OPTA—malnutrition in chronic renal failure
1Vivantes Klinikum im Friedrichshain, Berlin, Germany, 2University Hospital, Essen, Germany, 3Dialysezentrum, Kiel, Germany, 4University Hospital, Vienna, Austria
Correspondence and offprint requests to: Prof Dr Martin K. Kuhlmann, MD, Vivantes Klinikum im Friedrichshain, Klinik für Innere Medizin, Nephrologie, Landsberger Allee 49, 10249 Berlin, Germany. Email: martin.kuhlmann{at}vivantes.de
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Abstract |
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 Top Abstract Definition of protein-energy...Epidemiology and pathophysiologyDiagnosis of malnutritionDietary recommendations in...Treatment of malnutrition in...References |
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Protein–energy malnutrition (PEM) is common among patients with advanced chronic kidney disease (CKD stages 4 and 5) and is associated with an increased risk of morbidity and mortality. Early recognition and treatment of malnutrition is essential to improve the outcome of patients with advanced CKD and those undergoing maintenance peritonealdialysis and haemodialysis treatment.
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Definition of protein–energy malnutrition |
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TopAbstractDefinition of protein-energy...Epidemiology and pathophysiologyDiagnosis of malnutritionDietary recommendations in...Treatment of malnutrition in...References |
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Protein–energy malnutrition (PEM) is defined as a lack in supply of sufficient energy or protein to meet the body's metabolic demands as a result of either an inadequate dietary intake of protein, intake of poor quality dietary protein, increased demands due to disease, or increased nutrient losses.
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Epidemiology and pathophysiology |
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TopAbstractDefinition of protein-energy...Epidemiology and pathophysiologyDiagnosis of malnutritionDietary recommendations in...Treatment of malnutrition in...References |
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According to published reports roughly 20–50% of patients on maintenance haemodialysis or peritoneal dialysis suffer from PEM. In the majority of dialysis patients, malnutrition is mild to moderate, only in approximately 10% of patients severe PEM can be found. Protein–energy malnutrition develops during the course of chronic kidney disease (CKD). CKD stages 3 and 5 are associated with a spontaneous reduction of the mean protein intake from 1.0 g/kg body weight/day to about 0.5 g/kg body weight/day [1] accompanied by a reduction in energy intake. There are little data on the prevalence of PEM in pre-dialysis CKD stages, but a change in body composition including a reduction in body cell mass has recently been reported [2]. The presence of protein–energy malnutrition at the initiation of dialysis therapy is associated with higher risks of mortality and morbidity [3].
Cardiovascular disease is the number one cause of death among dialysis patients, followed by infections. Despite its high prevalence, malnutrition is rarely listed as cause of death, probably due to the fact that malnourished patients rather die from complications, such as heart disease or infection than from malnutrition itself. A strong association between malnutrition, inflammation and arteriosclerosis (MIA-syndrome or malnutrition inflammation complex syndrome, MICS) has been found in dialysis patients and among patients with chronic renal failure, suggesting that chronic inflammation contributes to accelerated atherosclerosis and the development of malnutrition [4–6].
Two forms of MIA syndrome have been described, type 1 and type 2: type 1 MIA originates primarily from insufficient dietary protein and energy intake and is rarely associated with concomitant diseases. Serum albumin is not reduced or at most to a moderate level and C-reactive protein (CRP) levels are not or only slightly increased. Possible causes for type 1 MIA are listed in Table 1.
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In contrast, type 2 MIA develops on the basis of chronic inflammation and shows a strongcorrelation with accelerated atherosclerosis and cardiovascular disease. Patients with type 2 MIA usually have multiple comorbidities, serum albumin levels are substantially reduced and CRP levels increased. A dysbalance between pro-inflammatory and anti-inflammatory cytokines favoring inflammation is advocated as the pathophysiological concept for type 2 MIA [6].
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Diagnosis of malnutrition |
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TopAbstractDefinition of protein-energy...Epidemiology and pathophysiologyDiagnosis of malnutritionDietary recommendations in...Treatment of malnutrition in...References |
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The nutritional status of a patient can best be judged by combination of clinical parameters, laboratory findings and certain technical examinations. There is no single measure that provides a comprehensive evaluation of the nutritional status.
Clinical parameters
Clinical symptoms
The leading clinical symptom of malnutrition is a continuous weight loss which may be masked by an increase in body water content. The weight loss is slow and often does not even bother the patient before it is accompanied by a reduction in physical stamina and by muscle weakness. Reductions in subcutaneous fat and in muscle mass in specific locations are the clinical hallmark of a loss in body mass. In more advanced stages of malnutrition vomiting and diarrhoea may occur before in later stages the development of oedema and ascites due to visceral protein deficiency can be observed.
Body weight
Body weight should always be interpreted under the aspect of the oedema-free normal body weight, which is the height-corrected average normal body weight in the absence of oedema (men: height (cm) – 100; women: [height (cm) – 100] – 10%). To accurately assess changes in body weight, oedema- and ascites-free dry weight needs to be achieved. In dialysis patients weight changes may be due to gain or loss of body mass or due to alterations in hydration status.
Body mass index (BMI)
The Quetelet-Index, calculated from a subject's height and weight, is widely used for categorizing underweight, normal weight, overweight and obesity. By current definition a BMI <18 kg/m2 is defined as underweight. Since malnutrition is a dynamic process going along with a steady weight loss even in overweight subjects, the threshold of 18 kg/m2 is a very late indicator of malnutrition and should not be used as a sole indicator of nutritional status.
Anthropometry
Anthropometry is a semiquantitative quantification of the various body compartments, particularly bone, muscle and fat. Anthropometric assessment includes besides body weight, height and skeletal frame size, the measurement of skin-fold thickness (fat mass) and mid-arm muscle circumference (muscle mass) [7]. The method depends, however, to some degree on experience and skills of the examiner. Anthropometric measurements are currently not applied in routine clinical use.
Subjective global assessment (SGA)
This simple technique is a reproducible and useful instrument for bed-side assessment of the nutritional status based on subjective and objective aspects of the medical history in conjunction with physical examination. The degree of malnutrition is evaluated by means of a structured evaluation form focusing on nutrient intake, physical activity and body composition. Patients are asked about weight changes during the last 6 months, eating behaviour, gastrointestinal symptoms and nutrition-related functional symptoms. The physical examination includes an evaluation of the patient's muscle mass and subcutaneous fat mass for detection of any fat and muscle wasting. Following these procedures the nutritional status is classified into three categories by a composite scoring system: normal nutritional status, mild to moderate malnutrition and severe malnutrition. SGA has been used in many clinical studies, and its value for assessment of nutritional status is well established [8]. However, the results obtained through SGA can vary depending on experience and skills of the examiner [9].
Assessment of dietary protein and energy intake
Patients tend to overestimate the quantity of their own nutrient intake [10]. Therefore, a detailed analysis of the patient's eating habits and nutrient intake is required to identify changes in nutrient intake. It is recommended that dialysis patients periodically maintain 3-day dietary records followed by dietary interviews conducted by an individual trained in calculating nutrient intake from diaries and interviews. The interview should include questions about meal frequency, meal composition as well as clinical symptoms associated with malnutrition (nausea, vomiting, diarrhoea and intestinal problems). The interdialytic weight gain besides drinking habits depends on the solid nutrient intake. Therefore, sudden changes in interdialytic weight gain are important and early indicators of alterations in eating behavior [11].
Assessment of appetite
Diminished appetite is a major cause for anorexia and malnutrition in end-stage renal disease patients. Kalantar-Zadeh et al. [12] reported diminished appetite in 38% of the 331 haemodialysis patients investigated, 7% had poor appetite and 31% had fair appetite. In the Hemodialysis (HEMO) Study, one-third of the 1846 patients reported a diminished appetite, 23.8% had fair appetite and 8.8% had poor or very poor. A higher percentage of patients had poor or very poor appetite on dialysis treatment days (12.7%) as compared with non-dialysis treatment days (5.4%). Poor appetite is a risk factor for hospitalization and probably for death of haemodialysis patients [12,13].
Pathogenesis of anorexia in haemodialysis patients is multifactorial and includes
- accumulation of middle molecules
- altered amino acid pattern (reduced essential/non-essential amino acid ratio, low-branched chain amino acids, high level of tryptophan)
- hormones, such as leptin or ghrelin
- neuropeptides, such as neuropeptide Y [14].
Laboratory parameters
Laboratory techniques allow determination of the visceral protein levels (negative acute phase reactants). The laboratory parameters listed below differ with regard to their half-life (T1/2). They allow a longitudinal assessment of nutritional status.
Total protein (T1/2: 6 weeks)
The total protein concentration is a long-term parameter of nutritional status. Total protein levels represent to a large extent serum albumin levels which are in turn influenced by inflammation.
Serum albumin (T1/2: 20 days)
Serum albumin concentration is influenced by hepatic synthesis and degradation as well as by the loss via urine and dialysate. Dietary factors are not the single cause of hypoalbuminaemia in CKD patients. In uraemia patients, hypoalbuminaemia is most closely linked to the presence of inflammation and/or metabolic acidosis. Reduced protein intake leads to decreased albumin synthesis, while a chronic inflammatory state and chronic or acute stress results in increased albumin degradation [15]. Serum albumin does not only serve as an indicator of nutritional status but as a negative acute phase reactant, also serves as an indicator of chronic inflammation. Serum albumin concentration is negatively correlated with mortality in patients on maintenance dialysis [16]. Although no single ideal measure of nutritional status exists, the serum albumin concentration is considered to be a useful indicator of protein–energy nutritional status in dialysis patients. Intensive dietary counselling results in an increase in serum albumin concentration [10].
Prealbumin (T1/2: 2–3 days)
As a precursor of serum albumin, prealbumin (transthyretin) reflects protein intake and visceral protein generation over the previous 2–3 days. Like albumin, prealbumin also is a negative acute phase reactant and thus bears the same problems in interpretation as albumin. Prealbumin levels <30 mg/dl are associated with increased mortality risk and correlate with other indices of PEM in dialysis patients [17].
Transferrin (T1/2: 8 days)
Transferrin levels are affected by the visceral protein generation rate but are primarily influenced by iron status, with iron deficiency increasing, and iron excess reducing hepatic transferrin synthesis. Transferrin, thus is not a sensitive indicator of nutritional status.
Serum cholesterol
Serum cholesterol concentration is affected by carbohydrate but not by protein intake. In the presence of malnutrition, serum cholesterol levels <150–180 mg/dl are frequently observed. However, the use of lipid lowering medication and the fact that cholesterol, like albumin, is negatively influenced by acute or chronic inflammation, renders this protein too insensitive and non-specific to be used as an indicator of protein–energy nutritional status. Dialysis patients with serum cholesterol concentrations <150–180 mg/d should be evaluated for nutritional deficits as well as for other comorbid conditions.
Serum pahosphate
The recommended dietary protein intake of 1.2–1.3 g/kg body weight/day for patients on maintenance dialysis is associated with a phosphate intake which is clearly higher than 1000 mg/day. Decreased dietary protein intake is associated with hypophosphataemia unless phosphate resorption from bone due to pronounced secondary hyperparathyroidism masks the decrease in serum phosphate. In catabolic states, hyperphosphataemia may prevail despite low dietary phosphorus intake. The presence of a low serum phosphate in dialysis patients who do not receive phosphate-binding agents indicates insufficient dietary protein intake.
Bicarbonate
Metabolic acidosis activates protein catabolism, whereas proteolysis is reduced when acidosis is compensated [18]. Pre-dialysis bicarbonate concentrations should be aimed to be 
22 mmol/l.
C-reactive protein (CRP)
As a positive acute phase reactant hepatic CRP synthesis is stimulated by acute and chronic inflammation/infection and stress. Serum albumin CRP and behave in an inverse proportional fashion during an acute phase reaction. CRP is not an indicator of nutritional status but is helpful in interpreting levels of other visceral proteins.
Serum creatinine
Creatinine is a breakdown product of muscle metabolism. While creatinine generation is dependent on muscle mass and dietary intake of foods rich in creatine or creatinine, the serum creatinine concentration also depends on the level of residual renal function. In anuric dialysis patients the predialysis serum creatinine level will be proportional to dietary protein intake and skeletal muscle mass. There is no threshold for serum creatinine concentration as an indicator for nutritional status. It is recommended that the nutritional status should be evaluated in anuric dialysis patients with pre-dialysis serum creatinine levels less than approximately 10 mg/dl [19].
Pre-dialysis blood urea nitrogen (BUN) concentration
The BUN concentration is a result of the balance between urea generation rate, protein synthesis and degradation and urea excretion by dialysis or the native kidney. Under conditions of a balanced metabolic situation, BUN is directly dependent on dietary protein intake. Under catabolic conditions, endogenous protein is metabolized resulting in additional nitrogen appearance and an increase in BUN. In anabolic situations dietary protein is utilized for protein synthesis, thus reducing nitrogen appearance and BUN levels. Both, a repeatedly low pre-dialysis BUN or a longitudinal decrease of pre-dialysis BUN may be used as indicator for insufficient dietary protein intake.
Normalized protein equivalent-nitrogen-appearance (nPNA)
The normalized protein equivalent-nitrogen-appearance (nPNA) or nPCR (protein catabolic rate), is a measure of nitrogen balance. The nPNA is calculated from total nitrogen appearance, which comprises the sum of dialysate, urine and fecal nitrogen losses, and the post-dialysis increment in body urea-nitrogen content. In clinically and metabolically stable patients, PNA can be used to estimate protein intake. However, in a catabolic situation PNA will exceed protein intake due to net degradation and metabolism of endogenous protein. Conversely, in anabolic situations PNA will underestimate actual protein intake dietary protein due to accrual of new body protein pools. Thus, especially in malnourished patients nPNA will not be a sensitive indicator of realistic protein intake. On the other hand, nPNA seems better suited for monitoring the nutritional status during treatment of malnutrition.
Technical methods
Dual energy X-ray absorption spectrometry (DEXA)
Whole body DEXA is a reliable, non-invasive method to assess fat mass and fat-free mass in dialysis patients with high levels of precision and accuracy in dialysis patients [20]. DEXA is currently the best method available for analysis of body composition, however, DEXA is cost intensive and only available at a limited number of clinical centres and therefore, cannot be employed for routine clinical use.
Bioimpedance
Body cell mass (BCM) and body water content can be assessed using single frequency bioimpedance analysis or multifrequency bioimpedance spectroscopy [21,22]. Nevertheless, there is still some controversy with regard to the value of this method.
Hand grip muscle strength
The measurement of hand grip muscle strength correlates with nutritional status when measurements are made using normalized devices. This method is amenable for routine clinical use as a measurement of muscle strength and nutritional status [23].
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Dietary recommendations in chronic kidney disease stages 3–5 |
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TopAbstractDefinition of protein-energy...Epidemiology and pathophysiologyDiagnosis of malnutritionDietary recommendations in...Treatment of malnutrition in...References |
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CKD Stage 3 (glomerular filtration rate (GFR) 60 – 30 ml/min per 1.73m2)
A reduced protein intake (0.6–0.8 g/kg body weight/day) with a caloric intake of at least 35 kcal/kg body weight/day is recommended for patients with CKD. Data on the effects of dietary protein restriction on progression of renal insufficiency are contradictory, however, a meta-analysis came to the conclusion that reducing protein intake appears to slow progression to kidney failure [24]. It is unclear however, if dietary protein restriction represents an additive effect in addition to the effects of adequate blood pressure reduction and of blood pressure-independent renal protection by angiotensin-converting enzyme inhibitors or angiotensin II receptor antagonists. In type I diabetics, progression of renal insufficiency was reduced by dietary protein reduction and optimal blood pressure control in an additive manner [25]. Dietary protein supplementation to compensate for renal protein loss in the nephrotic syndrome is not recommended. Dietary protein restriction generally bears the risk for development of malnutrition. Any dietary intervention thus needs to be accompanied by dietary counseling.
CKD Stages 4–5 (GFR < 30 ml/min per 1.73m2)
A dietary protein restriction of 0.6–0.8 g/kg body weight/day with a caloric intake of 30–35 kcal/kg body weight/day is recommended for patients with advanced (CKD). However, in patients consuming uncontrolled diets a decline in spontaneous protein and energy intake is particularly notable below a GFR of about 25 ml/min together with a progressive decline in anthropometric values, and biochemical markers (e.g. serum albumin, transferrin, cholesterol and total creatinine excretion) of nutritional status [1]. Therefore, a dietary protein restriction should only be prescribed to patients with documented excessive nutrient intake. Dietary protein restrictions should be discontinued if signs of malnutrition develop.
Maintenance dialysis treatment
Dietary protein requirements increase in patients on maintenance dialysis. This is due to catabolic effects of the dialysis procedure itself as well as to the loss of amino acids and proteins through the dialysate [26]. Basal energy expenditure and energy requirements increase in chronic dialysis patients [27]. Dietary protein intake greater or equal to 1.0–1.2 g/kg body weight/day (based upon oedema-free normal weight) is recommended. This corresponds to approximately 100 g protein/day for an 80 kg patient. In addition, any peritoneal protein loss in peritoneal dialysis patients should be compensated for by increased dietary protein intake. Caloric intake should correspond to the activity level of the patient. Under conditions of light physical activity, patients younger than 60 years old should receive approximately 35 kcal/kg body weight/day, whereas older patients require approximately 30 kcal/kg body weight/day [19]. Consumption of a protein- and energy-riched meal during the hemodialysis session decreased whole-body protein breakdown and increased protein synthesis and oxidation abolishing the negative effect of dialysis on whole protein balance [28].
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Treatment of malnutrition in dialysis patients |
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TopAbstractDefinition of protein-energy...Epidemiology and pathophysiologyDiagnosis of malnutritionDietary recommendations in...Treatment of malnutrition in...References |
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At present, only a limited number of studies on treatment of malnutrition in dialysis patients are available. Some data show that increases in protein and energy intake lead to increases in body weight and serum albumin concentration. In two independent studies, the regular ingestion of energy- and protein-enriched dietary supplements resulted in an improved nutritional status of dialysis patients [29,30]. The meal supplements were given orally, either daily [29] or during dialysis sessions exclusively (3x per week, 475 kcal and 16.6 g protein per dose) [30]. Prior to the initiation of any dietary intervention, the target oedema-free standard weight of the patient should be determined using NHANES data tables. Initially the patient should be counseled to maintain a dietary protein intake of at least 1.2 g protein/kg target weight/day, energy intake should be set according to physical activity between 30 and 35 and maximally 40–45 kcal/kg target weight/day. Fat intake should not exceed more than 30% of the total caloric intake. An enhanced protein and caloric intake can primarily be achieved through specific dialysis-adapted oral dietary supplements. In cases of severe malnutrition, tube feeding or the placement of a percutaneous gastrostomy tube may be required.
Practical considerations for diagnosis and therapy of malnutrition (Figure 1)
Patient-screening
Patients suffering from advanced CKD stages 4 and 5 which do not require maintenance dialysis, should be screened at least once per year for the presence of malnutrition. After initiation of dialysis, the nutritional status of the patient should be determined within 4–6 weeks and in regular intervals every 6–12 months following the initial examination. Screening should involve an interview with an emphasis on dietary history. Significant changes in interdialytic weight gain, as well as absolute changes in weight or BMI should be noted. Serum albumin, cholesterol, phosphate and urea (pre-dialysis) should be analysed. If malnutrition is suspected, additional parameters should be investigated.
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Additional diagnostic procedures
Subjective global assessment together with measurements of pre-albumin, transferrin, bicarbonate and CRP levels as well as determination of the Kt/V and nPNA are required for further assessment of the nutritional status. Based on these results a decision on the necessity for dietary intervention should be made. If no evidence for malnutrition is obtained, additional dietary supplementation is not required, and recommendations for protein and caloric intake should be made according to oedema-free normal body weight.
Treatment strategies
If malnutrition has been confirmed, dietary counselling by a trained renal dietician should be initiated. Counselling should involve a detailed and quantitative evaluation of dietary protein and energy using dietary diaries. The patient or a relative should keep a dietary record over a period of at least 3 days. Possible causes of malnutrition (Table 1) should be treated, and the administered dialysis dose (Kt/V) should be adapted to the patient's target weight. Dialytic adequacy has a critical role in prevention and treatment of malnutrition. Daily haemodialysis or six haemodialysis sessions weekly improves appetite and food intake probably caused by
- decreased dose of medications (e.g. phosphate binders, antihypertensive drugs)
- fewer dietetic restrictions
- lower levels of uraemic toxins [10,14].
Further treatment strategies depend on the extent of malnutrition. Dietary interventions should always be accompanied by physical exercise in order to promote the build-up of muscle mass instead of fat mass.
Patients with mild to moderate malnutrition should receive detailed dietary counseling with the aim to increase dietary protein and energy intake. Dietary recommendations should be oriented toward the pre-defined oedema-free target weight. The use of special dietary products may not be necessary in patients suffering from mild to moderate malnutrition. An increase in protein intake will necessarily be associated with an increased dietary phosphorus intake and the development or worsening of hyperphosphataemia. Phosphate binder prescription need to be adjusted in these cases.
In cases of severe malnutrition, an intensive dietary counseling should be undertaken to increase spontaneous protein and energy intake. However, a sole increase in spontaneous dietary energy intake is unlikely to meet the metabolic needs of those patients. Patients in this category are treated most effectively through oral administration of dietary products formulated specifically for dialysis patients (high protein and energy density with low potassium and phosphorus content). Intradialytic administration of oral supplements may improve patient compliance and motivation. If the administration of such preparations fails to improve nutritional status within a given time frame, insertion of a gastric tube or a percutaneous gastrostomy tube (PEG) should be considered. The use of intradialytic parenteral nutrition (IDPN) should be limited to severely malnourished patients in whom oral intake is insufficient to meet nutritional needs [10]. IDPN without interdialytic therapeutic measures does not seem suitable for the treatment of severe malnutrition. Intradialytic oral nutrition has recently been shown to improve the nutritional status in malnourished dialysis patients [31].
Malnutrition is an unusual cause of decreased muscle mass in uraemia. Muscle protein loss is caused by activitation of caspase-3, which cleaves the complex structure of muscle to provide substrates for the ubiquitin-proteasome pathway [32]. Protein breakdown by caspase-3 and the ubiquitin-proteasome system in muscle are stimulated by the same signal: a low caspase-3 activity [33]. Thus, a therapeutic strategy for blocking muscle loss that occurs in uraemia is to stimulate the activities of phosphatidylinositol 3-kinase [32,33].
Treatment monitoring
After therapy initiation the nutritional status should be assessed regularly at 6–8 weeks intervals. Dietary records, nutrition-related laboratory parameters and nPNA should be analysed regularly to evaluate therapeutic progress and to monitor patient compliance. Nutrition therapy must be intensified if malnutrition persists or worsens. In cases with only moderate malnutrition but resistance to dietary interventions, the insertion of gastric or PEG tube should be considered early enough before further deterioration occurs. Treatment intensity may be reduced stepwise if the nutritional status improves.
Practical suggestions for dialysis units
- The importance of adequate patient nutrition should be emphasized with patients and nursing staff.
- Nursing staff should be encouraged to regularly participate in courses pertaining to nutrition.
- ‘Nutrition specialists’ should be designated and trained from amongst the nursing staff who are available to patients and colleagues as a consultant for questions related to nutrition.
- Time required for dietary counseling of patients by nursing staff should be taken into account when planning work schedules (approximately 8–10 h/week for 80 dialysis patients).
- Dietary counselling should be established for every new dialysis patient.
- Cooperation with other dialysis units should be developed to facilitate access to and exchange of nutrition-specific information.
- Nephrologists should be aware of current scientific advances in the area of nutrition related to CKD patients.
Conflict of interest statement. None declared.
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TopAbstractDefinition of protein-energy...Epidemiology and pathophysiologyDiagnosis of malnutritionDietary recommendations in...Treatment of malnutrition in...References |
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