Abstract
A number of nutrition-related and catabolism-related complications arise with the loss of kidney function. These abnormalities are collectively termed protein-energy wasting (PEW) syndrome and have important consequences on patients’ quality of life and clinical outcomes. This chapter discusses key concepts in the etiology, diagnosis, and management of PEW in chronic kidney disease.
Keywords
albumin, body composition, catabolism, diagnosis, inflammation, mortality, nutrition, oral nutrition supplements, protein, protein-energy wasting, quality of life, screening assessment
Outline
The Role of the Kidney in Nutrient Homeostasis, 194
Rationale and Nutritional Requirements for Patients with Chronic Kidney Disease, 194
Rationale, 194
Energy Requirements, 194
Protein Requirements, 195
Electrolytes, 197
Dietary Quality, 197
Protein-Energy Wasting in Chronic Kidney Disease, 197
Concept of Protein-Energy Wasting, 197
Causes of Protein-Energy Wasting in Chronic Kidney Disease, 199
Prevalence of Protein-Energy Wasting in Chronic Kidney Disease, 200
Consequences of Protein-Energy Wasting in Chronic Kidney Disease, 201
Nutrition Screening and Assessment, 201
Treatment of Protein-Energy Wasting in Chronic Kidney Disease, 203
Dietary Counseling and Use of Oral Nutritional Supplements, 204
Intradialytic Parental Nutrition, 205
Nonnutritional Interventions, 206
Summary and Conclusions, 207
The Role of the Kidney in Nutrient Homeostasis
The kidneys regulate dietary sodium, potassium, and phosphate levels in the body. As kidney function declines, there are alterations in maintaining nutrient homeostasis. As kidney disease progresses, there is a reduction in the excretion of solutes, resulting in their accumulation in body fluids. The body is therefore less able to adapt to changes in dietary intake. Table 13.1 summarizes the role of the kidney in maintaining nutrient homeostasis and nutritional implications in chronic kidney disease (CKD).
| Kidney Functions in Nutrient Homeostasis | Nutritional Disorders That Appear in CKD |
|---|---|
| Regulation of sodium and potassium via tight control of body fluid osmolality | Dietary sodium, potassium, and fluid modification |
| Peptide and amino acid balance via the synthesis, degradation, filtration, and reabsorption of amino acids and the elimination of urea, uric acid, and creatinine | Reduced appetite, nausea, vomiting, and anorexia and thus increased risk for suboptimal energy and nutrient intake |
| Glucose homeostasis via hormone degradation, excretion, and reabsorption | Altered glucose regulation |
| Clearance of low-molecular-weight proteins, including insulin, growth hormone, and leptin | Altered appetite signaling |
| Acid–base balance—the regulation of pH by removing excess hydrogen ions | Acidosis; may consider dietary acid load |
| Vitamin D 3 activation via hydroxylation of calcidiol to calcitriol for the regulation of calcium, phosphorous, and parathyroid hormone | Altered renal bone metabolism May require modification of dietary phosphorous |
Rationale and Nutritional Requirements for Patients with Chronic Kidney Disease
Rationale
CKD is a global health problem, and appropriate nutritional intervention strategies are an essential component in the management of CKD across the spectrum of disease. Adopting a healthy diet, addressing obesity, and achieving optimal diabetes control might slow the decline in glomerular filtration rate and reduce the rates of reaching end-stage renal disease (ESRD). Limiting the intake of certain foods or nutrients may reduce the accumulation of metabolic products and prevent hypertension, proteinuria, and other cardiovascular and bone abnormalities. Nutritional management must consider the failing principle functions of the kidney, such as excretion and homeostatic and hormonal regulation ( Fig. 13.1 ). A large body of research has been focused mainly on individual dietary characteristics (single nutrients). More recently, however, there has been a shift toward the evaluation of whole dietary patterns in understanding the role of diet in the development and progression of CKD.
Energy Requirements
Understanding energy needs in the CKD population is important to enable adequate provision of nutrition to avoid protein-energy wasting (PEW) and conversely to limit overweight and obesity given their contribution to the progression of cardiovascular and renal damage. CKD-specific energy intake guidelines suggest that patients with CKD require 30 to 35 kcal/kg/day, which is greater than individuals without CKD because of their increased resting energy expenditure (REE). Inflammation and comorbidities associated with CKD and ESRD may all contribute to an increased REE. Adequate energy intake is usually required to maintain neutral or positive nitrogen balance ; however, assessment should be made on an individual basis.
Both protein and energy requirements should be adjusted to attain a healthy body weight (express as per ideal body weight [IBW]) and be adjusted for age because of the higher protein needs of the elderly population. A patient’s daily energy expenditure should be considered too, because it has been suggested that current energy recommendations (30 to 35 kcal/kg/day) may overestimate a patient’s needs. Lean body mass is the primary determinant of energy expenditure, and a low lean body mass is common within the CKD population, offering a possible explanation for their lower than anticipated energy requirements. Furthermore, although reduced food intake is often seen in patients with CKD, a degree of underreporting in energy intake cannot be excluded. As a whole, some authors propose that energy requirements for patients with CKD (30 to 35 kcal/kg/day) should be revised or individualized, especially for those who are sedentary.
A final consideration for determining energy requirements is glucose-based exchanges that take place within peritoneal dialysis (PD). These provide in the region of 300 kcal per exchange, contributing up to 30% of the total daily energy intake of patients undergoing PD. This should be taken into consideration when assessing energy intake in these patients.
Protein Requirements
For stable patients with CKD not requiring dialysis, the recommended protein intake is 0.6 to 0.8 g/kg/day, of which more than two-thirds should be of high biological value. Habitual protein intakes in the general population are usually higher; hence, this level of protein intake is often called low or reduced protein intake. Reducing protein intake (compared with usual intake in the general population) may result in a reduction in uremic symptoms and slower progression of kidney failure. Lower protein diets may also improve hyperkalemia and hyperphosphatemia. Furthermore, in patients with established CKD, a lower protein intake, compared with an unrestricted intake, has been associated with a 32% lower occurrence of renal death. However, the optimal level and type of protein intake (animal vs. plant) remains unclear. Recent studies have suggested that plant proteins may be more protective than animal proteins in the primary prevention of CKD. Nonetheless, confounding factors make drawing conclusions challenging given that plant protein is not consumed in isolation. Fig. 13.2 illustrates the key differences in the nutritional profile of plant and animal proteins, highlighting that the benefits of consuming a plant-based diet probably go beyond the source of protein.
The efficacy and safety of a “low-protein diet” remain equivocal. The arguments for and against are illustrated in Table 13.2 .
| Rationale | For | Against |
|---|---|---|
| Efficacy of low- protein diet | Improves signs and symptoms of insulin resistance, osteodystrophy, and peripheral neuropathy. | Benefits reported in experimental models, but clinical evidence is lacking. |
| Slowing CKD progression rate | Findings are inconsistent findings because of variation in study design. Meta-analysis (Hahn et al., 2018, in press/under review, Cochrane ) suggests very low protein diets (0.3–0.4 g/kg) may delay progression to end stage. | Benefits reported in experimental models, but publication bias favors positive results. Meta-analysis (Hahn et al., 2018 in press/under review, Cochrane ) reported no difference in progression to end stage between low- (0.5–0.6 g/kg) and normal-protein (0.8–1.0 g/kg) diets. |
| Renoprotective effects | May help decrease albuminuria, proteinuria, and total sodium and phosphate intake. | No additional benefit beyond renin-angiotensin-aldosterone system blockade and blood pressure reduction. |
| Safety and lack of adverse effects | Supervised diet management preserves nutritional status, does not jeopardize survival, improves symptom score. | May induce or exacerbate malnutrition if unsupervised. |
| Adherence | Good adherence noted in a number of intervention studies. | Quality-of-life outcome measures have not been assessed. |
Use of a very-low-protein diet (0.3 g/kg IBW/day plus keto-analog of amino acid supplements) in patients with advanced CKD is regarded as an effective treatment to delay renal death by delaying commencement of dialysis for 1 to 2 years. Switching to a very-low-protein diet should be carefully considered and managed to avoid nutritional inadequacies.
Protein intake should be increased on starting dialysis, because those with higher protein intakes have had improved rates of survival. Higher protein requirements are a result of dialysis-related protein loss, greater energy expenditure, and persistent inflammation. PD protein loss can be considerable; however, variation among individuals in transporter status and energy and protein intake and choice of dialysate should also be considered.
Nutritional recommendations tend to be made based on total nutrient intakes (i.e., total protein intake per day); however, the dietary pattern (timing and portion size) of protein intake may be an important consideration in the CKD population. In muscle metabolism research in healthy and older populations, there has been a shift away from total daily protein intake targets toward specific dose and timing recommendations. In healthy individuals, protein ingestion is a key stimulus for preserving skeletal muscle mass under rest and increasing skeletal muscle mass under exercise training conditions. Although dependent on age and recent exercise stimuli, general recommendations suggest that each meal should contain approximately 0.25 g of high-quality protein per kilogram of body weight (or an absolute dose of 20 to 40 g) evenly distributed across three to four meals each day to optimize muscle protein synthesis. Furthermore, the amino acid content of dietary proteins should be considered, because leucine content appears to be a critical factor in postprandial muscle protein synthesis. Studies are yet to be conducted in populations with CKD; however, it seems prudent to consider an even distribution of protein intake across each day when nutritional counseling or education is undertaken with patients.
Electrolytes
Sodium and Fluid Balance
Hypertension is a well-established cause and complication of CKD, and dietary interventions reducing salt intake have been found to be effective in reducing hypertension. Sodium is thus an important nutritional consideration given its influence on blood pressure as well as fluid retention and its role in exacerbating renal damage. Dietary assessment should identify sources of packaged and preprepared foods (e.g., canned soups, processed meats, and ready-made meals) given that sodium is often added during manufacturing. In the early stages of CKD it is recommended to restrict salt intake to moderately low levels (<6 g/day of salt or <100 mmol of sodium). Furthermore, the restriction of salt may help manage thirst and thus aid compliance with fluid restrictions ( Table 13.3 ).
| Strategies to Decrease Fluid Intake | Strategies to Decrease/Manage Thirst |
|---|---|
| Spread out fluid allowance throughout day. | Avoid savory snacks. |
| Use smaller cups or tea cups. | Limit adding salt during cooking/at the table. |
| Use the jug method to aid awareness. | Hard-boiled sweets/mints/chewing gum can stimulate saliva production. |
| Perform self-monitoring of intake and output. | Suck on frozen segments of lemon or lime. |
| Administer artificial saliva spray. | |
| Sparingly use ice cubes. |
Phosphorus
Those with renal impairment gradually lose the ability to excrete phosphorous, resulting in hyperphosphatemia, which has been found to be a strong predictor of mortality in patients with advanced stages of CKD. The role of serum phosphate in the pathogenesis of vascular calcification and left ventricular hypertrophy might explain the link between elevated concentrations of serum phosphate and a higher mortality in dialysis patients. Inorganic phosphorous found as an additive in processed foods is more biologically available compared with organic phosphorous found in plant and animal foods. Excess consumption of phosphorus-rich food can be managed via dietary change targeting inorganic phosphorus and nutrient-poor foods first, then taking into account the phosphorous-to-protein ratio of animal and plant origin and the use of phosphorous binders and dialysis ( Table 13.4 ).
| Electrolyte | Nonfood Causes | Food Causes |
|---|---|---|
| Potassium | Constipation Acidosis—bicarbonate Hyperparathyroidism Missed/inadequate dialysis Insulin insufficiency Drugs Potassium containing Affecting potassium excretion (ACE inhibitors, ARBs, beta blockers, NSAIDs) Potassium-sparing diuretics (spironolactone, amiloride) Cellular trauma (hemolyzed blood samples, post–blood transfusion, infection, GI bleed, crush injury, gangrene) | Salt substitutes Chips, crisps, potato products Nuts, chocolate Fruit juice Not boiling vegetables Excessive fruit consumption |
| Phosphate | Binder compliance Binder dose/regimen Parathyroid hormone/Ca 2+ management | Dark-colored carbonated drinks, chocolate drinks, condensed and evaporated milks, malted milk drinks, fudge Processed foods such as sausages, ham, corned beef, breaded chicken, cheese spread, processed cheese, and instant sauces (often contain phosphates or phosphoric acid) Organ meats (liver, kidney, heart, pate) Oily fish |
Potassium
Individuals with CKD are at risk for hyperkalemia given the role of the kidneys in potassium homeostasis. Hyperkalemia has been associated with higher mortality in ESRD and dialysis patients because of its arrhythmogenic effects. Recognizing nondietary causes, avoiding medications that might promote potassium retention (such as renin-angiotensin-aldosterone system inhibitors), and reducing intake of high-potassium foods with low nutritional value are recommended as initial steps to address and prevent hyperkalaemia (see Table 13.4 ). Potassium is associated with healthy, desirable foods such as fruit and vegetables; hence, practitioners should prioritize the avoidance of foods with poor nutritional value first when considering food causes of hyperkalemia so as not to compromise the nutritional adequacy of the diet.
Dietary Quality
Traditionally, dietary management in CKD/ESRD has focused only on modifying single nutrients, such as protein, phosphorus, potassium, or sodium, that can accelerate kidney damage or result in adverse outcomes. It is possible that the overall dietary pattern may be more influential in the development and progression of CKD than an excess or deficiency of specific macro- or micronutrients. Recent observational studies have indicated that a diet rich in fruits, vegetables, fish, cereals, whole grains, dietary fiber, and polyunsaturated fatty acids (and low in saturated fatty acids), such as the Mediterranean and DASH (Dietary Approaches to Stop Hypertension) styles of eating, may be beneficial for patients with CKD. Thus a shift away from interventions that focus on single nutrients toward the overall dietary picture may be advantageous given that healthy dietary patterns have been associated with lower mortality in observational studies. In contrast, the “Western diet” is characterized by a high intake of red meat, animal fat, sweets, and desserts and a low intake of fruits, vegetables, and low-fat dairy products. Adherence to a Western diet has been associated with increased risk for albuminuria, more rapid kidney function decline, and increased inflammation.
Several small studies using dietary pattern interventions, such as increasing fruit and vegetables and the Mediterranean diet pattern, have reported improvements in blood pressure and blood lipids; however, no dietary pattern intervention studies have yet examined mortality or CKD progression outcomes.
Protein-Energy Wasting in Chronic Kidney Disease
Concept of Protein-Energy Wasting
PEW was proposed in 2007 by the International Society of Renal Nutrition and Metabolism as a concept defining the multifactorial nature of metabolic processes and nutritional consequences of uremia in CKD. PEW involves a hypermetabolic state that promotes protein catabolism, attributed to both metabolic consequences of CKD—including inflammation, oxidative stress, uremia, metabolic acidosis, diminished efficacy of anabolic hormones, and a multimorbid condition—and the catabolic nature of hemodialysis (HD), which can lead to protein losses and muscle and fat wasting ( Fig. 13.3 ). Therefore the reduction in energy and protein intake associated with PEW is often secondary to other factors, rather than a primary consequence of inadequate access to adequate energy and protein to meet nutritional needs, as in primary malnutrition. In clinical practice the reduction in nutritional intake and causes may be difficult to separate because they are synergistic and may exacerbate each other.
Causes of Protein-Energy Wasting in Chronic Kidney Disease
Understanding the features that contribute to the etiology of PEW is critical to inform appropriate assessment and treatment strategies. Box 13.1 lists the major contributing factors to PEW in CKD, and it is important to note that inadequate intake is just one of the five major causes of PEW. Furthermore, adequate nutritional intake will not alter some of the contributing factors, such as hypermetabolism secondary to inflammation, the reduction in anabolic response, the catabolic nature of HD, insulin resistance, or frailty associated with reduced physical activity. A multifaceted therapeutic approach for this complex syndrome is therefore necessary.
- 1.
Decreased protein and energy intake
- a.
Anorexia, problems in organs involved in nutrient intake
- b.
Dietary restrictions
- c.
Depression, frailty, dependency
- a.
- 2.
Hypermetabolism
- a.
Increased energy expenditure
- b.
Metabolic acidosis
- c.
Inflammation
- d.
Hormonal disorders
- i.
Insulin resistance of CKD
- ii.
Increased glucocorticoid activity
- i.
- a.
- 3.
Decreased anabolism
- a.
Resistance to GH/IGF-1
- b.
Testosterone deficiency
- c.
Low thyroid hormone levels
- a.
- 4.
Comorbidities and lifestyle
- a.
Comorbidities (DM, CHF, depression, CAD, PVD)
- b.
Poor physical activity
- c.
Unhealthy dietary pattern
- a.
- 5.
Dialysis
- a.
Nutrient losses into dialysate
- b.
Dialysis-related inflammation and hypermetabolism
- a.
CAD, Coronary artery disease; DM, diabetes mellitus; GH, growth hormone; IGF-1, insulin-like growth hormone 1; PVD, peripheral vascular disease.
Decreased Protein and Energy Intake
Several observational studies have found that spontaneous protein intake decreases as CKD progresses. In addition, the dietary modifications prescribed to reduce protein intake and to prevent hyperkalemia and hyperphosphatemia in CKD stages 4 and 5 may further contribute to poor nutrient intake if these modifications are presented as restrictions only and are not accompanied with counseling on alternative food choices and strategies to ensure adequate nutrient intake. An important cause of undernutrition in CKD is reduced appetite, which decreases with declining estimated glomerular filtration rate and is reported by as many as 35% to 50% of dialysis patients. Appetite is typically driven by the endocrine system; however, in HD patients, factors related to the dialysis and alterations in the gastrointestinal system, as well as hedonic and social implications, can reduce appetite, and meal times can be missed if eating is not permitted during dialysis.
Hypermetabolism
Increased energy expenditure
REE is usually normal in stable maintenance dialysis or CKD patients. However, REE is increased during the HD procedure or in the presence of comorbidities such as cardiovascular disease, severe hyperparathyroidism, poorly controlled diabetes, inflammation, and PEW. Higher energy intake may correct the energy deficit because of increased REE under these circumstances, although it will not reverse the cause of increased energy expenditure and higher intakes may need to be maintained over the long term to prevent unintentional weight loss.
Persistent inflammation
Increased concentration of inflammatory cytokines in CKD is the result of both reduced renal clearance and increased production, stimulated by comorbidities, dialysis, and genetic factors. Inflammation induces appetite loss through central mechanisms blocking specific receptors in the melanocortin system, inhibiting feeding behavior and promoting energy expenditure and protein catabolism. Peripheral effects include mucosal inflammation in the mouth, periodontitis, gastritis, and bacterial infections, which can also have a secondary effect via a reduction in nutritional intake as a result of pain or discomfort during or after eating.
Metabolic acidosis
Metabolic acidosis causes protein catabolism through a reduction in albumin synthesis contributing to hypoalbuminemia. Correction of acidosis has been found to improve nutritional status, likely through decreased protein turnover, improved appetite, and total protein intake. The mechanism of action through decreased protein degradation has been demonstrated in both HD and PD.
Decreased Anabolism
Resistance to insulin/insulin-like growth factor 1
Resistance to insulin, growth hormone (GH), and insulin-like growth factor 1 (IGF-1) are implicated in loss of muscle mass in adult patients with CKD. Insulin and IGF-1 normally bind distinct cell surface receptors to prevent loss of muscle protein. Although current evidence suggests that myofiber shrinkage caused by accelerated protein degradation is the predominant mechanism for loss of muscle mass, both myofiber shrinkage and muscle cell fusion are regulated by insulin and IGFs. This has led to the hypothesis that the integrated outputs of these insulin/IGF–activated signaling pathways determines the balance between protein accretion and loss, determining overall changes in muscle mass.
Testosterone deficiency and low thyroid hormone levels
Testosterone is an anabolic hormone that induces skeletal muscle hypertrophy by promoting nitrogen retention, stimulating fractional muscle protein synthesis, inducing myoblast differentiation, and augmenting the efficiency of amino acid reuse by the skeletal muscle. In CKD, more than 40% of dialysis patients are testosterone deficient. Testosterone deficiency in CKD patients has been associated with anemia and erythropoietin hyporesponsiveness, as well as with reduced muscle mass and strength.
Available data cannot distinguish if low thyroid hormone levels in CKD patients with PEW are an adaptation that reduces energy expenditure and minimizes protein catabolism in PEW. Low triiodothyronine (T3) levels in CKD correlate with systemic inflammatory markers, endothelial dysfunction, and both all-cause and cardiovascular mortality, although the relationship with mortality is mediated through inflammation. Correction of metabolic acidosis in dialysis patients improves these hormonal derangements.
Comorbidities and Poor Physical Activity
Comorbidities
Common comorbidities that arise as a consequence of the failing kidney also contribute to catabolism, resulting in PEW. As Table 13.5 shows, these factors share common etiological mechanisms with PEW.
| Comorbidity | Possible Effects Related to Cause of PEW |
|---|---|
| Diabetes | Gastroparesis, inflammation/oxidation, insulin deprivation (type I), insulin resistance |
| Cardiovascular disease/heart failure | Cachexia, inflammation, glucocorticoid release, sympathetic nerve overactivity, increased circulating angiotensin II, insulin resistance, decreased activity, pain |
| Peripheral vascular disease | Reduced activity, ulcers, inflammation, pain |
| Edema | Inflammatory cytokine release, gut edema, leg ulcers, decreased physical activity, pain |
| Hyperparathyroidism, CKD-MBD | Increased energy expenditure, glucose intolerance, hypovitaminosis D, muscle wasting, gastric ulcers, heart disease |
| Anemia | Frailty, decreased activity, iron deficiency, high-output heart failure |
| Infections | Inflammation, reduced appetite, increased REE, pain |
| Depression/dementia | Unwillingness to eat, anorexia, inability to obtain/prepare food, inflammation, decreased activity |
Poor physical activity
Reduced physical activity plays a major role in both the cause of PEW and the associated adverse outcomes. Individuals with poor physical activity are at higher risk for developing CKD as a result of associated obesity, diabetes, hypertension, and heart disease. Furthermore, complications of CKD, including anemia, edema, and muscle wasting, limit exercise capacity, which, at the extreme level, can affect the ability to perform usual activities of daily living. In CKD stage 3 to 5, median peak oxygen consumption is decreased, which can limit exercise capacity, and muscle weakness is common, although exercise training can improve functional capacity and muscle strength.
Dialysis
Hemodialysis
The HD procedure activates an inflammatory cascade, and amino acid and protein losses occur during dialysis. This catabolic process together with low nutrient intake reduces nutrient availability for muscle synthesis and acute-phase reactant synthesis, resulting in the breakdown of muscle protein. Concurrent amino acid supplementation during the dialysis session can prevent or reverse these effects. Further, optimizing dialysis provision or increasing the frequency of the dialysis procedure has been associated with improvements in nutritional markers because of a reduction in uremic factors. Finally, HD results in a more rapid loss of residual renal function, which is also associated with poor nutritional status.
Peritoneal dialysis
In PD, losses of amino acids into the dialysate of up to 60 g/week occur. In addition, greater losses occur during an episode of peritonitis, as inflammation leads to muscle catabolism. In both cases, these losses increase the protein requirement for dialysis patients. It has been found in PD patients that loss of residual kidney function contributes to PEW.
Prevalence of Protein-Energy Wasting in Chronic Kidney Disease
The prevalence of undernutrition in CKD patients varies depending on the assessment methodology employed, geographical region, and criteria used to define nutritional status. There is no single measure of nutritional status in CKD, and a combination of biochemical anthropometric and nutritional intake assessment measures is recommended.
Few PEW prevalence studies have been done among nondialysis CKD patients. Those that used subjective global assessment (SGA) describe a prevalence of 12% to 18% in CKD stage 3 to 4 patients. Those using serum albumin suggest that PEW is present in 20% to 40% of patients with CKD stage 3 to 5 who are not on dialysis, although this suggests that inflammation is present, and may not be associated with a poorer nutritional status, which may account for the higher prevalence rates when albumin is used rather than a global measure of nutritional status.
PEW becomes much more common in the ESRD/dialysis patient. Studies suggest prevalence rates of between 20% to 70% for PEW or undernutrition in patients undergoing either HD or PD, using malnutrition‐inflammation score (MIS) or SGA methods to assess nutritional status and PEW. Differences in nutritional status in dialysis patients across the world may be due to the adequacy of dialysis treatment in different countries, the usual diet, socioeconomic status, and the type of dialysis treatment used. Improvements in dialysis membranes and water purity over time are also likely to affect the inflammatory processes associated with dialysis and may have contributed to a reduction in the prevalence of undernutrition in more recent studies.
Consequences of Protein-Energy Wasting in Chronic Kidney Disease
Nutrients are the substrates for energy, tissue synthesis, and metabolism and are necessary for life. Undernutrition and hypermetabolism, the two features of PEW, lead to a number of metabolic abnormalities, such as inflammation, oxidative stress, and impaired immune function, which per se or in addition to other factors increase the risk for poor quality of life, infection, hospitalizations, cardiovascular disease, and mortality.
Mortality, Cardiovascular Events, Infections, and Hospitalizations
Most markers of PEW have been associated with adverse patient outcomes in HD patients, including the incidence of hospitalizations, increased healthcare costs, and increased risk for infections, cardiovascular events, and death.
An important aspect of epidemiological studies is their observational nature, which does not allow us to differentiate whether these associations with adverse outcomes are causal in nature. It is ethically difficult to design randomized controlled trials targeting treatment of PEW to assess the impact on mortality and quality of life. Several epidemiological studies have explored this issue based on the potential of providing oral nutritional support to hypoalbuminemic patients through quality improvement initiatives. In one study hypoalbuminemic individuals receiving nutritional support had a 34% reduction in 1-year mortality risk compared with those who did not receive it. Nutritional support in persistently hypoalbuminemic HD patients reduced hospitalizations rates during the subsequent year by approximately 20% versus those who did not receive it. Implementation of a protocol to provide nutritional support during HD on diagnosis of hypoalbuminemia and to maintain albumin within normal range was associated with a 30% reduction in mortality compared with similar patients not receiving nutritional support.
Frailty and Poor Quality of Life
PEW plays an important role in the development and progression of frailty and poor quality of life in patients with CKD. Frailty and the individual components of frailty (unintentional weight loss, self-reported exhaustion, measured weakness, slow walking speed, low physical activity, and reduced muscle mass less than the 90th percentile for the age- and sex-matched general population) are common, closely related with PEW and muscle wasting, and associated with morbidities and mortality in patients with CKD, especially those requiring maintenance dialysis therapy. The Chronic Renal Insufficiency Cohort study revealed that the prevalence of frailty in CKD stage 2 and stage 4 is 7% and 43%, respectively, indicating that muscle loss and frailty, as with PEW, may develop and progress during the course of CKD. In a study of nondialysis CKD and incident HD patients, muscle mass, evaluated by multislice computed tomography, declined over time. PEW also is strongly associated with a poor quality of life. In a cohort study of quality of life, as evaluated with the Short Form 36 questionnaire, and PEW, measured using the MIS, in 800 stable prevalent HD patients in the United States, PEW was associated with worse quality-of-life scores for general health and physical and mental health component scores.
Nutrition Screening and Assessment
Systematic screening and assessment of nutritional status are essential in the management of patients with CKD. Nutrition screening aims to identify nutritional risk and initiates the systematic process of nutrition assessment. Nutrition assessment involves collecting and interpreting relevant information to identify nutrition-related problems, including PEW. This allows for the implementation and monitoring of an appropriate intervention.
There is no single measure that can provide a valid diagnosis of PEW in CKD given that its cause is multifactorial in nature. A range of measures should therefore be assessed, including anthropometric changes, biochemical parameters, and dietary intake. Data should, however, be interpreted with caution because nutritional markers such as albumin may be influenced by fluid status, inflammation, and renal replacement therapy. Furthermore, anthropometric measurements may be skewed by the presence of edema. Careful consideration of these confounding factors must be given before making a diagnosis.
Screening Tools
The goal of screening is to identify individuals who are at risk for undernutrition (and PEW) or who are malnourished and require nutrition intervention, including referral to a registered dietitian for nutrition assessment. Screening tools use measures that can be routinely collected in clinical practice, including body weight, other visual and palpable signs of muscle wasting, and changes in food intake. Screening can virtually be performed by any healthcare professional. There is no consensus on the frequency of nutritional screening in chronic diseases such as CKD, although monthly to 3-month intervals have been proposed. Table 13.6 describes several screening tools currently used in clinical practice. Is it important to screen patients for nutritional status, but the choice of screening tool is less important. These screening tools, however, are generic and may not be able to identify individuals with CKD who are at risk for malnutrition if changes in body weight are a key component of the tool, because often loss of body mass is masked by a concomitant increase in edema in advanced stages of CKD.
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