Last updated: Lesson of the Month - March 2016…
on 08 Mar 2016

Renal Nutrition


Andrew Stein  -  UNDER REVIEW (Senior Editor Andy Stein)

Few systematic investigations in the area of renal nutrition have been performed, and controlled trials with an acceptable study design are rare. Therefore:

Key Point: Most recommendations in this chapter should be regarded as expert opinion only.

Albumin and Outcome

In 1990, Lowrie and Lew published a landmark paper which applied logistic regression analysis to more than 12,000 hemodialysis patients; and evaluated the association of various patient descriptors, treatment time (hours/treatment), and various laboratory tests, with the probability of death. Advancing age, white race, and diabetes were all associated with a significantly increased risk of death. Short dialysis times were also associated with high death risk before adjustment for laboratory variables.

Of the laboratory variables, low serum albumin (less than 40 g/L) was most highly associated with death probability. This is one of the reasons why it is thought that nutritional state, especially at the start of dialysis, is thought to be of such prognostic importance. Whether malnutrition can be reversed, and whether that can improve mortality, has not been proven.

In a study of 190 pateints Gamba (1993), and in the CANUSA study (Churchill, 1996) (680 patients), serum albumin just prior to starting CAPD was the most powerful predictor of patient mortality. Blake (1993) found similar results, also in PD patients, with serum albumin correlating with morbidity and mortality. Blake also found that albumin level was primarily influenced by factors (eg age, body size) that are difficult to alter. Jones (1997), in a retrospective analysis of 225 patients, observed that the better predictor of patient and technique survival is not serum albumin at start of CAPD, but the trend of serum albumin over time on CAPD. Kalantar-Zadeh (2003) have described the unexpected relationships between commonly measured biomedical and biochemical parameters and mortality in HD patients (eg higher mortality with low cholesterol).

Controversy Regarding Albumin and Outcome

The biological basis of hypoalbuminaemia in ESRD, is multifactorial and complicated (Kaysen, 1998). This may explain why associations of serum albumin with mortality cannot be easily extrapolated to treatment.

According to Kaysen, "Serum albumin concentration is determined by its rate of synthesis, by the catabolic rate constant (the fraction of the vascular pool catabolized per unit time), by external losses, and by redistribution from the vascular to the extravascular space. Hypoalbuminemia in dialysis patients is primarily a consequence of reduced albumin synthesis rate in both HD and PD patients,and in the case of PD patents, of transperitoneal albumin losses as well. Continuous ambulatory peritoneal dialysis patients are able to increase albumin synthesis to replace losses".

Kaysen continues .. "Thus, ESRD does not directly suppress albumin synthesis. The rate of albumin synthesis is inversely proportional to the serum concentration of one potential acute phase protein (a2 macroglobulin), and albumin concentration is inversely proportional to that of either C-reactive protein on serum amyloid A in both HD and PD patients. The cause of decreased albumin synthesis is primarily a response to inflammation (the acute phase response), although it is possible that inadequate nutrition may also contribute. The cause of the inflammatory response is not immediately evident".

Even though much has been made of the association of a low serum albumin with mortality in ESRD, it is by no means clear that:

  • Malnutrition is the cause of that low serum albumin
  • Malnutrition (as marked by its surrogate, ie albumin) causes death
  • Even if does, that it is possible to correct malnutrition (or serum albumin) over the longterm
  • Even if one could correct malnutrition, this intervention prevents death

Metabolic Acidosis

Even though it is known that the metabolic acidosis of renal failure increases protein breakdown (Straumann, 1992), the role of the correction of acidosis in renal failure remains controversial. In two epidemiological studies a U-shape relationship between serum bicarbonate levels and mortality has been demonstrated in haemodialysis patients. Lowrie and Lew (1990) demonstrated an increased risk of dying if serum bicarbonate levels were <17.5 or >25 mmol/l.

In the DOPPS study, in which a rise in mortality was present if predialysis bicarbonate level was <17 or >27 mmol/l (Bommer, 2004). In this study, it was demonstrated that serum bicarbonate levels between 20.1 and 21.0 mmol/l faced the lowest risk for mortality, and levels of 21.1–22.0 the lowest risk of hospitalisation. From these epidemiological data it can be concluded that predialysis serum bicarbonate levels of 20–22 mmol/l seem to be optimal.

Kraut (2011) has summarised the metabolic consequences of metabolic acidosis in CKD.


The word 'nutrition' was first recorded in the 1550s. Derived from Latin nutritionem ( 'a nourishing'), from nutrire ( 'nourish, suckle')



Acute Kidney Injury


AKI not only affects water, electrolyte and acid–base metabolism but also induces a global change of the 'milieu interieur', with specific alterations in protein and amino acid, carbohydrate and lipid metabolism. Additionally, it exerts a pro-inflammatory reaction and has a profound effect on the antioxidative system. AKI, especially in the ICU setting, rarely represents an isolated disease process. In fact, metabolic changes in these patients are also determined by the underlying disease process and/or co-morbidities, by other organ dysfunction, and by the method and intensity of RRT.

Protein Catabolism

Protein catabolism is the metabolic hallmark of AKI. The metabolism of various amino acids is abnormal. Several non-essential amino acids (eg tyrosine) become conditionally essential, and there are alterations in the intra- and extracellular amino acid pools - as well as in the utilisation of exogenously infused amino acids.

There is hyperglycaemia, caused both by peripheral insulin resistance and the activation of hepatic gluconeogenesis. In contrast to patients with CKD and healthy subjects, this increased glucose formation cannot be suppressed by exogenous nutrient supply. Insulin resistance as defined by hyperglycaemia in the setting of higher insulin concentrations may be associated with mortality in critically ill patients with AKI (Basi, 2005).

Alterations in lipid metabolism are characterised by hypertriglyceridaemia due to an inhibition of lipolysis (Druml, 1996).

Other features include: depletion of antioxidants, induction of a pro-inflammatory state and impaired immunocompetence. Plasma concentration of water-soluble vitamins is reduced. Activation of vitamin D3 is impaired, resulting in secondary hyperparathyroidism. Vitamins E and A and selenium levels are low and there is a profound depression of the antioxidant system.

RRT and Metabolism

Continuous renal replacement therapies (CRRTs), and especially veno-venous haemofiltration (CVVHF) and veno-venous haemodiafiltration (CVVHD-F), have become the treatment modality of choice in the critically ill patients with AKI. Because of their continuous nature and the high filtration rates, these therapies may exert a negative influence on electrolyte and nutrient balance (Druml, 1999).

CRRT causes a significant loss of water-soluble, small molecular weight substances including several nutrients.

Key Point: In continuous RRT, there is a loss of 0.2 g amino acid/L of filtrate, leading to a total daily loss of 10–15 g amino acid, and a protein loss of 5-10 g (depending on the type of therapy and the membrane material used).

Water-soluble substances such as vitamins are also lost in significant amounts (Bellomo, 1991). The administration of large amounts of lactate as substitution fluid, or citrate as anticoagulant, can cause complications such as hyperlactacidaemia or metabolic alkalosis. CRRT also frequently induces electrolyte disturbance, eg hypophosphataemia, hypomagnesaemia and or hyponatraemia.

AKI and Gastrointestinal Function

The influence of AKI on gastrointestinal function remains poorly understood. A positive correlation between impaired gastrointestinal motility and the presence of renal failure has been documented (Barnert, 1998). Moreover, multiple factors are known to negatively affect gastrointestinal function in critically ill patients, eg medications (sedatives, opiates, catecholamines etc), glucose and electrolyte disorders, diabetes or mechanical ventilation.

AKI  is a well-defined major risk factor for gastrointestinal haemorrhage, especially in the upper-gastrointestinal tract. Nutritional support could exert protective effects on the risk of stress ulcers/bleeding.

Nutrition Status and Outcome

Nutritional status is one of the main factors determining outcome. A prospective cohort study in 309 patients showed that severe malnutrition, as evaluated at admission by subjective global assessment (SGA), was present in 42% of patients with AKI (Fiaccadori, 1999). In this study, in-hospital length of stay and mortality were increased in undernourished patients.

Furthermore, malnutrition appeared to be a predictor of in-hospital mortality independently of complications and co-morbidities.

Nutritional Support and Outcome

Several nutrients have an impact on renal function. Both intravenously and enterally administered amino acids increase renal plasma flow and creatinine clearance (renal reserve). There are indications that NG feeding is associated with an improvement in survival in ITU patients with AKI. Experimental studies have reported accelerated recovery of renal function in tube-fed rats. Enteral was superior to parenteral nutrition in this respect. Two clinical studies have suggested that NG feeding is associated with improved outcome in ICU patients (Metnitz, 2002; Scheinkestel, 2003). The effect of oral nutritional supplements (ONS) on renal function in uncomplicated AKI is not known.

Indications for Nutritional Support

Undernutrition is the main but not the only indication for enteral nutrition. In uncomplicated AKI, NG feeding is indicated if normal nutrition and oral supplements are not sufficient to meet estimated requirements. In severe AKI, the recommendations for NG feeding are the same as for other ICU patients. If possible, feeding should be started within 24h. The majority of enteral and parenteral supplements designed for patients with AKI are low in sodium. Freqent dialysis may be necessary to allow adequate volumes of nutrition to be given.

Chronic Kidney Disease, Nephrotic Syndrome and Transplantation

Chronic Kidney Disease

Causes of Malnutrition

The uraemic syndrome leads to undernutrition. Causes include:

• Reduced intake
  - Inadequate dialysis
  - Poor dentition
  - Inability to obtain or prepare food
  - Slow gastric emptying
  - Depression
• Endocrine abormalities
  - Insulin resistance
  - Hyperleptinaemia
  - Secondary hyperparathyroidism
  - Impairment of vitamin D3 activation
• Metabolic abnormalities
  - Altered amino acid metabolism
  - Metabolic acidosis
  - Insulin resistance
  -Abnormal plasma lipid clearance
• Chronic inflammation (MIA Syndrome)
• Intercurrent illness; increased protein catabolism due to enhanced catabolism in intercurrent acute illness, acidosis and inflammation

Low Protein Diet

The uraemic syndrome is associated with loss of appetite and a variety of gastrointestinal adverse effects, which result in reduced nutritional intake. There is a direct correlation between degree of renal insufficiency and reduced intake of normal food. CKD patients spontaneously reduce protein intake, when GFR < 10 mls/min. The MDRD showed that a low-protein diet does not delay the onset of dialysis in patients with CKD (Klahr, 1994). Indeed, protein-restricted diets can result in undernutrition, if not closely monitored.

Malnutrition Inflammation and Atherosclerosis (MIA)

Intercurrent acute illnesses and/or the chronic inflammatory state also augment protein catabolism and can compromise the efficacy of nutritional support. In other words, wasting is part of the inflammatory state associated with atherosclerosis, and is not responsive to dietary nutrient intake. This phenomenon is sometimes called Type 2 Malnutrition, or  'MIA syndrome' ( = malnutrition + inflammation + atherosclerosis) (Stenvinkel, 1999). MIA was proposed to explain the increased CV risk associated with ESRD.

The evolution of atherosclerosis is an inflammatory proces, and there is increasing evidence that C-reactive protein (CRP) enhances this process. There is a strong association between a low serum albumin and a high CRP (Stenvinkel, 1999). In a study by Qureshi (1998), on HD patients, elevated serum CRP (> 20 mg/L), which reflected the presence of infection/inflammation (and was associated with hypoalbuminemia), was more common in malnourished patients than in patients with normal nutritional status - and also more common in elderly than in younger patients.

Patients with CKD have raised circulating levels of CRP and a number of proinflammatory cytokines including IL-6. The low serum albumin levels seen in MIA rather than reflecting poor nutritional intake, may reflect on-going inflammation - as well as the cytokine action on the GI tract.

Nutritional therapy cannot be considered in isolation from other metabolic interventions, such as the therapy of secondary hyperparathyroidism or correction of metabolic acidosis. In diabetic patients, accurate management of glucose metabolism and hypertension is mandatory. Intercurrent disease (eg infection) should be treated.

CKD and Gastrointestinal Function

Nearly all gastrointestinal functions, mainly gastric emptying, can be compromised in CKD patients. Impaired gastric emptying, impaired intestinal motility and disturbances of digestive and absorptive function (eg, biliary and pancreatic secretions), and alterations in intestinal bacterial flora can occur in CKD patients (Kang, 1993). Intestinal fat absorption is delayed. Disturbed intestinal motility is of particular importance clinically. Gastroparesis is most pronounced in patients with diabetic nephropathy. Gastric prokinetic agents (metoclopramide), control of diabetes and treatment of diabetic neuropathy can improve tolerance to enteral feeding (Silang, 2001).

Nutritional Requirements of CKD Patients

An energy intake of 35 kcal/kg body weight/day is associated with better nitrogen balance and is recommended in stable CKD patients in the range of ideal body weight +/- 10%. Overweight or undernourished patients may need adjustments of energy supply. ESPEN's (2006) recommendations for protein requirements of metabolically stable patients are: GFR 25–70 ml/min, 0.55–0.60 g/kg/day; and GFR <25 ml/min, 0.55–0.60 g/kg/day (ie protein restriction). As previously stated, there is no evidence that such an approach delays the onset of dialysis, and it may lead to protein-calorie malnutrition.

For mineral requirements, ESPEN recommends: Phosphate 600–1000 mg/day, Potassium 1500–2000 mg/day and Sodium 1.8–2.5 g/day (ie phosphate, potassium and salt restriction). Salt restriction may help with blood pressure control.

Note: such recommendations, regarding nutritional intake, have to be interpreted as part of a holistic assessment of the patient - eg if the patient is elderly, and supportive care is appropriate, tight dietary restrictions are inappropriate.

Need for Enteral Nutritional Support

In undernourished CKD patients, oral food supplements can be provided in order to optimise nutrient intake. NG feeding is indicated when adequate oral intake is not possible despite dietary counselling and oral food supplements.

Enteral feeding should be considered in the following patient groups with CKD:

  1. Patients with CKD and other catabolic intercurrent acute conditions in whom oral feeding is not possible. These patients should be treated metabolically and nutritionally like AKI patients
  2. CKD patients in whom adequate oral intake cannot be achieved. Overnight NG feeding can be considered in order to optimise nutrient intake
  3. Elderly patients with CKD may require special attention. The nutrient requirements and the need for nutritional support in elderly patients with renal failure have not been studied, although the prevalence of uraemic patients older than 75 years is increasing (Abras, 1982)

Low-protein diets (LPD) should only be prescribed with strict monitoring of energy intake and of nutritional status, in order to prevent undernutrition in patients entering dialysis.

Enteral Feeding Formulae in CKD

Standard formulae can be used for short-term enteral feeding in undernourished CKD patients. But, if feeding is required for more than 5 days, special or disease-specific formulae (protein-restricted formulae with reduced electrolyte content) should be used. There is little evidence for the use of essential amino acids and ketoanalogues, which have been used with very low protein formulae, in an attempt to preserve renal function in conservatively treated CKD patients.

Metabolic Acidosis

Metabolic acidosis in uraemia is an important factor in the activation of protein catabolism. Alkalisation therapy should be considered in all patients with CKD3-4. Though it is uncertain whether better correction of acidosis improves nutrition, and outcome in CKD patients.

In a small prospective study in CKD patients, Verove (2002) found that metabolic acidosis (serum bicarbonate levels <21 mmol/l) could be corrected by oral sodium bicarbonate supplementation (serum bicarbonate levels in both studies after treatment was >24 mmol/l). This resulted in a rise in serum albumin levels, but no other changes in nutritional parameters.

Roderick et al (2007) in a Cochrane Review, assessed the evidence for the benefits and risks of correcting metabolic acidosis. They found that very limited evidence for this therapy, with no RCTs in pre-ESRD patients, none in children, and only three trials in dialysis patients. These trials suggest there may be some beneficial effects on both protein and bone metabolism but the trials were underpowered to provide robust evidence.

Nephrotic Syndrome

Key Point: Long-standing severe nephrotic syndrome (NS) produces a kwashiorkor-like syndrome, which is only partly due to low serum albumin levels, and albuminuria.

For example, reduced hepatic protein synthesis is also a feature of the syndrome. As well as the disturbances of visceral protein and lipid metabolism (increased VLDL, LDL and IDL), abnormalities of muscle metabolism have also been described (Guarnieri, 1989).

In the past, nutritional treatment of NS was traditionally characterised by a high protein intake, in order to compensate for the protein urinary loss and low albumin/protein plasma levels. Higher protein intake experimentally induces increased protein synthesis and increased proteinuria with a negative nitrogen balance and lower plasma protein levels (Kaysen, 1984).

In man, high protein intake (1.6±2.0 g/kg/day) is able to increase: albumin synthesis, at the site of albumin in RNA transcription; fractional catabolic rate of albumin; renal excretion of albumin and protein; plasma phosphate and renin activity. Increased expression of TGF-b, IGF-1 and PDGF are described with higher protein intake. But neither plasma proteins nor skeletal muscle protein synthesis are improved. Therefore, a high protein intake seems to be harmful for the kidney and for nutritional status. With a lower protein intake, protein excretion is definitely decreased.

Changes in glomerular capillary pressure and haemodynamics are responsible for changes in proteinuria. The quality of dietary proteins/amino-acids might be involved. Branched chain amino acid infusion does not influence renal haemodynamics. A direct beneficial relationship between the reduction of urinary protein loss obtained by low protein diet in patients with nephrotic syndrome and the subsequent course has been described (El Nahas, 1987).

An interesting evolution in the nutritional treatment of nephrotic syndrome was more recently proposed: a low protein diet (0.6-0.7 g/kg/day), all of vegetable origin, supplemented with essential amino acids (EAA) or keto-analogues. This treatment has been shown to decrease proteinuria and hyperfiltration, while improving the lipid pattern. The albumin plasma level is not negatively affected. A similar effect on plasma lipid was described using a soy-based vegetal protein diet (0.7 g/kg/day), and no evidence of malnutrition was noticed.

Key Point: For all these reasons, ESPEN (Toigo, 2000) has recommended the following nutritional requirements for patients with nephrotic syndrome: protein: relatively low-protein diet (0.8±1.0 g/kg/day), without replacement of urinary protein loss; energy: 35 kcal/kg/day or more, according to physical activity.

These recommendations are very controversial.


Pre-transplantation Period

Nutritional monitoring and dietetic counselling are required in transplant recipient candidates. Elderly, diabetic, obese, and young people must be particularly followed. If severe malnutrition is recognised, a period of artificial nutritional support may be indicated.

If uncontrolled diabetes, obesity, severe dyslipidaemia and/or hypertension are present, patients are at risk of developing or rapidly worsening atherosclerosis. It is logical that correction of these risk factors by means of diet and drugs be initiated before patients are transplanted. Smoking adds further risk and should be stopped. A prudent programme of weight control should be begun in obese patients. Evidence for these recommendations is not strong. Bariatric surgery should also be considered to make a patient transplantable.

Early Post-transplantation Period

The surgical trauma during transplantation is generally mild and bowel function is rapidly restored. Enteral or parenteral nutrition are not generally needed, as spontaneous oral nutrient intake is resumed. However, surgical trauma, short-term starvation, high-dose steroid therapy, pre-existing protein-energy malnutrition, and a variable delay in restoring kidney function, make transplanted patients prone to develop acute protein-energy malnutrition in the early post-transplant period.

Recovery from uraemic protein-energy malnutrition is slow: 3 months after transplantation, muscle abnormalities (low protein, changed water content and amino acid concentration) are not fully corrected, possibly because of immunosuppressive therapy. Altered water, electrolyte and protein pattern, typical of CKD, has been found 13 months after transplantation. Whilst after 9 years, muscle composition is normal despite chronic steroid therapy (Qureshi, 1984). Ciclosporin has a nitrogen sparing effect in comparison with high-dose steroid therapy (Edelstein, 1992).

The effect of obesity on outcome is unclear. Johnson (2002) showed that obesity was associated with an increase in wound complications, which were generally of minor consequence. No effect on transplant outcomes was discovered. However, Cacciola at al (2008) examined 2 groups with different degrees of obesity. They showed that the patient survival rate at 1 year in overweight patients was 98.9% and 95.6% at 5 years. In obese patients, the survival rate at 1 year was 87.5% and at 5 years was 79.2%. Graft survival rates were also better in the overweight patients.

Teplan (2003) showed that obesity and hyperhomocysteinaemia after renal transplantation can be treated effectively by a combination approach: including modified immunosuppression (corticosteroid withdrawal), long-term diet (IHHD), folic acid and vitamin B6 supplementation, and drugs suppressing digestion or absorption.

Late Post-transplantation period

The late phase of the post-transplant period can still be characterised by increased protein catabolism, and muscle protein status can be impaired in this phase. However, as said above, it has been reported that muscle metabolism and nutrition are normal 9 years after transplantation (Qureshi, 1984). Low protein dietd have been investigated in transplanted patients. Salahudeen (1992) showed that LPD was associated with a significant reduction in plasma renin activity, suggesting that part of the beneficial effect of protein restriction was related to the suppression of the renin-angiotensin system.

One of the most severe metabolic risks in transplanted patients is hyperlipidaemia. The most common lipid pattern is characterised by high total cholesterol and high LDL cholesterol levels (with low HDL3 cholesterol and normal HDL cholesterol). Prednisolone, renal dysfunction, proteinuria, ciclosporin, increased body weight and inappropriate food intake are important factors responsible for dyslipidaemia (Teplan, 1999).


Despite the increasing number of patients on HD and the high incidence of malnutrition in this patient group, experience with enteral nutrition is limited and few systematic studies have been performed.

Risk of Malnutrition in HD

HD patients have a high risk of developing undernutrition. Malnutrition has been reported in 10–70% of HD patients. Moderate to severe undernutrition, which can compromise survival, has been reported in more than 20%. The prognostic impact of undernutrition suggests monitoring of dietary intakes and of nutritional indices may be of benefit (Toigo, 2000; NKF, 2000).

Several large series have demonstrated the high prevalence of malnutrition in HD patients as well as its impact on survival. In a European studyf more than 7000 patients, albumin, transthyretin (prealbumin) and normalised protein nitrogen appearance (nPNA) were below the high-risk thresholds of 35 g/l, 300 mg/l and 1g/kg/day in 20%, 36% and 35%, respectively (Aparicio, 1999).

The following simplified nutritional monitoring has been proposed, based on ESPEN (Toigo, 2000) and US National Kidney Foundation (NKF, 2000) recommendations:

  • Dietary interviews every 6 months
  • SGA every 3 months
  • Body mass index and nPNA monthly
  • Serum albumin and transthyretin every 1–3 months according to nutritional status

Effect of HD on Nutritional Status (above that of CKD)

Several dialysis-specific factors further aggravate the impairment of subjective well being, loss of nutrients, and induction of protein catabolism - thereby contributing to the high incidence of undernutrition. In addition to the above-mentioned factors seen in CKD, anorexia is a major cause for the development of malnutrition in HD (Kalantar-Zadeh, 2004). Most HD patients eat much less than they should.

A further factor is inadequate dialysis prescription. Moreover, the uraemic syndrome, as well as HD per se, is a microinflammatory condition that induces persistent activation of protein catabolism. Intercurrent disease processes, such as infection, enhance catabolism and must be treated consistently. Other 'treatable' causes of undernutrition are acidosis, hyperparathyroidism and gastroparesis (Kopple, 1997).

Effect of HD on Metabolism and Substrate Requirements

The metabolic alterations due to CKD are not completely compensated by HD therapy. Fluid and electrolyte problems are aggravated and several dialysis-associated factors become relevant. Metabolic alterations associated with HD include loss of nutrients (amino acids, vitamins and carnitine), the induction of dialysis-related catabolism, an increase in susceptibility to intercurrent acute conditions (infection) and dialysis-induced amyloidosis. Because of dialysis-induced catabolism, nitrogen balance is usually negative on HD days.

Nutritional Requirements

In acutely ill HD patients the requirements are the same as in AKI patients. ESPENs (2006) recommendations for the requirements of metabolically stable patients are:

Key Point: protein intake: haemodialysis 1.2–1.4 g/kg/day; PD 1.2–1.5; both HD and PD: energy intake 35 kcal/kg BW/day.

ESPENs recommendations for mineral and water requirements are:

Key Point: phosphate 800–1000 mg/day; potassium 2000–2500 mg/day; sodium 1.8–2.5 g/day; fluid 1000mls + urine volume per day.

Due to dialysis-induced losses, water-soluble vitamins can be given: folic acid (1mg/day), pyridoxine (10 mg/day) and vitamin C (100 mg /day). Vitamin D should be given according to serum calcium, phosphate and parathyroid hormone levels.

Routine haemodialysis does not induce significant trace-element losses. However, in depleted patients, zinc (15 mg/day) and selenium (50–70 lg/day) supplementation may be useful.

Effect of Malnutrition in HD on Morbidity and Mortality

Malnutrition is an independent determinant of morbidity and mortality in HD patients. Nutritional status at the beginning of dialysis predicts mortality after 1 year of substitutive treatment (Beddhu, 2003). Several parameters of nutritional state (albumin, transthyretin, cholinesterase, creatinine, cholesterol, and BMI) have a close association with survival in HD patients; albumin and transthyretin showing the strongest predictive value (Avram, 1995; Combe, 2001). It should be noted that the concentration of plasma proteins is also influenced by the inflammatory state of the patient Kopple,1994).

Nutritional Support

Nutritional support is indicated in undernourished HD patients as defined by low nutritional indices, mainly BMI less than 20 kg/m2, body weight loss more than 10% over 6 months, serum albumin less than 35 g/l and serum prealbumin less than 300 mg/l. Oral nutritional support (ONS) improves nutritional status in undernourished HD patients. If nutritional counselling and ONS are unsuccessful, NG feeding should be proposed. A systematic review with meta-analysis has shown that ONS and NG feeding increased serum albumin by 2.3 g/l (95% confidence interval, 0.37–4.18) in maintenance HD patients (Stratton, 2005).

In a randomised controlled trial in 182 undernourished HD patients, standard ONS induced a sustained improvement of serum albumin and transthyretin independently from inflammatory status. The increase in transthyretin during ONS was associated with better survival (Cano, 2005).

HD patient groups, in whom enteral nutrition should be considered, are:

  1. HD patients with intercurrent catabolic acute conditions in whom normal nutrition is not possible
  2. HD patients in whom adequate oral intake cannot be achieved
  3. Unconscious patients on HD (eg on neurology wards or in nursing homes) in need of enteral nutrition

In undernourished HD patients with poor compliance to ONS and not requiring daily enteral NG feeding, intradialytic parenteral nutrition should be considered (Pupim, 2002).

Metabolic Acidosis

The effects of better correction of acidosis on nutritional state in HD patients remains unclear. In a single-blind crossover study design, Williams et al (1997) demonstrated that 27% of patients had metabolic acidosis defined as pH < 7.36 when treated with a 30 mmol/l bicarbonate dialysis solution. When the bicarbonate content of the dialysate was increased to 40 mmol/l (raising pH to > 7.36), this was associated with a rise in triceps skinfold thickness but no change in serum albumin or other nutritional parameters.

Movelli (2009) carried out an uncontrolled trial of oral sodium bicarbonate supplementation in HD patients. They found that oral bicarbonate was effective in correcting metabolic acidosis (MA) in HD patients and did not affect interdialytic weight gain, plasma Na, and blood pressure. The correction of MA was effective in reducing protein catabolism (nPCR) in both inflammed and less inflammed HD patients, but increased serum albumin only in patients without inflammation. In inflammed patients, the correction of MA was not sufficient per se to improve serum albumin concentration.

Treatment of the Malnourished HD Patient

The aetiology of malnutition is multifactorial, so treatment needs to address all possible factors:

  • Dialysis dose
  • Inflammation
  • Metabolic acidosis
  • Consider nutritional support (remains controversial); ONS, NG and PEG feeding should be considered in HD patients
  • Referral to renal dietician




Peritoneal Dialysis

Metabolic Characteristics

Since PD patients usually have better residual renal function, metabolic abnormalities are less pronounced than in patients on HD. However, peritoneal losses of proteins, amino acids and micronutrients are relevant and absorption of glucose is increased.

Protein losses during PD are higher than in HD (5–15 g/day), as are losses of protein bound substances, such as trace elements. Protein loss is further exacerbated by peritonitis, and remains increased for weeks after resolution of the episode. Elimination of amino acids and other water-soluble substances is lower than in HD.

Because most peritoneal solutions have a very high glucose content, PD is associated with a high glucose uptake. Patients on PD, on average, absorb 70% of glucose infused from dialysate. Total energy intake is therefore normal or even enhanced. The high glucose intake can cause obesity, hypertriglyceridaemia, hyperglycaemia, induction or aggravation of diabetes.

Body Composition and Nutritional State

In PD patients, body composition is characterised by fluid overload, low fat-free mass and low serum albumin and prealbumin. Normalisation or an increase in body fat can be observed during PD without concomitant increase in body mass.

Protein-energy malnutrition is present in a significant proportion of incident and prevalent patients undergoing chronic peritoneal dialysis (for review, see Mehrotra, 2003). In a cross-sectional study, patients were found to be more severely undernourished than HD patients (42% versus 30%). In PD versus HD patients, serum total protein and albumin was lower, midarm muscle circumference similar, and relative body weight, skinfold thickness, and estimated percent body fat greater (Cianciaruso, 1995).

Fluid overload is associated with a reduction of nutrient intake (Wang, 2003). As a consequence of excess energy over protein net balance, fat mass can increase concealing a kwashiorkor-like protein malnutrition.

Chronic or acute peritoneal inflammation is per se a catabolic stimulus. The loss of lean body mass is further increased by physical inactivity related to the time-consuming dialysis procedures (Toigo, 2000).

Nutritional Requirements

Acutely ill PD patients have the same nutritional requirements as AKI patients. ESPENs (2006) recommendations for the energy, protein and minerals requirements of metabolically stable PD patients are summarised in the Haemodialysis section of this chapter. Some authors recommend vitamins, pyridoxine (10 mg) and vitamin C (100 mg) supplements.

Nutritional Support

Nutritional support is indicated in malnourished PD patients, based on the same nutritional indices as in HD patients. In patients on PD with insufficient oral intake, oral nutritional support (ONS) can help to optimise nutrient intake. NG feeding is indicated when adequate normal nutrition and ONS are insufficient.

Selected patient groups in whom NG feeding should be considered, are:

  1. PD patients with inadequate oral intake despite nutritional counselling and ONS
  2. PD patients with intercurrent catabolic acute conditions in whom an adequate oral intake is not possible
  3. Unconscious PD patients (eg on neurology wards or in nursing homes) in need of enteral nutrition

Metabolic Acidosis

Stein (1997) demonstrated that better correction of acidosis improves nutritional state and outcome (eg hospitalisation) in a prospective RCT of 200 PD patients.  Furthermore Szeto (2007) has shown positive effects of oral sodium bicarbonate in PD patients.

Key Point: Better correction of metabolic acidosis improves nutritional outcome in PD (and possibly HD) patients.

In 2013, Vashistha found measured bicarbonate significantly higher in peritoneal dialysis patients than HD patients; suggesting that the therapy provides a more complete correction of metabolic acidosis. He also stated "survival data suggest maintaining serum bicarbonate>22 mEq/L for all ESRD patients, irrespective of dialysis modality".

Treatment of the Malnourished PD Patient

The aetiology of malnutition is often multifactorial, so the treatment needs to address all possible factors:

  • Dialysis dose
  • Inflammation
  • Metabolic acidosis
  • Consider nutritional support (remains controversial); consider ONS or NG feeding. PEG feeding is normally avoided in adult PD patients because of the risk of peritonitis
  • Referral to renal dietician


Top Tip: Starting RRT with an albumin <35 g/L carries a poor prognosis. Focus on nutrition in these patients

  1. Most recommendations in this chapter should be regarded as expert opinion only
  2. Continuous renal replacement therapy (eg CVVHF) causes a loss of 0.2 g amino acids/l filtrate, giving a total daily loss of 10–15 g amino acids, with a protein loss of 5-10g per day
  3. Long-standing severe nephrotic syndrome produces a kwashiorkor-like syndrome, which is only partly due to low serum albumin levels, and albuminuria
  4. Protein and energy intake recommendations (European guidelines): haemodialysis 1.2–1.4 g/kg/day; PD 1.2–1.5; both HD and PD; energy intake 35 kcal/kgday
  5. Mineral and water recommendations (European guidelines): phosphate 800–1000 mg/day; potassium 2000–2500 mg/day; sodium 1.8–2.5 g/day; fluid 1000mls + urine volume per day
  6. Better correction of metabolic acidosis improves nutritional outcome in PD (and possibly HD) patients






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