Nutritional problems in adult patients with chronic kidney disease

c l i n i c a l q u e r i e s : n e p h r o l o g y 1 ( 2 0 1 2 ) 2 2 2 e2 3 5

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Review article

Nutritional problems in adult patients with chronic kidney disease Anita Saxena* Associate Professor, Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Raebarely Road, Lucknow 260014, India

article info

abstract

Article history:

Chronic renal failure (CRF) impairs not only appetite but also impairs immune function,

Received 28 June 2012

resulting in increased susceptibility to infections and poor wound healing and may

Accepted 8 July 2012

predispose to inflammatory diseases. Every strategy should be used to avoid complications

Available online 6 August 2012

of chronic kidney disease (CKD) manifested in uremic state including anorexia, nausea, vomiting leading to malnutrition, fluid and electrolyte imbalance leading to volume

Keywords:

overload, hyperkalemia, metabolic acidosis, and hyperphosphatemia, as well as abnor-

Chronic kidney disease

malities related to hormonal or systemic dysfunction such as hypertension, anemia,

Nutrition

hyperlipidemia, bone disease, pericarditis, peripheral neuropathy, and central nervous

Hyperphosphatemia

system abnormalities. With decline in GFR, nutrient requirements change. Nutritional

Hyperkalemia

status should be assessed periodically. Low protein diets are beneficial for CKD stages 1e5,

Fluid balance

but nutritional management should be such that the nutritional status is not compromised. In order to maintain proper nutritional status patients on maintenance dialysis require high protein diet. Timely diagnosis of protein-energy-wasting (PEW) is important for early initiation of nutritional intervention and treatment. Management of hypertension, bone mineral disease, fluid overload and gastroparesis should be given prime importance. Copyright ª 2012, Reed Elsevier India Pvt. Ltd. All rights reserved.

The term “protein-energy-wasting” (PEW) has been proposed to describe conditions such as protein-energy malnutrition, malnutrition-inflammation complex syndrome, malnutrition-inflammation atherosclerosis syndrome, kidney wasting disease and uremic cachexia which are associated with inadequate nutrient intake, decreased body protein and/or reduced energy reserves.1,2 PEW defines loss of somatic and circulating body protein mass and energy reserves2 (Table 1).

1.

2.

Diagnosis of PEW

Timely diagnosis of PEW is important for early initiation of intervention and treatment.1 Criteria for diagnosing PEW2 are given in Table 3.

3. Nutritional implications and complications of renal dysfunction

Causes of malnutrition

Malnutrition and inflammation are two major causes of PEW. Table 2 summarizes nutritional and non nutritional causes which lead to PEW in CKD population.

Chronic renal failure (CRF) impairs appetite.3 Several studies have reported a statistically significant association between poor appetite and decreased survival.4,5 PEW by virtue of its malnutrition component may lead to impaired immune

* Tel.: þ91 9453019812 (mobile). E-mail addresses: [email protected], [email protected]. 2211-9477/$ e see front matter Copyright ª 2012, Reed Elsevier India Pvt. Ltd. All rights reserved. http://dx.doi.org/10.1016/j.cqn.2012.06.007

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Table 1 e Types of malnutrition in kidney disease.2,91 Factors

Type 1

Type 2

Associated with uremic syndrome

Associated with MIA syndrome

Normal/low Uncommon No Decreased Normal Increased Decreased Yes

Low Common Yes Low/Normal Elevated Markedly Increased Increased No

Serum albumin Comorbidity Presence of inflammation Food intake Resting energy expenditure Oxidative stress Protein catabolism Reversed by dialysis and nutritional support

function and host resistance, resulting in increased susceptibility to infections and poor wound healing. Low protein diets prescribed to CKD patient are also atherogenic because patients may tend to consume high amounts of atherogenic fat in order to maintain adequate energy. Patients may also have low dietary mineral and vitamin intake.6 They are susceptible to zinc, vitamin B6, vitamin C and folic acid deficiencies most of which can induce alterations in host defense, such as diminished antibody response, lymphocytic dysfunction and impaired wound healing.7e9 Vitamin D deficiency, refractory anemia and iron depletion is also a consequence of PEW which may lead to increased platelet count and/or activation and increased mycloperoxidase activity.10 Impaired host resistance, aggravated by PEW may predispose to inflammatory diseases such as hepatitis C infections, which is associated with increased death in CKD.11 In CKD population, inflammation (increased serum CRP levels and IL6 concentrations) has been shown to be associated with increased risk of cardiovascular death.12 Inflammation induces endothelial cell damage and endothelial dysfunction, predisposing to atherosclerosis plaque

formation. Inflammation may both be a cause and a consequence of PEW. Furthermore, derangements of gastrointestinal tract are characteristic of malnutrition, with atrophy of the gut lining, decreased intestinal secretion, and altered gut flora leading to further reduction in gut function and ability to absorb nutrients.13 Sarcopenia (muscle wasting) may lead to reduced skeletal, respiratory and cardiac muscle function, compromising the vital functions of these organ systems. It may also restrict muscle based oxidative metabolism and thus lead to a decreased antioxidant defense.14 Tissue damage can affect protective actions of certain molecules such as gelsolin (vitamin D binding protein) and is consumed by circulating actin.15,16 Gradual loss of body fat content during the progression of CKD may result in decreased sequestration of uremic toxins and lower production of certain anti-inflammatory cytokines and adiponectine. The endotoxinelipoprotein hypothesis17 explains the link between low levels of serum cholesterol and increased cardiovascular disease and death in both CKD and chronic heart failure patients; hence, higher concentrations of unbound endotoxins occurring in the setting of low serum

Table 2 e Causes of protein-energy-wasting92 (PEW). Inflammation 1. Associated with infected vascular access sites, systemic infectious illness including tuberculosis, diabetes mellitus, myocardial infarction, stroke, peripheral vascular ischemia, vasculitis. 2. Unassociated with clinically apparent disease such as, inflammatory reaction to vascular access catheters, grafts, peritoneal dialysis catheters, dialysis tubing, impure dialysate, old nonfunctioning transplant kidney, kidney failure per se Decreased food intake 1. Anorexia caused by uremic toxicity, medication, inflammatory disorders 2. Loss of taste, unpalatable prescribed diets 3. Nonanorexic causes (financial constraints), medical or surgical illness, particularly of gastrointestinal tract, impaired cognitive function, other mental disability, physical disability, loss of dentures Dialysate nutrient losses 1. Losses of amino acids, peptides and protein into dialysate 2. Losses of water soluble vitamins and minerals during dialysis Metabolic acidemia Anemia and loss of blood due to 1. Gastrointestinal bleed 2. Frequent blood sampling Hormonal disorders 1. Resistance to anabolic hormones such as insulin, growth hormone, insulin-like growth factor-1 2. Increased levels of counter regulatory hormones such as glucagon, parathyroid hormone Increased fecal excretion of nitrogen Decreased level of antioxidants such as vitamin E, C, selenium, reduced glutathione (GSH) Physical conditioning

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Table 3 e Criteria for diagnosing protein-energy-wasting (PEW). Serum chemistry 1. Serum albumin level <3.8 g/dL 2. Serum pre-albumin level <30 mg/dL 3. Serum cholesterol level < 100 mg/dL Body mass 1. BMI<22 kg m2 (for age >65 years), <23 kg m2(for age >65 years) 2. Unintentional weight loss over time 5% in three months; or 10% in 6 months; Total body fat percent< 10% Muscle mass 1. Muscle wasting, reduced muscle mass 5% in three months; or 10% in 6 months; 2. Reduced midarm muscle circumference area >10 reduction in relation to 50th percentile of reference population 3. Creatinine appearance Dietary intake 1. Unintentional low dietary protein intake <0.8 g/kg/d for at least 2 months for maintenance dialysis patients or <0.60 g/kg/d for patients with CKD stage 2e5 with 5 g/d of urinary protein loss. 2. Unintentional low dietary energy intake <25 kcal/kg/d for least 2 months

cholesterol may activate the proinflammtory cytokine cascade leading to endothelial dysfunction and atherosclerosis.18 Every strategy should be used to avoid complications of CKD manifested in uremic state including anorexia, nausea, vomiting leading to malnutrition, fluid and electrolyte imbalance leading to volume overload, hyperkalemia, metabolic acidosis, and hyperphosphatemia, as well as abnormalities related to hormonal or systemic dysfunction such as hypertension, anemia, hyperlipidemia, bone disease, pericarditis, peripheral neuropathy, and central nervous system abnormalities (ranging from loss of concentration and lethargy to seizures, coma, and death). Restriction of dietary protein intake has been a relevant part of the management of CKD for more than 100 years, but even today, the principal goal of protein-restricted regimens is to decrease the accumulation of nitrogen waste products, hydrogen ions, phosphates, and inorganic ions while maintaining an adequate nutritional status to avoid deterioration of renal function.19,20 Every gram of nitrogen absorbed by the body is eliminated into urine after metabolic processing. Since, proteinuria is an important independent risk factor for progression of CKD, nutritional intervention is directed toward not only lowering proteinuria to a minimal level but also to replenish losses of the same.21

3.1.

Goals of nutritional therapy

Adequate nutritional support can maintain protein stores and correct pre-existing or disease-related deficits in lean body mass. Overnutrition, on the other hand, is associated with altered renal hemodynamics, particularly if the excess consists of high protein intake, high aminoacid intake, or both. Glomerular protein trafficking induces hypermetabolism and oxidative stress, and a low protein diet (LPT), is associated with reduced oxygen consumption and monoaldehyde production.2,22 Nutritional intervention is directed toward overall patient outcome and comorbid conditions such as anemia, bone disease, and cardiovascular disease (CVD). As glomerular filtration rate (GFR) declines, the stages of kidney disease23 change, and the nutritional requirements also change (Table 4). Therefore, the primary objective of nutritional intervention for patients with renal disease is to

 Control progression of disease and to maintain adequate nutritional status  Prevent appearance of uremic symptoms  Delay renal replacement initiation  Improve outcomes in CKD patients  Improve nutrition  Build up body stores for good transplant outcome (if planned)  Improve quality of life

3.1.1.

Energy

Increasing or decreasing energy requirement is not necessary for patients with CKD before ESRD develops. For individuals with CRF (GFR <25 mL/min) who are not undergoing maintenance dialysis the energy intake should be 35 kcal/kg/day provided they are below 60 years of age and 30 kcal/kg/day those who are more than 60 years of age. Research data show that basal rate metabolism and energy requirements in these patients do not differ from those in healthy adults. Metabolic balance studies of such individuals indicate that a diet providing about 35 kcal/kg/d engenders neutral nitrogen balance and maintains serum albumin and anthropometric indices.24 Energy requirements are given in Table 4. Spontaneous reduction in energy and protein intake have been reported when renal function is impaired and intake as low as 21 kcal/kg/d and 0.85 g protein/kg/d have been observed in patients with CKD stage 3 i.e., GFR <30 mL/min. With restricted protein intake risk for intake of hypocaloric diet increases when GFR declines below 50 mL/min. Careful evaluation of protein energy intake is necessary to prevent setting in of PEW.

3.1.2.

Protein restriction

Multiple well-designed randomized controlled human trials have evaluated both the efficacy and safety of protein restriction in patients with progressive CKD.25e29 Moderate protein restriction (0.6e0.8 g/kg per day) is associated with a modest but not significant benefit of protein restriction on progression of renal disease. It is generally well tolerated and does not lead to malnutrition in patients with CKD providing caloric goals are met, dietary protein is of high biologic value,

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Table 4 e Stages of chronic kidney disease23 and changes in nutrient requirement. Stage

Description

GFR mL/min/1.73 m2

1

Kidney damage (presence of protein in urine) with normal GFR

>90

2

Kidney damage with mild decrease in GFR

60e<89

3

Moderate decrease in GFR

30e59

4

Severe reduction in GFR

15e<30

5

Kidney failure (End-stage renal disease)

<15

and metabolic acidosis is avoided. Low protein diet (0.6e0.8 g/ kg per day) should be used in select predialysis patients who are highly motivated to follow such a diet. According to KDOQI guideline 24,30 individuals with CRF (GFR <25 mL/min) who are not undergoing maintenance dialysis institution of a planned low-protein diet providing 0.60 g/kg/d should be considered. For individuals who will not accept such a diet or who are not able to maintain adequate daily energy intake with such a diet, an intake of up to 0.75 g protein/kg/d may be prescribed.30 Target dietary protein intake for people with

Nutrient requirement Recommended dietary allowances Energy 30e35 kcal/kg/d (35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d) Water soluble Vitamins and minerals as per RDA Low protein 0.6e0. 75 g/kg/d Energy 30e35 kcal/kg/d (35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d) Phosphorus 800e1000 mg Non-calcium based phosphate binder with meals Calcium 1000e1500 mg/d Sodium <2.4 g/d Potassium 1 mEq/kg Cholesterol <200 mg/d Water soluble Vitamins and minerals as per RDA Low protein 0.6e0.75 g/, Energy 30e35 kcal/kg/d (35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d) Phosphorus 800e1000 mg Non-calcium based phosphate binder with meals Calcium 1000e1500 mg/d Sodium <2.4 g/d Potassium 1 mEq/kg Cholesterol <200 mg/d Water soluble Vitamins and minerals as per RDA Low protein 0.6 g-75/kg/d, Energy 30e35 kcal/kg/d (35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d) Phosphorus 800e1000 mg Non-calcium based phosphate binder with meals Calcium 1000e1500 mg/d Sodium <2.4 g/d Potassium 1 mEq/kg Cholesterol <200 mg/d Water soluble vitamins and minerals as per RDA Low protein 0.6 g/kg/d, if on conservative management, 1.2e1.3 g/kg/d if on maintenance dialysis phosphorus 800e1000 mg Energy 30e35 kcal/kg/d (35 < 60 years; 30 > 60 years; Diabetics <30 kcal/kg/d) Non-calcium based phosphate binder with meals Calcium 1000e1500 mg/d Sodium <2.4 g/d Potassium 1 mEq/kg Cholesterol <200 mg/d Water soluble Vitamins and minerals as per RDA6 Treat anemia with folic acid, B12, iron supplements (check iron profile) and erythropoietin stimulating agents as per requirements of the patients.

diabetes and CKD stages 1e4 should be the RDA of 0.8 g/kg body weight per day.31

3.1.2.1. Efficacy of low protein diet. Relatively small studies have suggested that a low protein diet may protect against progression of CKD in at least some diseases, such as diabetic nephropathy and chronic glomerular diseases.32e35 It has been shown that in diabetic nephropathy, the rate of decline in GFR slowed by 75 percent with dietary protein restriction.36 Even patients with an initial GFR as low as 15 mL/min

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appeared to benefit.34 In contrast to these positive results, a much larger controlled trial (Northern Italian Cooperative Study Group) involving patients with a variety of renal diseases found that a low protein diet produced only a small, not statistically significant trend toward benefit at two years.36 There were, however, two potential problems with this study: the GFR was measured indirectly by the often inaccurate creatinine clearance and, more importantly, noncompliance with protein restriction minimized the difference in dietary intake between control and treated groups. Protein intake (as estimated from the formula derived below) has been close to 1 g/kg per day in the control group in most studies. Whereas protein intake was reduced by 29e43 percent in the treated group in the smaller successful trials.32e34 It was reduced by only 16 percent in the Italian trial.36 Difficulty with compliance occurred despite the availability of much greater dietary counseling and monitoring than is available to the typical practitioner. Modification of Diet in Renal Disease (MDRD) study analyzed patients with nondiabetic CKD and a mean GFR of 39 mL/min per 1.73 m2 (all patients with GFR less than 55 mL/ min per 1.73 m2).37 Protein intake was 1.3 or 0.58 g/kg per day with or without aggressive blood pressure control and followed for a mean of 2.2 years. The achieved protein intake in the low protein group was between 0.6 and 0.8 g/kg per day. Despite good compliance, there appeared to be little overall benefit with the low protein diet. A similar lack of substantial benefit was noted in a second part of this study involving patients with more advanced disease (mean GFR 19 mL/min per 1.73 m2) who were randomized to a low protein diet or a very low protein diet (0.3 g/kg per day) with a ketoacid-amino acid supplement. A long-term follow-up analysis of the MDRD study38,39 reflected on outcomes during the first six years after the trial ended, the next six year period, and the total 12-year period. Analysis of outcomes after the first six years revealed a small but significant benefit of low-protein intake on renal failure and all-cause mortality (hazard ratios of 0.68, CI 0.51e0.93 and 0.66, CI 0.50e0.87, respectively). However, there was no benefit of protein restriction when outcomes between 6 and 12 years were analyzed. Another trial also provided evidence of modest benefit from dietary protein restriction (control group mean protein intake 1.06 g/kg per day) versus protein intake 0.8 g/kg per day, higher than the desired level of 0.6 g/kg per day in treatment group) in nondiabetic CKD.40 Reviews published in 2006 and 2008 evaluated eight randomized controlled trials that compared low protein diets (0.3e0.6 g/kg per day) with standard protein intake (>0.8 g/kg per day) in nondiabetic.41,42 Low protein diet was associated with a decreased risk of need for dialysis, kidney transplantation, or death during follow-up (RR 0.69, 95% CI 0.56e0.86). These studies provide some evidence that a low protein diet may benefit some patients with CKD. Some studies have evaluated the effects of a very low protein diet in patients with significant proteinuria or reduced GFR. Study on nephrotic syndrome patients evaluated the effects of a very low protein diet (0.3 g/kg per day supplemented with 10e20 g/ day of essential amino acids), which was administered for an average of ten months in 16 patients.43,44 Eleven of the 16 patients with clearances below 30 mL/min upon entrance into the study exhibited modest improvement

with treatment, but all eventually required dialysis. Among the remaining five patients with clearances greater than 30 mL/min, however, dietary treatment for 3e14 months resulted in several beneficial effects such as decreased proteinuria (9.3 versus 1.9 g/day), increased serum albumin concentration (2.5 versus 3.8 g/dL), increased GFR (52 versus 70 mL/min) and upon resumption of a relatively normal diet, four of the five patients continued to remain in clinical remission (or near-remission) at a follow-up of 6e24 months. Some44 studies suggest that a very low protein diet may help delay the requirement for renal replacement therapy among patients with near-end-stage renal failure (GFR of less than 6e10 mL/min). Nutritional studies in patients with CKD suggest that protein intake can be safely lowered to 0.6 g/kg per day.28 However, a very low protein diet has been associated with increased mortality over the long term. Lower levels of protein ingestion are associated with diminished energy intake and significant, but small, absolute declines in serum transferrin, body weight, percent body fat, and arm muscle area at a mean follow-up of 2.2 years (http:// www.uptodate.com/contents/protein-restriction-and-progre ssion-of-chronic-kidney-disease/abstract/16) and increased risk of death among patients who received the very low protein diet compared to patients who received the low protein diet (hazard ratio 1.92, 95% CI 1.15e32).39 However, these observations suggest that there are important long-term safety risks associated with the very low protein diet among patients with advanced CKD. Modest protein restriction to 0.6e0.8 g/kg per day appears to be safe. We observed moderate to severe malnutrition with high CRP levels, low albumin levels, protein intake of 0.8 g/kg/d and energy intake of 25e28 kcal/kg/d in our patients (SGPGI, Lucknow) on maintenance hemodialysis (Unpublished data). To prevent malnutrition:  Patients should maintain adequate caloric intake.  At least 60 percent of the ingested protein must be of high biologic value or contain a high percentage of essential amino acids.25  Metabolic acidosis should be treated to prevent skeletal muscle stimulation and protein breakdown and to limit net nitrogen loss.  Properly supervised resistance training may help maintain muscle mass.45

3.1.2.2. Hyperkalemia. Hyperkalemia is a common clinical problem that is most often a result of impaired urinary potassium excretion due to acute or chronic kidney disease and/or disorders or drugs that inhibit the renineangiotensinealdosterone axis. Therapy for hyperkalemia due to potassium retention is ultimately aimed at inducing potassium loss.46e48 In some cases, the primary problem is movement of potassium out of the cells, even though the total body potassium may be reduced. Redistributive hyperkalemia most commonly occurs in uncontrolled hyperglycemia (e.g., diabetic ketoacidosis or hyperosmolar hyperglycemic state). In these disorders, hyperosmolality and insulin deficiency are primarily responsible for the transcellular shift of potassium from the cells into the extracellular fluid, which can be reversed by the administration of fluids and insulin.

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Many of these patients have a significant deficit in whole body potassium and must be monitored carefully for the development of hypokalemia during therapy. Hyperkalemia generally develops in the patient who is oliguric or who has an additional problem such as a highpotassium diet, increased tissue breakdown, or hypoaldosteronism (due in some cases to the administration of an ACE inhibitor or ARB).49 Impaired cell uptake of potassium also may contribute to the development of hyperkalemia in advanced chronic kidney disease. Hyperkalemia due to ACE inhibitor or ARB therapy is most likely to occur in patients in whom the serum potassium concentration is elevated or in the high normal range prior to therapy. In addition to treating hyperkalemia, there are several measures that can help prevent hyperkalemia in patients with chronic kidney disease. These include ingestion of a low potassium diet (e.g., less than 40e70 meq/day [1500e2700 mg/day] or 1 mEq/kg/d) (Table 5) and avoiding, if possible, the use of drugs that raise the serum potassium concentration such as non-steroidalanti-inflammatory drugs. Nonselective beta-blockers make

the postprandial rise in the serum potassium concentration but do not produce persistent hyperkalemia.

3.1.3.

Approach to hyperphosphatemia

Dietary manipulations should be considered as one of the main approaches in the management program of CKD patients and that a reasonable number of patients with moderate or severe CKD benefit from dietary protein phosphorus restriction.19 To optimally manage elevated phosphate levels in patients with CKD, it is important to first assess the presence or absence of other mineral abnormalities, vascular calcifications, and note the administration of concurrent therapies. Therefore baseline phosphate, calcium, and parathyroid hormone (PTH) levels must be obtained and then on an ongoing basis, particularly after changes in therapeutic measures. Among dialysis patients, aim is to maintain serum phosphate levels between 3.5 and 5.5 mg/dL. Initial step should be to restrict dietary phosphate to 900 mg/day. Among dialysis patients with elevated phosphate levels that are refractory to maintenance dialysis therapy and diet,

Table 5 e Potassium content of common foods.a High-potassium foods Citrus fruits Apricots Banana (1 small) Dates (1/4 cup) Honeydew melon Nectarines Orange juice Prune juice Melons Kiwi Tomatoes Sweet potatoes Spinach Beans (baked, kidney, lima, pinto) Avocado Beets Brussels sprouts Chard Greens (beet, collard, etc.) Kohlrabi Parsnips Pumpkin

Moderate-potassium foods

Lower-potassium foods

Cantaloupe Figs (2 whole) Grapefruit Grapefruit juice Mango nectar Papaya Peach (fresh) Pear (fresh) Rhubarb Prunes (5) Raisins Cherries Asparagus Broccoli Celery Kale Mixed vegetables Peas Peppers Potato Summer squash Turnips Zucchini

Apple, Apple juice, Apple sauce Apricot nectar Blackberries Blueberries Cranberries and Cranberry juice Fruit cocktail Gooseberries Grape juice Grapes Lemon or lime (1) Papaya nectar Pear (canned) Pear nectar Pineapple Plums Raspberries Strawberries Tangerines Watermelon Cabbage Cauliflower Mustard greens Broccoli Alfalfa sprouts Bamboo shoots (canned) Corn Cucumber Eggplant Green beans Lettuce (1 cup) Mushrooms Radishes Water chestnuts Watercress

a Source: United States Department of Agriculture (USDA) National Nutrient Database for Standard Reference, Release 17-1 (www.nal.usda. gov/fnic/foodcomp/Data/SR17/wtrank/sr17a306.pdf (PDF, 211 KB); accessed June 3, 2005); Nutritive value of Indian Foods Gopalan G, Rama Sastri BV and Balasubramaniam SC, National Institute of Nutrition, 1996 Indian Council of Medical Research Hyderabad.

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administration of phosphate-binding agents is a must. Table 6 shows approach to treating hyperphosphatemia based upon the serum calcium level. Some patients do not achieve the recommended serum phosphate goals with the regimen given in Table due in part to the use of various agents to help control PTH levels. Vitamin D analogs may contribute, raising both phosphate and calcium concentrations. A possible alternative is the use of cinacalcet, which acts by a different mechanism and produces significant reductions in PTH, calcium, and phosphate levels. More frequent and more intensive dialysis can also lower phosphate levels.50 Extremely long and/or frequent dialysis, such as that provided by nocturnal hemodialysis, clears a large amount of phosphate. Among patients with refractory hyperphosphatemia, nocturnal hemodialysis is an option among those who are willing to accept this form of dialysis. Avoid aluminum hydroxide except for short-term therapy (four weeks for one course only) of severe hyperphosphatemia. Many such patients are candidates for parathyroidectomy.51 First step in the management of hyperphosphatemia in patients with stage 3e5 CKD not on dialysis is to restrict dietary phosphate to 900 mg/day. Among patients with serum phosphate levels greater than target levels despite dietary phosphorus restriction after one month, administer phosphate binders. While restricting dietary phosphates following points must be considered: 1. Restrict phosphate but nutritional status should not be compromised. 2. Approximately 900 mg per day level/day is acceptable. 3. Phosphate restriction includes processed foods and colas but high biologic value foods such as meat and eggs should not be restricted (Table 7). A large number of dialyzed patients having either overt or borderline malnutrition are advised protein supplements. Plant-derived phosphorus is less easily absorbed because it is in the form of phytate phosphorus, and the human intestine does not secrete phytase, the enzyme required for absorption. The patient should be encouraged to avoid unnecessary dietary phosphate (as in phosphorus-containing food additives, dairy products, certain vegetables, many processed foods, and

colas) while increasing the intake of high biologic value sources of protein (such as meat and eggs).52,53 Table 6 shows strategies for management with and without comorbidities. Since hypercalcemia is unusual in CKD stage 3e5, evaluation for secondary non-PTH mediated causes should be undertaken if PTH values are not significantly elevated and patients are not receiving active vitamin D therapy. Primary hyperparathyroidism can be present in hypercalcemic patients with stage 3e4 CKD and when serum phosphate level is low in the absence of phosphate binders. In patients without comorbidities, but high phosphate levels, dose of calcium-containing phosphate binders is generally increased until the serum phosphate falls to normal values. The safe dose of calcium is not known in stage 3 and 4 CKD but likely exceeds the 1500 mg/day limit in end stage renal disease patients suggested by the K/DOQI work group.54 The 2009 KDIGO practice guidelines provide recommendations for the evaluation and management of chronic kidney disease-mineral and bone disorder (CKDMBD).55

3.1.3.1. Calcium. Close attention to the prevention and management of cardiovascular disease should be a priority among patients identified with chronic renal dysfunction. Increased intake of calcium for treating hyperphosphatemia enhances coronary arterial calcification which may be associated with the development of coronary atherosclerosis. The combination of hypercalcemia (calcium >10.2 mg/dL corrected for serum albumin) and persistent hyperphosphatemiais a limitation with calcium therapy and active vitamin D analog administration, possibly leading to extraskeletal calcium phosphate deposition. Dose of calcium-based phosphate binders should be decreased or therapy discontinued, and/or therapy should be switched to sevelamer to control phosphate (Table 6).50 In addition, the dose of active vitamin D sterols should be lowered or therapy should be discontinued until calcium levels return to 8.4e9.5 mg/dL. In dialysis dependent hypocalcemic patients, calcium supplements should be taken in between the meals and non-calcium based phosphate binders should be administered with meals. Since patients on maintenance dialysis are advised to take high protein diet, therefore in these patients dietary calcium (especially from milk and milk products) should also be taken

Table 6 e Treating hyperphosphatemia based upon the serum calcium level. Patient’s calcium level

Treatment

>9.5 mg/dL Non-calcium containing phosphate binder (Sevelamer or lanthanum) rather than calcium containing binders Between 8.4 and 9.5 mg/dL a) Without comorbiditiesi) ii) iii)

calcium-based phosphate binder (up to 1500 mg of elemental calcium from binders alone). Higher doses of calcium if patients are not receiving vitamin D analogs or who have hypocalcemia while being treated with calcimimetics. If phosphate remains above 5.5 mg/dL despite this strategy, add non-calcium containing phosphate binder

b) Presence of a dynamic bone disease, low PTH levels, and/or vascular calcification: <8.4 mg/dL

i) Prefer non-calcium based phosphate binder Calcium based phosphate binders

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Table 7 e High and low phosphorus containing foods.a High phosphorus foods Dairy foods: milk (condensed milk, evaporated milk, dried milk.), cheese (cheddar, Edam, Gruyere, Cheese spreads, cheese sauce), yogurt, ice cream Calcium enriched milk Peanut butter Beans (baked, kidney, lima, pinto) Nuts and peanut butter Processed meats (hot dogs, canned meat) Cola Pepsi Canned iced teas and lemonade Bran cereals Egg yolks

Low phosphorus foods Milk/Dairy Foods/Eggs Cottage cheese, Ricotta cheese, cream cheese, Cream, sour cream Egg whites Liquid non-dairy creamer Sherbet Pasta rice Rice and corn cereals Popcorn Green beans Lemon-lime soda Root beer Powdered iced tea and lemonade mixes Biscuits and Cakes Cream crackers, water biscuits, digestives, plain sweet biscuits, shortbread, crumpets, cream biscuits Sugars All sugars, jams, honey, golden syrup, Cordials and soft drinks, (not cola, Pepsi)

a Source: United States Department of Agriculture (USDA) National Nutrient Database for Standard Reference, www.nal.usda.gov/fnic/ foodcomp/Data/SR17/wtrank/sr17a305.pdf (PDF, 211 KB) June 3, 2005); Nutritive value of Indian Foods Gopalan G, Rama Sastri BV and Balasubramaniam SC, National Institute of Nutrition, 1996 Indian Council of Medical Research Hyderabad.

into account, both while prescribing calcium supplements and while calculating total calcium intake/day.

3.1.3.2. Sodium and its association with hypertension. Hypertension is a common comorbidity associated with CKD. There is a large body of evidence that patients with CKD have a substantial increase in cardiovascular risk that can be in part explained by an increase in traditional risk factors such as hypertension, diabetes, and the metabolic syndrome. CKD alone is also an independent risk factor for cardiovascular disease.56 Among patients with CKD, the risk of death, particularly due to cardiovascular disease, is much higher than the risk of eventually requiring dialysis therefore hypertension requires not only medical management but also nutritional management which includes dietary salt and fat and cholesterol restriction, changes in life style. 2011 KDIGO clinical practice guideline for management of blood pressure in CKD states that goal blood pressure depends upon the degree of proteinuria:  In patients with proteinuric CKD (500e1000 mg/day or more), the blood pressure should be lowered to less than 130/80 mmHg.  In patients with nonproteinuric CKD (less than 500e1000 mg/day), the blood pressure should be lowered to less than 140/90 mmHg in all patients, and to less than 130e135 mmHg systolic if it can be achieved without producing significant side effects. Sodium balance remains virtually normal until very late in the course of CKD, because the kidney can markedly increase the amount of sodium excreted per nephron by reducing tubular sodium reabsorption. Although sodium balance is maintained, the kidney loses its ability to adapt to large variations in salt intake. Indeed, intake of large amounts of

sodium can easily overwhelm the excretory capacity of the failing kidney and result in fluid retention, edema, and hypertension. Likewise, if diuretics are used overzealously, the patient may become volume-depleted, with further aggravation of the kidney failure.57 Clinically evident edema is uncommon until the GFR falls to less than 15 mL/min/1.73 m2. However, edema can occur at higher GFR levels in patients with glomerular disease and significant proteinuria (i.e., nephrotic syndrome) and in those with heart failure. The cornerstone of treatment of edema (and hypertension) is restriction of dietary sodium to a level lower than that recommended for uncomplicated hypertension (<100 mEq/day; 2.3 g of sodium or 6 g of salt).58 If sodium restriction is not effective or not achieved, diuretics should be used.59 Thiazide diuretics are usually ineffective if the serum creatinine level is greater than 3 mg/dL (>265 mmol/L). Thus, more potent loop diuretics are the agents of choice in patients with CKD. The initial aim is to determine the threshold dose that is effective. Patients with advanced CKD may require doses of furosemide (Lasix) as high as 400 mg per day. Lack of response to high doses of loop diuretics often is due to noncompliance with dietary sodium restriction. In such cases, a combination of a thiazide diuretic or metolazone (Mykrox, Zaroxolyn) given before the loop diuretic may induce diuresis. For maximum efficacy, the thiazide diuretic should be given 30 min before the loop diuretic. Potassium-sparing diuretics (e.g., spironolactone [Aldactone]) are contraindicated because of the risk of inducing hyperkalemia. The NKF-KDOQI Guidelines on Hypertension and Antihypertensive Agents in CKD recommended a version of the DASH diet with modifications for CKD stages 3 to 4.56,60 These modifications decreased dietary protein from 1.4 g/kg body weight per day to 0.6e0.8 g/kg body weight per day, as well as restricted phosphorus (0.8e1.0 g/d) and potassium (2e4 g/d). Based on concerns about potential detrimental effects of

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high-protein diets on the kidney and evidence for kidney and survival benefits at approximately the RDA level in diabetes and CKD stages 1e2, the Work Group concluded that a protein intake that meets, but does not exceed, the RDA would be prudent at earlier stages of CKD (Table 8). The ADA endorses a dietary protein intake of 0.8 g/kg body weight per day for people with DKD.61 An additional restriction to 0.6 g/kg body weight per day is suggested should glomerular filtration rate begin to decrease. The dietary protein recommendation should be based on idealized body weight because obesity, which is highly prevalent in the diabetes and CKD population, otherwise would lead to overestimating the dietary protein recommendation.62 Dietary sodium reduction to 2.3 g/d (100 mmol/d) is recommended based on the DASH and DASH-Sodium diets.60 Because most people with diabetes and CKD have hypertension characterized by enhanced sodium retention, this limitation should apply. Recommendations for phosphorus and potassium are the same for CKD with and without diabetes. Phosphorus binders may be needed in patients with advanced CKD because of the emphasis on whole grains and dairy products. Table 9 lists high and low sodium containing foods. The Institute of Medicine established guidelines for intake of omega-3 fatty acids. Adequate intake of alpha-linolenic acid was established as 1.6 g/d for men and 1.1 g/d for women, with substitution of up to 10% of these amounts by the more physiologically potent eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA).63 The AHA and the KDOQI CPGs for CVD in dialysis patients recommend including 1 serving of cold-water fish in the diet 3 times per week.64,65 It is possible that 3 servings of cold-water fish, such as salmon, mackerel, herring, and albacore tuna, would provide EPA and DHA in excess of the 10% of adequate intake amounts for men and women. In the opinion of the Work Group, these recommendations may be considered for the diabetes and CKD population.

3.1.3.3. Restriction of fat. Restriction of fat 20 g/d is advisable (Table 8). Avoid saturated fats (red meat, poultry, whole milk, butter, lard) and hydrogenated vegetable oils. Preference should be given to monounsaturated fats such as corn oil, safflower oil, olive oil, peanut oil, canola oil. Foods containing trans-fatty acids like commercially baked goods (cakes, pastries and biscuits, French fries, doughnuts) should best be avoided.56 3.1.3.4. Metabolic acidosis. There is an increasing tendency to retain hydrogen ions among patients with chronic kidney disease. This can lead to a progressive metabolic acidosis. Bicarbonate supplementation may slow the progression of chronic kidney disease. Bone buffering of some of the excess hydrogen ions is associated with the release of calcium and phosphate from bone, which can worsen the bone disease. Uremic acidosis can increase skeletal muscle breakdown and diminish albumin synthesis, leading to loss of lean body mass and muscle weakness. Classical studies in humans demonstrated the powerful effect of chronic metabolic acidosis, induced experimentally or resulting from chronic kidney disease, on the loss of bone mineral. Bone fractures are a relatively common manifestation of chronic metabolic acidosis. Chronic metabolic acidosis contributes, in part, to the osteodystrophy in patients with chronic kidney disease.66 Acidemia engenders protein catabolism and negative protein balance and enhances degradation of protein and amino acids.67,68 Acidemia due to metabolic acidosis is associated with increased oxidation of branched chain amino acids (valine, leucine and isoleucine),69,70 increased protein degradation and PNA and decreased albumin synthesis. Arterial pH of 7.43e7.45 is associated with a more positive protein nitrogen balance than an arterial pH of 7.36e7.38.71 The administration of bicarbonate increases serum albumin and the lean body mass.72 When academia occurs repetitively

Table 8 e A balanced approach to nutrition in CKD with or without diabetes: macronutrient.56

Table 9 e Food sources of sodium.a

Nutrient

High-sodium foods

Stage of CKD 1e2

Sodium (g/d) Total fata (% of calories) Saturated fat (% of calories) Cholesterol (mg/d) Carbohydrate (% of ca calories) Protein (g/kg/d, % of calories) No diabetes 1.4 (w18) Diabetes 0.8 (w10) Phosphorus (g/d) 1.7 Potassium (g/d) >4

1e4

3e4

<2.3 <30 <10 <200 50e60

0.5e0.8 (w8e13) 0.5e0.8 (w8e13) 0.8e1.0 2.4

Note: Adapted from the DASH diet and NKF-KDOQITM CPGs for hypertension and antihypertensive agents in CKD, modified for diabetes and stages of CKD.92 a Adjust so total calories from protein, fat, and carbohydrate are 100%. Emphasize such whole-food sources as fresh vegetables, whole grains, nuts, legumes, low-fat or nonfat dairy products, canola oil, olive oil, cold-water fish, and poultry.

Salt Chutney Pickles Papdams Coconut water Tomato sauce Canned vegetables Hot dogs Packaged rice with sauce Packaged noodles with sauce Frozen vegetables with sauce Canned soup Snack foods

Lower-sodium alternatives Salt-free herb seasonings Frozen vegetables Plain rice Plain noodles Unsalted popcorn

a United States Department of Agriculture (USDA) National Nutrient Database for Standard Reference, Release 17-1 (www.nal. usda.gov/fnic/foodcomp/Data/SR17/wtrank/sr17a307.pdf (PDF, 211 KB)). Adapted from National Renal Diet (Harvey KS. A Healthy Food Guide for People on Dialysis. Chicago, IL: American Dietetic Association Renal Practice Group; 2002).

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before hemodialysis treatments, alkali supplements can prevent this from occurring.1 Predialysis or stabilized serum bicarbonate levels should be maintained at or above 22 mmol/ L.67 According to K/DOKI guideline 15,66 in CKD Stages 3, 4 and 5, measurement and monitoring of the serum levels of total CO2 is warranted or in patients on maintenance dialysis. Steps to keep the measured serum levels of CO2 above 22 mmol/L are warranted for improvement in bone histology, and to ameliorate excess protein catabolism. The frequency of these measurements should be based on the stage of CKD. If necessary, supplemental alkali salts should be given to achieve this goal.66 The use of exogenous alkali salts containing citrate may increase the absorption of dietary aluminum in patients with CKD, both before dialysis and in those treated with dialysis; therefore, citrate alkali salts should be avoided in CKD patients exposed to aluminum salts.

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Patients with chronic kidney disease and volume overload generally respond to the combination of dietary sodium restriction and diuretic therapy, usually with a loop diuretic given daily. Limiting sodium intake may also help decrease progression of chronic kidney disease by lowering intraglomerular pressure (Table 4). Water overload may result in hyponatremia and a decrease in water intake may lead to hypernatremia. Hyponatremia does not usually occur with glomerular filtration rates above 10 mL/min. The use of diuretics in volume overload in CKD is useful to force natriuresis. Thiazides have little effect in advanced CKD. Loop diuretics are effective and should be used in higher than normal doses. The combination of thiazides and loop diuretics can be useful in refractory cases.73 Weight and volume should be monitored regularly in the hospitalized patient with CKD. In oliguric patients, the best advise to avoid fluid overload is to

3.1.3.5. Fluid balance. The kidneys are the key organs to maintain the balance of the different electrolytes in the body and the acidebase balance. Progressive loss of kidney function results in a number of adaptive and compensatory renal and extrarenal changes that allow homeostasis to be maintained with glomerular filtration rates in the range of 10e25 mL/min. With glomerular filtration rates below 10 mL/min, there are almost always abnormalities in the body’s internal environment with clinical repercussions.73 Other factors that contribute to the development of fluid volume overload are proteinuria and increased renin. Proteinuria occurs in response to damage of the glomeruli. High blood pressure can cause sclerotic changes in the glomeruli with a resultant loss of protein, especially albumin in the urine.74,75 The loss of albumin in the urine contributes to fluid shifting from the intravascular space to the interstitial space because of decreased oncotic pressure. As a response to decreased GFR, aldosterone is released from the adrenal cortex, causing the kidneys to reabsorb sodium and water. Fluid retention in turn results in the development of respiratory and cardiovascular clinical manifestations.76 Sodium and intravascular volume balance are usually maintained via homeostatic mechanisms until the GFR falls below 10e15 mL/min. However, the patient with mild to moderate chronic kidney disease, despite being in relative volume balance, is less able to respond to rapid infusions of sodium and is therefore prone to fluid overload. Therefore, as kidney disease progresses, limiting fluid intake is necessary in order to correct edema. In CKD stages 1e3 urine output is generally normal. Except in edematous states, a daily fluid intake of 1.5e2 L may be recommended.73 Urine output drops as kidney failure progresses therefore, most dialysis patients urinate very little or not at all, and therefore fluid restriction between treatments is very important. Daily fluid restriction should be based according to insensible fluid losses þ urine output þ amount to replace additional losses (e.g., vomiting, diarrhea, enterostomy output)  amount to be deficited.77 Without urination, fluid builds up in the body and causes fluid overload. In such patients, daily requirement of fluid depends upon e i) the amount of urine output in 24 h, ii) the amount of weight gain between the dialysis treatment, iii) amount of fluid retention, iv) levels of dietary sodium, v) congestive heart failure.

 Avoid or minimize eating food with high content of water (soups, fruit juices, grapes, melons, coconut water).  Use measuring glasses for proper charting of fluid intake.  Allow sips of water if patients feels dryness of mouth.  Minimize sodium intake. It is best to avoid salty foods.  If possible, freeze juices (with low potassium content) in an ice tray and suck them to minimize thirst.  Avoid extreme heat. Do not go out in the sun when its too hot.

3.1.4. Nutritional status, indications for nutritional support and monitoring nutritional adequacy in CKD Individuals undergoing maintenance dialysis (CKD Stage 5D) who are unable to meet their energy requirements with food intake for an extended period of time should receive nutrition support.78 Unfortunately, there is no single optimal laboratory test to assess and monitor nutritional adequacy in CKD patients. Criteria for diagnosis of PEW are given in Table 3. No single measure provides a comprehensive indication of nutritional status. Measures of intake, visceral and somatic protein stores, body composition, and functional status identify different aspects of nutrition status. Malnutrition may be identified with greater sensitivity and specificity using a combination of factors. Patients with CKD who are on a protein-restricted diet should be carefully monitored with close follow-up every three to six months for adequate caloric intake and evidence of protein malnutrition.79 Body weight, serum albumin, prealbumin, and cholesterol should be checked on every visit. More frequent monitoring (i.e., monthly) may be necessary in patients with advanced CKD (i.e., stages 4 and 5). Complementary measures for assessment should include medical history, physical examination, anthropometry (height, body weight, body mass index (BMI), skin fold thickness, mid upper arm mid upper arm muscle mass), waist/hip ratio. Subjective global assessment (SGA) score correlates with objective measures (albumin/weight/intake/anthropometry). Change in SGA rating by 1 point decreases relative risk of death by 25%. A higher SGA score is associated with a lower relative risk of death and fewer hospitalized days/year (CANUSA study). Methods of body composition like bioelectrical impedance analysis, infrared reactance and DEXA should be used to

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estimate water compartments and changes in body muscle, fat and protein stores. This will help in attainment of dry weight. Assessment of dietary Intake should be done at least once a month using, 1. Diet history questionnaires, 2. Food weighing and 3. Observation. Food weighing is a little difficult for patients who visit dialysis units on out patient basis. Assessment of food intake using diet history questionnaires is therefore more appropriate for such patients. Egg white, fish, chicken, milk and milk products (curd, chenna/paneer), dehusked (without outer covering to prevent hyperphosphatemia) lentils kidney beans, soy protein (milk and cheese marketed as Tofu) are good sources of protein with HBV for patients on maintenance dialysis.

3.1.4.1. Predialysis serum creatinine. This is a direct indicator of protein intake and muscle mass. It is directly proportional to skeletal muscle mass & dietary muscle intake According to NKF/KDOQI guideline 5 predialysis Serum Creatinine of<10 mg/dL is considered as high risk for PEW which warrants thorough evaluation of PEW. Mortality risk increases with creatinine below 9e11 mg/dL in patients on MHD or PD. But these data are based on Western population with significantly different body frame and size. A predialysis serum creatinine of higher than 10 mg/dL is not tolerated by Indian patients and they become highly uremic (anorexia, vomiting, loss of taste). Therefore, the threshold levels of predialysis serum creatinine for Indian are much lower than those recommended by NKF/KDOKi guidelines. A low predialysis or stabilized serum creatinine level in MD patients suggests decreased skeletal muscle mass and or low dietary protein intake. Therefore in Indian patients, low stabilized predialysis creatinine of between 2 and 4.5 mg/dL with negligible residual renal function should be investigated for low dietary protein intake and skeletal muscle wasting and risk for high mortality.

3.1.4.2. Anorexia. Chronic renal failure impairs appetite.3 Major proportion of patients treated with HD consume less protein and energy than is recommended. Factors that contribute to anorexia like underdialysis (to overcome this factor switch over to thrice weekly dialysis in place of twice weekly dialysis therapy), comorbidity, medication (in such circumstances discontinuing phosphate binders and iron and vitamin supplements for a short period of time helps improve appetite) psychosocial factors should be immediately addressed. Dialysis regimen should be regularly monitored and modified to treat intensification of the patient’s uremic state that is caused by superimposed illness. Maintain KT/V of 1.2 in HD patients. Because of the number of factors affecting the nutritional and metabolic status in patients with advanced chronic kidney disease or who are on maintenance dialysis, the prevention and treatment of PEW of chronic kidney disease should involve a comprehensive combination of maneuvers to diminish protein and energy depletion, in addition to therapies that will avoid further losses. The available evidence suggests that nutritional supplementation, administered orally or parenterally, is effective in the treatment of maintenance dialysis patients with PEW in whom oral dietary intake from regular meals cannot maintain adequate

nutritional status. Increased oral nutrient intake during dialysis and at home is the ideal choice for this intervention.79 In clinical practice, the advantages of intradialytic oral nutritional supplements include proven efficacy and compliance. Therefore, at a minimum, oral nutritional supplementation given intradialytically should be attempted in maintenance dialysis patients with PEW, accompanied by individualized dietary advice for appropriate intake at home. In ones who cannot tolerate oral feeding, intradialytic parenteral nutritional is a good alternative.80 Approximately one-third of maintenance dialysis patients have mild to moderate protein-energy malnutrition, and about 6e8 percent of these individuals have severe malnutrition.81 These statistics are of major concern because markers of protein-energy malnutrition are strong predictors of morbidity and mortality. The causes of protein-energy malnutrition in patients with chronic renal failure are given in Table 2. There is some evidence that the nutritional status of the hemodialysis patient can be influenced by the biocompatibility of the membrane.82e84 In particular, the elaboration of cytokines from cells activated after contact with BICM may be responsible for increased protein catabolism. One report demonstrated net protein catabolism when normal subjects were exposed to (not dialyzed by) cellulosic membranes but not when exposed biocompatible polysulfone or PAN membranes.85 It was estimated that a 150 min exposure to the cuprophane membrane resulted in the net degradation of approximately 15e20 g of muscle protein (measured by the release of amino acids). Of interest, the net release of amino acids occurred 3 h after the end of dialysis, not during dialysis, and continued for as long as six and one-half hours after dialysis. This time course is similar to that of monocyte activation, the release of cytokines, and their subsequent action on muscle cells.82 Two other observations are compatible with a beneficial effect of biocompatible membranes (BCM) on nutritional status. In one study, for a given dose of dialysis, protein intake (reflected by the protein catabolic rate) increased to a greater extent in patients dialyzed with PAN membranes compared to those treated with cuprophane membranes.83 In a multicenteric trial, patients treated with BCMs had higher plasma levels of albumin and insulin-like growth factor-1 and a greater degree of body-mass weight gain during the 18 months of the study.84

3.1.4.3. Gastroparesis. Gastroparesis can be a contributing factor to decreased food intake by delaying gastric emptying, thereby increasing the feeling of fullness. This complication is most common in diabetics (possibly affecting as many as 20 to 30 percent of diabetics with end-stage renal disease), but can also occur in nondiabetics.86,87 If gastroparesis is suspected from the history, the rate of gastric emptying can be accurately assessed by various methods, such as ingestion of a radiolabeled test meal with simultaneous gastric scanning. Patients with severe gastroparesis may be unable to tolerate any form of oral supplementation. Intravenous infusion and intradialytic parenteral nutrition (IDPN) or total parenteral nutrition (TPN) depending upon urine output in case of dialysis dependent patients may be beneficial. TPN is required in patients with severe malabsorption. Although generally well tolerated, TPN solutions typically contain added potassium,

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phosphorus, and magnesium. Thus, patients with end-stage renal disease receiving TPN are at risk for the development of hyperkalemia, hyperphosphatemia, and hypermagnesemia. Elimination of the added electrolytes can prevent these problems but carries the reverse risk of electrolyte deficiencies with prolonged therapy.

3.1.4.4. Obesity. Weight excess is associated with increased renal risk. Data in overt obesity suggest a role for altered renal hemodynamics. Study on the relation between BMI and renal hemodynamics in 102 healthy, non-obese (BMI <30 kg/m2) subjects suggests that the impact of BMI on renal function is not limited to overt obesity as in subjects with BMI <30 kg/m2, a higher BMI is associated with higher FF, that is, a higher GFR relative to effective renal plasma flow. This suggests an altered afferent/efferent balance and higher glomerular pressure (i.e., a potentially unfavorable renal hemodynamic profile) that may confer enhanced renal susceptibility when other factors, such as hypertension or diabetes are superimposed.88 Elevated BMI is not a biologically significant predictor of diminished GFR and therefore may be an insufficiently accurate measure of risk for the metabolic syndrome and CKD.89 Hypertension is a common obesity-related health problem and visceral obesity seems to be the major culprit. Obesity-related HTN pandemic and its CVD and CKD consequences call for prevention and treatment of obesity and to treat HTN to goal.90 It is recommended that obese patients be motivated to lose body weight by encouraging physical activity without compromising their nutritional status.

4.

Summary

Chronic renal failure (CRF) impairs not only appetite but also impairs immune function and host resistance, resulting in increased susceptibility to infections and poor wound healing and may predispose to inflammatory diseases. Every strategy should be used to avoid complications of chronic kidney disease (CKD) manifested in uremic state including anorexia, nausea, vomiting leading to malnutrition, fluid and electrolyte imbalance leading to volume overload, hyperkalemia, metabolic acidosis, and hyperphosphatemia. With decline in GFR, nutrient requirements change. Nutritional status should be assessed. Timely diagnosis of PEW is important for early initiation of nutritional intervention and treatment. Management of hypertension, bone mineral disease, fluid overload and gastroparesis should be given prime importance.

Conflicts of interest The author has none to declare.

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