton J. Medical nutrition therapy for CKD. ASN Kidney News. 2014;6(5):7.