|Year : 2013 | Volume
| Issue : 1 | Page : 46-51
Nutritional needs and dietary modifications in patients on dialysis and chronic kidney disease
Sukhminder Jit Singh Bajwa1, Ishwardeep S Kwatra2
1 Department of Anaesthesiology and Intensive Care, Gian Sagar Medical College and Hospital, Ram Nagar, Banur, Punjab, India
2 Department of General Medicine, Gian Sagar Medical College and Hospital, Ram Nagar, Banur, Punjab, India
|Date of Web Publication||1-Jan-2013|
Sukhminder Jit Singh Bajwa
House No-27-A, Ratan Nagar, Tripuri, Patiala, Punjab
Source of Support: None, Conflict of Interest: None
Nutritional needs in patients with chronic kidney disease are different from those of the normal population. As such, estimation of these nutritional requirements mandates a thorough understanding of the various physiologic and pathologic processes related to renal system. Many of these patients get admitted in intensive care and dialysis units at some stage of life for one indication or the other. Intensivists also have to update their knowledge when it comes to providing nutrition to these patients during their intensive care unit (ICU) stay. Majority of these patients are on chronic dialysis and this aspect has to be taken care of while they are treated in ICU. The assessment of nutritional needs and the various dietary modifications requires the services of a nephrologist on patient-to-patient basis depending upon the underlying co-morbid diseases. Majority of the studies involving patients with renal disease have been carried out in normal population, and as such, data is lacking from ICU and dialysis units. The present article is an attempt to discuss various aspects of patients with chronic kidney disease and their nutritional needs and the relevant dietary modifications and is an extrapolation of the present evidence of normal population to the patients admitted in ICU and dialysis units.
Keywords: Chronic ambulatory peritoneal dialysis, chronic kidney disease, dietary modifications, nutritional needs
|How to cite this article:|
Bajwa SS, Kwatra IS. Nutritional needs and dietary modifications in patients on dialysis and chronic kidney disease. J Med Nutr Nutraceut 2013;2:46-51
|How to cite this URL:|
Bajwa SS, Kwatra IS. Nutritional needs and dietary modifications in patients on dialysis and chronic kidney disease. J Med Nutr Nutraceut [serial online] 2013 [cited 2023 Dec 7];2:46-51. Available from: http://www.jmnn.org/text.asp?2013/2/1/46/105330
| Introduction|| |
Assessment of nutritional needs and designing modifications in dietary components in patients with various co-morbid diseases is a challenging task. Dietary factors are an important component in the treatment of patients with kidney diseases and also to minimize the complications arising due to renal insufficiency.  Many of these patients get admitted in intensive care units (ICUs) and dialysis centers at some stage of life for one indication or the other.  Nowadays, number of patients undergoing renal transplantation surgeries has also increased, and as such, their nutritional aspects also require special attention.  Therefore, it becomes essential that intensivists also update their knowledge about various renal pathologies and the underlying mechanisms of the disease when it comes to providing nutrition to these patients during their ICU stay. ,
| Dietary Modifications|| |
Dietary manipulations not only help to ameliorate the signs and symptoms of kidney disease, but also retard the progression of kidney disease regardless of its etiology. Timely and appropriate nutritional intervention optimizes patient care and outcomes at all levels of renal dysfunction. The same holds true for patients with chronic kidney disease (CKD) who require ICU admission or admission in dialysis units. It has been noticed that nutritional markers, such as serum albumin, are highly predictive of morbidity and mortality, and this further emphasizes the importance of nutritional concerns in the management of patients with kidney disease.
Dietary modifications depend on the level of renal insufficiency as well as the present nutritional status. High prevalence of malnutrition exists in patients with renal failure. Several surveys have reported protein-calorie malnutrition in up to 40% of this subset of patient population. , Malnutrition in renal failure is multifactorial, but inadequate oral intake is a major contributing factor. , Nutritional status can be highly variable in geriatric population, menopausal women, critically ill pregnant patients, patients with psychiatric diseases, and patients with polytrauma, who also suffer from either acute or chronic renal pathology, and as such, their requirements have to be estimated on an individual basis. ,,,, Diet restrictions, loss of nutrients in dialysate, and chronic inflammatory milieu associated with renal failure also contribute. Presence of co-morbid diseases pertaining to different organ systems can exaggerate the nutritional problems. Gastrointestinal (GI) complaints are also frequently seen in this patient population and contribute to decreased intake and malnutrition. ,, Evidence from the literature clearly suggests that addressing GI issues in patients with renal failure may improve the nutritional status. 
| Nutritional Needs|| |
No nutritional plan can be successful without prior estimation of the proper nutritional assessment. This is highly desired in patients of ICU and dialysis units who are invariably suffering from various co-morbidities and the resulting nutritional disorders.  It is pertinent to mention at the beginning that there are no large, prospective controlled randomized trials that guide about nutritional needs, especially in the critically ill patients suffering from renal diseases. Current recommendations have been based on various surrogate markers of nutritional status, indirect calorimetry measurements, and studies of protein catabolic rate which have been mainly carried out in not so critical patients.
A systematic review of various research studies concluded that caloric expenditure of stable hemodialysis and chronic ambulatory peritoneal dialysis (CAPD) patients was not significantly different from that of normal individuals.  The evidence from the studies in the chronic renal patients admitted in the ICU is lacking. The available evidence is solely from the studies carried out in patients with CKD requiring dialysis at some stage of their disease state. However, in a review of surveys of food intake in the dialysis patients, it was seen that calorie intake is frequently inadequate and is compromised to a greater degree than protein intake., The National Kidney Foundation's guidelines recommend30-35 calories/ kg for stable dialysis patients. Patients who receive peritoneal dialysis with a dextrose containing dialysate solution can absorb up to 70% of the dextrose from the solution that is instilled. Many patients often absorb 200-300 dextrose calories per day from CAPD and this must be taken into account when estimating calorie intake. For sedentary individuals older than 60 years and obese patients with edema-free body weight >120% of the desirable body weight for CKD may be prescribed 30 kcal/kg/d.
Nutritional assessment requires interpretation of a combination of clinical and biochemical parameters.
Physical examination for clinical signs of poor nutrition or nutritional deficiency (appearance of skin, hair, lips, tongue, gums, nails, and overall presence of subcutaneous fat loss or muscle wasting) should be looked for. Regular monitoring of dry weight is essential to highlight changes in body weight over time.
Body composition: Various methods include anthropometric measurements using calipers and a tape measure, commonly mid-upper arm circumference (MUAC) and triceps skin fold thickness (TSF); mid-arm muscle circumference (MAMC) can then be calculated. Comparison with standards must use renal anthropometric tables. Serial measurements are of more significance to highlight changes in muscle mass or fat. Other measures include bioelectrical impedance (BIA), dual-energy X-ray analysis (DEXA), and magnetic resonance imaging (MRI).
Functional assessment: Review activities of daily living and the ease of basic physical activity (stair climbing or walking). Muscle strength can be determined using hand-grip dynamometry.
Subjective global assessment (SGA): Uses eight clinical measures including dietary intake, co-morbid disease, or GI symptoms, physical examination, changes in body weight, and functional capabilities to produce a semiquantitative nutritional assessment. An overall assessment of nutritional status is generated from the scores in each category.
Biochemical markers: Serum albumin is a good predictor of mortality in end-stage renal disease (ESRD). A single measurement at any point after initiation of dialysis is strongly associated with survival. Patients with serum albumin <25 g/l have a risk ratio for dying 20 times higher than patients with serum albumin >40 g/l. Biochemical markers, which may indicate poor nutrient intake, include reduced serum urea, albumin, potassium, and phosphate. In the long term, reduction in serum creatinine may reflect reduced muscle mass and reduction in serum cholesterol may follow inadequate energy intake.
The calculation and administration of nutritional supplements based on energy requirements is slightly easier as dialysis machines have been set up in the various ICUs. This facilitates a close co-ordination between an intensivist and the nephrologist during designing and modification of dietary regimen of CKD patients. Caloric calculations should be done with actual edema-free body weight, determined post-dialysis for hemodialysis, and "post-drain" for peritoneal dialysis. The National Kidney Foundation recommends that when patients are <95% or >115% of the median standard weight (as determined from the National Health and Nutrition Examination Survey-II data), an adjusted body weight be used. If actual body weight is used to calculate calorie requirements in patients who are obese, energy requirements may be overestimated.
Adjusted body weight is calculated as follows:
Adjusted weight = ideal weight + [(actual edema-free weight-ideal weight) × 0.25]
From practical point of view, monitoring the trends in dry weight and clinical condition of patient should be used to adjust the calorie requirements. This assumes a greater significance as the body weight fluctuates markedly in patients during their stay in ICU or even in dialysis units. However, the modification involves the same principles which help in designing and modifying the diets in ambulatory patients with chronic renal pathology. A diet moderate to rich (depending on caloric needs) in complex carbohydrates is advised. Lower glycemic index carbohydrates (complex carbohydrates) are the preferred carbohydrate sources to prevent hyperglycemia due to insulin resistance. The high phosphorus and/or potassium content of many complex carbohydrates (legumes, whole grains, and fruit) create difficulties in those with stages 3-5 CKD and ESRD. Other strategies to control phosphorus and potassium levels may allow greater consumption of complex carbohydrates. The nutritive values of some common Indian foods have been shown in [Table 1].
Dietary protein in excess of daily requirements is degraded to urea, other nitrogenous waste, acid, phosphate, and sulfate. These waste products accumulate in patients with uremia, leading to muscle catabolism, bone loss, and vascular calcification. It also leads to metabolic acidosis. These pathophysiological changes are of immense significance in patients admitted in dialysis units and ICU with numerous critical states. The metabolic profile is invariably deranged in majority of these patients and requires urgent intervention. It has been shown that adequate correction of acidosis slows the rate of loss of kidney function. Dietary protein restriction also slows the progression of CKD as low protein diets have been reported to slow the rate of progression of chronic renal failure in various studies.,,,, Some studies have even suggested that very low protein diets supplemented with ketoacids, hydroxyacids, and essential amino acids may be particularly effective at slowing the rate of loss of renal function.,,,, However, the universal consensus is lacking as few studies do not agree with these results. The nitrogen-sparing effects of these essential amino acids or ketoacids supplemented diets are due, in part, to the branched-chain amino acids and ketoacids, particularly leucine and its ketoacid analog, alpha-ketoisocaproic acid, that promote protein anabolism., Among the participants in MDRD(Modification in diet in renal disease) study, those prescribed the low-protein diet had significantly faster declines in glomerular filtration rate (GFR) during the first 4 months than those on the usual protein diet. Thereafter, the rate of decline of the GFR in the low-protein, low-phosphorus group was significantly slower than in the group fed the usual protein and phosphorus diet. Over the course of the entire treatment period, there was no difference in the overall rate of progression of renal failure in the two diet groups. However, it is likely that the initial greater fall in GFR in the patients prescribed the low-protein diet may reflect a hemodynamic response to the reduction in protein intake, rather than a greater rate of progression of the parenchymal renal disease. This might in fact be beneficial, reflecting a reduction of intrarenal hyperfiltration and intrarenal hypertension. Clinical results of protein restriction vary due to primary diagnosis and variability in achieving goal protein intakes. In response to catabolic stimulus or inadequate protein or caloric intake, endogenous protein stores also are degraded. Inability to adapt to a low-protein diet may be due to inadequate caloric intake. When calories are inadequate, dietary amino acids are used for energy, increasing the need for muscle stores to supplement visceral protein synthesis. These scenarios are common in the usual ICU setup where majority of the patients exhibit such nutritional pathologies.
Neutral nitrogen balance is achieved in patients with nondialysis CKD with a minimum of 0.6 g/kg/d of high biological value protein in stable nonacidotic patients when adequate calories are given. High biological value protein contains a high fraction of the essential amino acids proportioned approximately according to daily dietary requirements for humans. At least 0.35 g/kg/d should be high biological value protein. Essential amino acids may be supplemented or can be administered as their ketoanalogs. This nutritional balance in critically ill renal patients cannot be achieved without the services of a nephrologist and a well-trained dedicated dietician.
There are no studies which have established any nutritional needs and modifications in patients with kidney disease having an unstable clinical state in ICU. However, the data from the other studies and guidelines can be extrapolated to the patients in ICU. The NKF K/DOQI (The National Kidney Foundation Disease Outcomes Quality Initiative) Clinical Practice Guidelines on Nutrition in CRF recommend 1.2 g protein/kg body weight/d for clinically stable patients on maintenance hemodialysis (MHD). To ensure adequate intake of essential amino acids, at least half of the dietary protein should be of high biologic value. This level of protein intake should maintain neutral or positive balance in almost all clinically stable patients undergoing MHD thrice weekly. In patients on chronic ambulatory peritoneal dialysis, protein intake should be 1.2-1.4 g/kg/d. Higher protein and amino acid losses in peritoneal fluid account for the differences.
Sodium and fluids
Electrolytes and fluid balance has always remained a challenging task for the attending intensivist, especially in patients with any form of CKD. Normally, dietary sodium intake is frequently restricted to 2000-4000 mg/d for patients with CKD in an effort to aid in the control of hypertension, and to avoid excessive thirst and fluid consumption in those patients with oliguria or anuria. Salt substitutes frequently contain potassium chloride, and patients should be instructed to avoid salt substitutes as they can precipitate hyperkalemia. When these patients get admitted in ICU, such therapeutic interventions should be elicited thoroughly so as to manage these patients smoothly. In most nondialyzed patients with advanced renal failure, a daily intake of 1000-3000 mg (40-130 mEq) of sodium and 1500-3000 mL of fluid will maintain sodium and water balance. The requirement for sodium and water varies markedly, and each patient must be managed on an individual basis. Patients undergoing MHD or chronic peritoneal dialysis(CPD) frequently are oliguric or anuric. For hemodialysis patients, sodium and total fluid intake generally should be restricted to 1000-2000 mg/d and 1000-1500 mL/d, respectively.  Because sodium and water can be removed easily with CAPD or other forms of CPD, a more liberal salt and water intake is usually allowed. Indeed, by maintaining a larger dietary sodium and water intake, the quantity of fluid removed from the CPD patient, and hence the daily dialysate outflow volume can be increased. This may be advantageous, since with CPD the daily clearance of small- and middle-sized molecules is directly related to the volume of dialysate outflow. Thus, for some CPD patients, a higher sodium and water intake (e.g. 6-8 g/d of sodium and 3 L/d of water) may enable the patient to use more hypertonic or hyperoncotic dialysate to increase the dialysate outflow volume, thereby increasing dialysate clearances and energy uptake from dialysate, if hypertonic glucose is used.
Renal compensatory mechanisms maintain normal serum potassium levels until the GFR drops below 15- 20 mL/ min. Dietary potassium is generally restricted to 2000-3000 mg/d for patients requiring hemodialysis and 3000-4000 mg/d for patients requiring peritoneal dialysis. There are a number of non-food factors that can cause or contribute to hyperkalemia. Correcting the underlying factors causing hyperkalemia, such as inadequate glucose control, will frequently allow patients a more liberal diet restriction that will encourage good oral intake. The management of such patients assumes a greater significance when they require ionotropic support for maintaining stable hemodynamics.
The rationale for controlling dietary phosphorus and the use of GI binders of phosphate is to prevent and treat hyperphosphatemia, a high serum calcium-phosphorus product, calcium phosphate deposition in soft tissue, and hyperparathyroidism. In renal failure patients, a large dietary phosphorus intake can lead to a high plasma calcium-phosphorus product with increased risk of calcium and phosphate deposition in soft tissues including arteries. Moreover, hyperphosphatemia, by lowering serum calcium, provides a strong stimulus to the development of hyperparathyroidism. Also, animal and human studies suggest that a low phosphorus intake may reduce the rate of progression of renal failure in individuals with CKD. ,,,
Patients with CKD frequently experience hyperphosphatemia when their GFR drops to 20- 30 mL/ min. These changes are more marked in patients requiring ICU admission. A dietary phosphorus restriction of 800-1000 mg/d should be implemented when serum phosphorus rises to >4.6 mg/dL. There is recent evidence that phosphorus excretion is affected when GFR drops below 60 mL/min, contributing to secondary hyperparathyroidism. This mandates the normalization of hemodynamics in critically ill patients with ionotropic support and other appropriate therapeutic interventions. The increased serum parathyroid hormone (PTH) normalizes serum phosphorus level until GFR drops below 20-30. mL/min A dietary phosphorus restriction of 800-1000 mg/d decreases the PTH levels and may reduce bone resorption in those patients with elevated PTH. Patients with hyperphosphatemia frequently receive calcium-containing phosphate binders, which can contribute to hypercalcemia or elevation of the serum calcium-phosphorus product. The National Kidney Foundation recommends that serum calcium-phosphorus product be maintained at <55 mg/dL to prevent soft tissue calcification. Calcium from phosphorus binders should be maintained below 1500 mg/d, and total calcium intake (supplements and diet) should not exceed 2000 mg/d.
Nutritional requirements for most vitamins are not well defined in patients with CKD, but there is some evidence that daily supplements of the following vitamins will prevent or correct vitamin deficiencies:
- Pyridoxine hydrochloride, 5 mg
- Folic acid, 1 mg
Recommended daily allowances for healthy individuals for other water-soluble vitamins
- Vitamin C, 60 mg; higher doses have been associated with increased plasma oxalate levels.
- Supplemental vitamin A is not recommended.
- Vitamin K often is not needed.
- Vitamin D should be supplemented to a plasma level >30 pg/mL.
These deficiencies are severe after institution of dialysis therapy because of the loss of water-soluble vitamins in dialysate on a thrice-weekly regimen. Replacement is similar to CKD, except that 75-90 mg/d of vitamin C, 10-50 mg/d of pyridoxine, and 1-5 mg/d of folate should be prescribed. However, in critically ill patients, such regimens have to be given intravenously wherever possible if enteral nutrition is difficult to establish.
| Conclusion|| |
The estimation of nutritional needs and dietary modifications in patients with CKD, although challenging, can become fairly easy with a close co-ordination between nephrologist, dietician, and intensivist, especially when these patients are admitted in ICU. The nutritional needs and requirement in patients with chronic disease have to be titrated on an individual basis with an emphasis on underlying diseases, nutritional status, severity of renal disease, and so on. To improve our knowledge and concepts of genomics, immunology, and various pathophysiological changes, more and more studies have to be undertaken in ICU involving various patients with chronic renal disease and failure. Such a confluence of studies can help in establishing and modifying the dietary requirements and supplementation, and thereby can possibly help in establishing our own guidelines in the nutritional management of patients in dialysis units and ICU.
| References|| |
|1.||Mitch WE, Remuzzi G. Diets for patients with chronic kidney disease, still worth prescribing. J Am Soc Nephrol 2004;15:234-7. |
|2.||Bajwa SJ, Kulshrestha A. Renal endocrine manifestations during polytrauma: A cause of concern for the anesthesiologist. Indian J Endocrinol Metab 2012;16:252-7. |
|3.||Bajwa SJ, Kulshrestha A. Anaesthesia considerations and challenges during renal transplantation: Current perspectives. Apollo Medicine 2012; 9: 126-132. |
|4.||Bajwa SJ, Kwatra I. Reno-endocrinal disorders: A basic understanding of the molecular genetics. Indian J Endocrinol Metab 2012;16:158-63. |
|5.||Bajwa SS, Kulshrestha A. Critical nutritional aspects in intensive care patients. J Med Nutr Nutraceut 2012;1:9-16. |
|6.||Mehrotra R, Kopple JD. Nutritional management of maintenance dialysis patients: Why aren't we doing better? Annu Rev Nutr 2001;21:343-79. |
|7.||Kopple JD. Pathophysiology of protein-energy wasting in chronic renal failure. J Nutr 1999;129(1S Suppl):247S-51S. |
|8.||Bajwa SK, Bajwa SS, Singh A. Nutritional facts and menopausal symptomatology: The role of nutraceuticals. J Med Nutr Nutraceut 2012;1:42-9. |
|9.||Bajwa SK, Bajwa SJ, Kaur J, Singh K, Kaur J. Is intensive care the only answer for high risk pregnancies in developing nations? J Emerg Trauma Shock 2010;3:331-6. |
|10.||Bajwa SK, Bajwa SJ. Delivering obstetrical critical care in developing nations. Int J Crit Illn Inj Sci 2012;2:32-9. |
|11.||Bajwa SJ, Jindal R, Kaur J, Singh A. Psychiatric diseases: Need for an increased awareness among the anesthesiologists. J Anaesthesiol Clin Pharmacol 2011;27:440-6. |
|12.||Bajwa SS, Kaur J, Bajwa SK, Kaur G, Singh A, Parmar SS, et al. Designing, managing and improving the operative and intensive care in polytrauma. J Emerg Trauma Shock 2011;4:494-500. |
|13.||Strid H, Simren M, Stotzer P. Patients with chronic renal failure have abnormal small intestinal motility and a high prevalence of small intestinal bacterial overgrowth. Digestion 2003;67:129-37. |
|14.||Van Vlem B, Schoonjans R, Vanholder R, De Vos M, Vandamme W, Van Laecke S, et al. Delayed gastric emptying in dyspeptic chronic hemodialysis patients. Am J Kidney Dis 2000;36:962-8. |
|15.||Ross EA, Koo LC. Improved nutrition after the detection and treatment of occult gastroparesis in nondiabetic dialysis patients. Am J Kidney Dis 1998;31:62-6. |
|16.||Natl. Kidney Found. I Init. K-DOQ. Clinical practice guidelines for nutrition in chronic renal failure. Am J Kidney Dis 2000;35:S1-140. |
|17.||Bergstrom J, Furst P, Alvestrand A, Lindholm B. Protein and energy intake, nitrogen balance, and nitrogen losses in patients treated with continuous ambulatory peritoneal dialysis. Kidney Int 1993;44:1048-57. |
|18.||Rigalleau V, Gin H. Carbohydrate metabolism in uraemia. Curr Opin Clin Nutr Metab Care 2005;8:463-9. |
|19.||Maschio G, Oldrizzi L, Tessitore N, D'Angelo A, Valvo E, Lupo A, et al. Effects of dietary protein and phosphorus restriction on the progression of early renal failure. Kidney Int 1982;22:371-6. |
|20.||Rossman JB, ter Wee PM, Meijer S, Piers-Becht TP, Sluiter WJ, Donker AJ. Prospective randomised trial of early dietary protein restriction in CRF. Lancet 1984;2:1291-6. |
|21.||Locatelli F, Alberti D, Graziani G, Buccianti G, Redaelli B, Giangrande A. Prospective, randomized, multicentre trial of effect of protein restriction on progression of chronic renal insufficiency. Lancet 1991;337:1299-304. |
|22.||Williams PS, Stevens ME, Fass G, Bone JM. A randomized trial of the effects of protein and phosphate restriction on the progression of CRF. Nephrol Dial Transplant 1987;7:285. |
|23.||Ihle BU, Becker G, Whithworth JA, Charlwood RA, Kincaid-Smith PS. The effect of protein restriction on the progression of renal insufficiency. N Engl J Med 1989;321:1773-7. |
|24.||D'Amico G, Gentile MG, Fellin G, Manna G, Cofano F. Effect of dietary protein restriction on the progression of renal failure: A prospective randomized trial. Nephrol Dial Transplant 1994;9:1590-4. |
|25.||Mitch WE, Walser M, Steinman TI, Hill S, Zeger S, Tungsanga K. The effect of a keto acid-amino acid supplement to a restricted diet on the progression of CRF. N Engl J Med 1984;311:623-9. |
|26.||Walser M, Hill S, Ward L, Magder L. A crossover comparison of progression of CRF. Ketoacids vs. amino acids. Kidney Int 1993;43:933-9. |
|27.||Teschan PE, Beck GJ, Dwyer JT, Greene T, Klahr S, Levy AS, et al. Effect of a ketoacid-aminoacid-supplemented very low protein diet on the progression of advanced renal disease: A reanalysis of the MDRD feasibility study. Clin Nephrol 1998;50:273-83. |
|28.||Walser M, Hill S. Can renal replacement be deferred by a supplemented very low protein diet? J Am Soc Nephrol 1999;10:110-6. |
|29.||Alvestrand A, Ahlberg M, BergstrÃm J. Retardation of the progression of renal insufficiency in patients treated with low-protein diets. Kidney Int Suppl 1983;16:S268-72. |
|30.||Buse MG, Reid SS. Leucine. A possible regulator of protein turnover in muscle. J Clin Invest 1975;56:1250-61. |
|31.||Mitch WE, Walser M, Sapir DC. Nitrogen sparing induced by leucine compared with that induced by its keto analogue, Î±- ketoisocaproate, in fasting obese man. J Clin Invest 1981;67:553-62. |
|32.||Klahr S, Levey AS, Beck GJ, Caggiula AW, Hunsicker L, Kusek JW, et al. The effects of dietary protein restriction and blood pressure control on the progression of chronic renal disease: The modification of diet in renal disease study. N Engl J Med 1994;330:877-84. |
|33.||Franch HA, Mitch WE. Navigating between the Scylla and Charybdis of prescribing dietary protein for chronic kidney diseases. Annu Rev Nutr 2009;29:341-64. |
|34.||K/DOQI Nutrition Workgroup. National Kidney Foundation kidney disease outcomes quality initiative. Clinical practice guidelines for nutrition in chronic renal failure. Am J Kidney Dis 2000;35:S1-S140. |
|35.||Institute of Medicine (U.S.) Panel on Dietary Reference Intakes for Electrolytes and Water: Dietary reference intakes for water, potassium, sodium, chloride and sulfate. In Ch xviii. Washington, DC: National Academies Press; 2005. p. 617. |
|36.||Heimburger O, et al. Nutritional effects and nutritional management of chronic peritoneal dialysis. In: Kopple J, Massry S, editors. Nutritional Management of Renal Disease. 2 nd ed. Philadelphia Lippincott, Williams and Wilkins; 2004. p. 477-512. |
|37.||Beto JA, Bansal VK. Hyperkalemia: Evaluation dietary and non- dietary etiology. J Renal Nutr 1992;2:28-9. |
|38.||Allon M. Hyperkalemia in end-stage renal disease: Mechanisms and management. J Am Soc Nephrol 1995;6:1134-42. |
|39.||Tomford RC, Karlinsky ML, Buddington B, Alfrey AC. Effect of thyroparathyroidectomy and parathyroidectomy on renal function and the nephrotic syndrome in rat nephrotoxic serum nephritis. J Clin Invest 1981;68:655-64. |
|40.||Ibels LS, Alfrey AC, Huffer WE, Craswell PW, Weil R 3rd. Calcification in end-stage kidneys. Am J Med 1981;71:33-7. |
|41.||Barsotti G, Giannoni A, Morelli E, Lazzeri M, Vlamis I, Baldi R, et al. The decline of renal function slowed by very low phosphorus intake in chronic renal patients following a long nitrogen diet. Clin Nephrol 1984;21:54-9. |
|42.||Lumlertgul D, Burke TJ, Gillum DM, Alfrey AC, Harris DC, Hammond WS, et al. Phosphate depletion arrests progression of CRF independent of protein intake. Kidney Int 1986;29:658-66. |
|43.||National Kidney Foundation. K/DOQI Clinical Practice Guidelines for Managing Bone Metabolism in Chronic Kidney Disease. Am J Kidney Dis 2003;42(suppl 1):S1-92. |
|44.||Kalantar-Zadeh K, Kopple JD. Trace elements and vitamins in maintenance dialysis patients. Adv Ren Replace Ther 2003;10:170-82. |
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