Part I-Nutrition in Kidney Disease: Core Curriculum 2022

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As chronic kidney disease (CKD) progresses, the requirements and utilization of different nutrients change substantially. These changes are accompanied by multiple nutritional and metabolic abnormalities that are observed in the continuum of kidney disease. To provide optimal care to patients with CKD (chronic kidney disease), it is essential to have an understanding of the applicable nutritional principles: methods to assess nutritional status, establish patient-specific dietary needs, and prevent or treat potential or ongoing nutritional deficiencies and derangements. This installment of AJKD’s Core Curriculum in nephrology provides current information on these issues for the practicing clinician and allied healthcare workers and features basic, practical information on epidemiology, assessment, etiology, and prevention and management of nutritional considerations in patients with kidney disease. Specifificemphasis is made on dietary intake and recommendations for dietary patterns, and macro-and micronutrients. In addition, special conditions such as acute kidney injury and approaches to obesity treatment are reviewed.

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Introduction

As chronic kidney disease (CKD) progresses, the requirements and utilization of different nutrients change substantially. These changes are accompanied by multiple nutritional and metabolic abnormalities that are observed in the continuum of kidney disease. To provide optimal care to patients with CKD (chronic kidney disease), an understanding of the applicable nutritional principles and the methods for assessing nutritional status, establishing patient-specific dietary needs, and preventing or treating potential or ongoing nutritional deficiencies and derangements is essential. This installment of AJKD’s Core Curriculum in Nephrology provides current information on these issues for the practicing clinician and allied health care workers, with basic, practical information on epidemiology, assessment, etiology, and prevention and management of nutritional considerations in patients with kidney disease. Specific emphasis is made on dietary intake and recommendations for dietary patterns, and macro-and micronutrients. In addition, special conditions such as acute kidney injury (AKI), and approaches to obesity treatment, are discussed separately.

Epidemiology

Individuals with CKD (chronic kidney disease) are at risk for a spectrum of nutritional disorders that encompass undernutrition, protein-energy wasting (PEW), and electrolyte disturbances. They also face other challenges such as obesity, secondary prevention of cardiovascular disease, and maintenance of a high-quality diet within the constraints of reduced glomerular filtration (Fig 1). Undernutrition includes protein-energy malnutrition and micronutrient deficiencies. Protein-energy malnutrition, which is caused by inadequate protein and energy intake, results in loss of muscle and fat which, if severe enough, can lead to increased frailty, susceptibility to illness, and even premature death. Undernutrition is different from PEW because the loss of muscle and fat may be due to a variety of causes such as illness, inflflammation, acidosis, and insulin resistance, in addition to inadequate nutrient intake.

Figure 1. Chronic kidney disease spectrum with nutritional disorders and nutritional interventions are considered to be important during each identifified phase. Abbreviations: CKD, chronic kidney disease; eGFR, estimated glomerular filtration rate.

Correctly diagnosing PEW is challenging because the suggested criteria are extensive and not always easily assessed in clinical settings. Studies suggest the worldwide prevalence ranges from 11% to 54% in persons with CKD (chronic kidney disease) stages 3-5 and is between 28% and54% in patients requiring dialysis. The global prevalence of protein-energy malnutrition in persons with CKD is difficult to estimate because it varies by region and country and lacks a single diagnostic test that is highly accurate, reproducible, and easy to perform in the clinical setting. Hence, the diagnosis is usually based on a combination of history and clinical examination.

There is some evidence that patients with CKD (chronic kidney disease) are at risk for micronutrients (vitamins, trace elements, electrolytes) defificiency as a result of possible inadequate dietary consumption, reduced absorption, adherence to dietary prescriptions that may limit micronutrient-rich foods, and dialysis procedures that contribute to micronutrient loss. These factors may be compounded by certain illnesses or the use of specific medications. However, the lack of high-quality evidence in this field and the almost complete absence of such studies in patients with CKD (chronic kidney disease) who are not on dialysis make it very difficult to determine the true prevalence of individual micronutrient deficiencies. Overnutrition, which encompasses the other end of the malnutrition spectrum, includes obesity and(rarely) toxicity from excess micronutrient intake. Though protein-energy malnutrition has historically been the major macronutrient derangement in patients with uremia and kidney failure, obesity is arguably now more common in all stages of CKD (chronic kidney disease), at least in theUnited States. Obesity is important as a major risk factor for the development and progression of CKD (chronic kidney disease) and AKI and as an impediment to optimal care of patients with CKD (chronic kidney disease). Obesity in the CKD (chronic kidney disease) population clearly shows a rising trend. From 2011-to 2014 over 44%of persons with CKD (chronic kidney disease) stages, 3-5 in the United States had obesity, with half of such individuals having severe obesity (ie, body mass index [BMI] > 35 kg/m2). This represented a 5 percentage point rise over the prior decade. Similar upward trends can be seen in kidney transplant recipients and patients initiating dialysis. Such trends are likely to continue at least into the near future as the prevalence of obesity in the overall population continues to rise.

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Assessment of Nutrition Stores

Case 1: Ms. P is a 62-year-old woman regularly attending a CKD (chronic kidney disease) clinic, with an estimated glomerular filtration rate (eGFR) of 14 mL/min/1.73 m2. Her weight, 95 kg, has been stable over the last 2 months, ranging from 92 to 94 kg. Upon examination, you note that she is short of breath and has bilateral ankle edema. She says she has been eating less than usual and is less active due to weakness and fatigue.

Question 1: Which of the following is the gold standard for body composition assessment in this patient?

a) Anthropometrics and subjective global assessment (SGA)

b) Dual-energy x-ray absorptiometry (DEXA)

c) Bioelectrical impedance analysis (BIA)

d) Magnetic resonance imaging (MRI)

For the answer to this question, see the following text.

The metabolic changes that occur with declining kidney function often result in altered appetite and changes in food intake. Over time this results in the loss of nutritional reserves, which are the body stores of muscle and fat tissue. Uremia and the associated inflflammation, altered hormones, metabolic acidosis, and changes in gut motility can lead to reduced dietary intake as CKD (chronic kidney disease) progresses. Taste changes, poor appetite, and reduced or restricted nutritional intake result in fat and lean tissue loss, which if coupled with volume expansion and edema may remain undetected. Therefore, monitoring body weight alone is not a sufficient means of assessing changes in nutritional stores.

Bodyweight may remain stable in a state of negative energy balance or undernutrition if edema develops contemporaneously. In dialysis, PEW can be common, and the catabolic state, often due to a combination of reduced intake and inflflammation, leads to loss of muscle and fat tissue. The 2012 consensus statement from the Academy of Nutrition and Dietetics and the American Society of Enteral and Parenteral Nutrition recommends that a diagnosis of malnutrition requires that 2 or more of the following reidentified: insufficient energy intake, weight loss, loss of muscle mass, loss of fat mass, fluid accumulation (which may mask weight loss), and diminished functional status. Assessment of all these characteristics—including assessment of nutritional stores including muscle mass, body fat, and fluid accumulation—is part of the comprehensive nutrition assessment undertaken in patients with CKD (chronic kidney disease). At the simplest level, nutritional status is likely compromised if there is unintentional weight loss or fluid accumulation together with reduced food intake.

Muscle wasting and subcutaneous fat mass loss can be deidentified at specific anatomical sites using a physical examination, as in all forms of SGA of nutrition status. Nephrologists, dietitians, nutrition assistants, and nurses can all undertake the SGA as part of routine care, and many dietitians are trained to do so. Specifically, muscle loss at the temples (temporalis), clavicle (pectoralis, trapezius, and deltoids), shoulder (deltoid), scapula (deltoids, trapezius, infraspinatus, latissimus dorsi), between the thumb and forefinger (interosseous), leg (quadriceps), and lower leg (gastrocnemius) can be identifified by the prominence of bone or hollowing, both identifying loss of muscle tissue. Depletion of fat stores can easily be detected under the eyes (orbital fat pads) and in the upper arms(triceps and biceps skinfold). Fluid accumulation in the extremities or ascites can mask body mass loss if assessed by weight alone. If edema-free weight is not assessed regularly in individuals undergoing dialysis, a reduction in muscle and fat stores may remain undetected until the resulting fluid accumulation is identified clinically.

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Handgrip strength measured using a calibrated grip dynamometer serially in an individual can detect a decrease in physical function. Serum albumin, pre albumin, or BMIare no longer considered useful as single markers of nutritional status. Methods requiring specialist equipment and/or significant training and accreditation in technique, such as assessment of body fat by DEXA or skinfold measurements, are not usually available for routine use. DEXA is considered suitable for the assessment of fat mass in clinical populations. DEXA is a valid technique for measuring body composition in adult patients with CKD (chronic kidney disease), including post-transplant patients. Although DEXA is also influenced by hydration status in maintenance hemodialysis (HD) and peritoneal dialysis (PD) patients, it is considered the gold standard. Therefore, the correct answer to question 1is (b).

Etiology and Implications of Nutritional and Metabolic Derangements in Kidney Disease

Case 2: A 74-year-old woman with a history of CKD (chronic kidney disease) secondary to diabetes is visiting her nephrologist with concerns of anorexia, nausea, and occasional vomiting. During her evaluation, it is noted that her serum creatinine has risen compared with her most recent (6 months prior) levels, from 2.5 mg/dL to 3.6 mg/dL (eGFR 19 and 12 mL/min/1.73 m2, respectively). She has been mostly at home with limited activity since her husband died 6 months ago.

Question 2: Which problem(s) may best explain her recent nutrition and functional decline?

a) Advanced CKD-uremia

b) Depression

c) Decreased physical activity

d) All of the above For the answer to the question, see the following text

Multiple factors affect the nutritional and metabolic status of patients with moderate to advanced kidney disease, and this can lead to adverse consequences. Accordingly, prevention and treatment strategies should involve an integrated approach to reduce nutrient depletion along with interventions that would avoid further losses and replenish already wasted stores. Table 1 displays the dietary and metabolic changes occurring in progressive CKD (chronic kidney disease), their mechanisms, and the resulting symptoms, which may be addressed with nutritional interventions.

A frequent and important cause of PEW in patients with advanced kidney disease is dietary protein and energy intake that is inadequate compared to their needs, primarily due to “uremic” anorexia. The spontaneous and progressive decrease in dietary protein and energy intake seen in CKD (chronic kidney disease) patients not yet on kidney replacement therapy usually improves once maintenance dialysis is commenced or a patient undergoes kidney transplantation. Nevertheless, a substantial portion of patients on maintenance dialysis may still have anorexia due to inadequate dialysis and retention of uremic toxins, intercurrent illnesses, chronic systemic inflflammation, or depression. Some of the dietary restrictions implemented before initiation of maintenance dialysis are often continued to prevent excessive accumulation of electrolytes such as sodium, potassium, and phosphate, although this practice as a preventative measure is no longer encouraged. Maintenance dialysis is also considered to be a catabolic procedure requiring increased energy intake relative to the needs of CKD (chronic kidney disease) patients not yet on kidney replacement therapy.

Provision of an adequate dialysis dose to remove uremic toxins is considered a key measure for preventing and treating PEW in maintenance dialysis patients, and a minimum dose of dialysis has been recommended to avoid uremia anorexia and maintain adequate dietary nutrient intake. Data from randomized controlled trials of HD patients (HEMO study) and PD patients (ADEMEX Trial)suggest that what various guidelines consider adequate dialysis is sufficient to maintain nutritional status, although the HEMO study showed that over time patients lose weight regardless of whether they receive an “adequate” dialysis dose. Raising the dialysis dose above the targets determined in these trials has not been shown to improve the nutritional status any further. The results of the Frequent Hemodialysis Network Trial found no meaningful difference in nutritional markers when in-center HD patients were randomized to 6 times per week compared with those receiving the standard 3 times per week.

Nutrient losses through HD membranes (6-8 g per HDsession), loss of residual kidney function, increased systemic inflflammation from indwelling catheters, use of bioincompatible HD membranes, and PD dialysis solutions can also cause an overly catabolic milieu and increase the minimal amount of nutrient intake required to preserve a neutral nitrogen balance and hence acceptable nutritional stores. Patients who are unable to compensate for this increased need will fall into a state of semistarvation, leading to the development or worsening of PEW.

Systemic inflflammation is a major contributor to wasting in patients with advanced kidney disease. Increased systemic levels of inflflammatory cytokines such as interleukin 1 (IL-1), interleukin 6 (IL-6), and tumor necrosis factor α (TNF-α)are critical in causing exaggerated protein and energy catabolism, leading to sarcopenia and frailty in chronic disease states. Beyond causing greater protein breakdown, the chronic inflflammatory state is associated with lessened physical activity and impaired anabolic actions of insulin and growth hormone; it may also be linked to anorexia on account of its effects on the central nervous system.

In patients with advanced CKD (chronic kidney disease), metabolic acidosis is associated with increased muscle protein catabolism and promotes PEW. Several studies have found improved nutritional status in CKD (chronic kidney disease) patients who are given oral bicarbonate supplementation. Based on recent epidemiologic data showing adverse outcomes with high levels of serum bicarbonate before a dialysis session, a target of 24-26 mmol/L is required for patients to avoid metabolic alkalosis after HD. There is evidence that loss of muscle mass in patients with advanced CKD (chronic kidney disease) is related to 2 key endocrine abnormalities, namely resistance to insulin and to the growth hormone-insulin-like growth factor 1 (IGF-1) axis. Enhanced protein catabolism occurs in insulin-defificient and insulin-resistant states alike. Patients with advanced CKD (chronic kidney disease) also often have other metabolic and hormone disorders (elevated parathyroid hormone concentration, low levels of testosterone, or abnormalities in the thyroid hormone profile), which may also boost hypermetabolism and lower anabolism, leading to excess protein and energy catabolism.

Other comorbid diseases are common in CKD (chronic kidney disease) patients and may worsen their nutritional status. In addition to the well-established role of diabetes, CKD (chronic kidney disease) patients are also likely to be protein depleted on account of gastrointestinal disturbances (eg, diabetic gastroparesis, nausea, vomiting, pancreatic insufficiency, bacterial overgrowth, and impaired protein absorption in the gut). Polypharmacymakes these gastrointestinal complications worse. The answer to question 2 is, therefore (d), all of the above.

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Nutritional Management of Patients With Kidney Disease

In the last decade, there has been a paradigm shift in the nutritional management of CKD (chronic kidney disease). The focus has moved away from the management of specific nutrients and toward the broader perspective of whole diets and dietary patterns. Observational studies suggest that dietary patterns that promote cardiovascular health, such as diets based on eating vegetables, nuts, legumes, whole grains, and fish and poultry, with less red meat and fewer processed foods, are associated with reduced mortality and reduced risk of CKD progression. Evidence from a small number of clinical trials of dietary patterns or nutritional interventions that address the whole diet has demonstrated the beneficial effects of whole-diet interventions for slowing kidney function decline in stages 3-4 CKD and improving protein and energy intake in patients receiving HD and improving the lipid profile in kidney transplant recipients.

Medical Nutrition Therapy

Case 3:

Ms. B is a 56-year-old woman with CKD (chronic kidney disease) secondary to diabetes. Her eGFR is 19 mL/min/1.73 m2, and her diabetes is poorly controlled. Her blood work indicates random blood glucose of 162 mg/dL (9 mmol/L), serum potassium of 5.8 mEq/L (5.8 mmol/L), and serum bicarbonate of 18 mEq/L (18 mmol/L).

Question 3: What factor(s) would you address to treat hyperkalemia?

a) Reduce fruit and vegetables.

b) Correct the acidosis.

c) Treat hyperglycemia.

d) b and c. If hyperkalemia is not resolved, then review her whole diet. For the answer to the question, see the following text.

Medical nutrition therapy in CKD (chronic kidney disease) aims to meet nutritional requirements for food groups, macronutrients, and fiber while reducing the risk of hyperkalemia and hyperphosphatemia. Achieving the balance between adequate and varied nutritional intake and safety is achievable with the skills of a dietitian to educate patients and provide individualized recommendations based on a detailed holistic assessment. Dietitians are also skilled in addressing barriers to improving nutritional intake; they can help improve energy and protein intakes via behavior change approaches. Providing generic advice focused on safety without also ensuring access to a dietitian may increase the likelihood of patients adopting overly restrictive diets resulting inadequate nutrition.

Dietary patterns are rapidly becoming a major focus of medical nutrition therapy in CKD (chronic kidney disease). Encouraging certain dietary patterns is a sharp contrast with the restrictive dietary approaches that have dominated nutrition interventions for decades. The guidelines now suggest that specific nutrient restriction is not needed unless serum levels are elevated unsafely. Therefore, a more individualized approach is encouraged, and dietitians experienced in managing CKD can expand dietary choices for fruit, vegetables, nuts, legumes, and whole grains in a stepwise manner when serum levels permit. Furthermore, adopting a dietary pattern approach enables providers who do not have specific nutrition expertise to provide holistic dietary recommendations to their patients with CKD.

Nutritional therapy in early CKD (chronic kidney disease) should focus on high fruit and vegetable intakes for their beneficial effects on blood pressure, blood lipids, acid-base balance, and fiber content. With mild to moderate reductions in eGFR, a diet high in fruit and vegetables, with moderate amounts of dairy foods and meat and poultry, may be beneficial due to several mechanisms. In studies by Goraya et al (2013)comparing high fruit and vegetable intake to sodium bicarbonate and to control conditions, the fruit and vegetable intake was as effective as sodium bicarbonate for reducing acidosis and slowing the decline in eGFR without increasing serum potassium, and it was superior to sodium bicarbonate for decreasing body weight, systolic blood pressure, and low-density lipoprotein (LDL) cholesterol. Overall, when intake of fruit and vegetables was increased by 2 cups per day, it led to a lower acid load and higher dietary fiber, which may be protective against hyperkalemia due to faster bowel transit time and have favorable effects on gut microbiota.

The Mediterranean diet pattern—which is high in fruits, vegetables, legumes, whole grains, nuts, and olive oil, with moderate amounts of poultry and seafood, and contains little red meat, sweets, or processed foods—can improve the lipid profile of kidney transplant patients and may be beneficial in CKD (chronic kidney disease) to slow down the onset of kidney failure. Dietary patterns based on fresh foods and whole grains are naturally lower in salt and absorbable phosphate, so they have beneficial effects on blood pressure and serum phosphate levels. Dietary education can encourage patients with CKD (chronic kidney disease) to consume a healthy diet by favoring home cooking and reducing the intake of processed and convenience foods.

Table 2 lists the major considerations for nutrition interventions in CKD (chronic kidney disease) and some examples of how more generalized interventions may be delivered in CKD (chronic kidney disease) when medical nutrition therapy is not available. Specific, tailored medical nutrition therapy is implemented by dietitians, who follow a holistic assessment to derive a nutritional diagnosis and consider multiple factors that impact food-related behaviors.

As eGFR declines and hyperkalemia develops, there are several potential contributing factors to consider. Hyperglycemia and metabolic acidosis can cause potassium to shift extracellularly. Correction of acidosis with sodium bicarbonate or treatment of hyperglycemia with insulin can restore equilibrium and allow the potassium to shift back into cells. Thus, the best answer to question 3 is (d). If serum potassium is elevated with normal acid-base balance and euglycemia, dietary modifications to reduce potassium intake from lower nutritional value foods are recommended after other non-dietary causes such as medications are considered and addressed, if medically appropriate to do so. Meat, fish, and dairy foods often contribute more dietary potassium than fruits and vegetables, so consideration of the dietary pattern or a wholediet plan is required for optimal management. It is important to note that dietary modifications are now recommended only to treat hyperkalemia and not as a preventative measure. When possible, individuals with CKD should be encouraged to eat a variety of plant foods for dietary fiber, cardioprotection, and the beneficial effect on the gut microbiome.

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