protein energy malnutrition in ckd

Protein Energy Malnutrition (PEM),

Protein-Energy Wasting (PEW)

Kidney Disease Wasting (KDW),

Kidney Disease-Related PEM By

Mabrouk Ramadan Al-SheikhProf. of nephrology and Internal Medicine

Faculty of MedicineTanta University

زينتكم” خذوا آدم بني ياوكلوا مسجد كل عند

إنه تسرفوا وال واشربوا“ المسرفين يحب ال

العظيم الله صدق(31األعراف) -

Eat right to feel and live right

Do not starve your patient

Let the food be the medicine and not let the medicine be the food. “Hippocrates”

لنأكل نعيش ال لنعيش، نأكل نحن

Agenda Definition Prevalence Factors contributing to malnutrition Nutritional assessment Nutritional therapy Conclusion and Recommendations

Agenda DefinitionPrevalence Factors contributing to malnutritionNutritional assessment Nutritional therapy Conclusion and Recommendations

The International Society of Renal Nutrition and Metabolism (ISRNM) expert panel defined PEM (2012):

“state of decreased body stores of protein and energy fuels i.e. body protein and fat masses”

Definition

DefinitionComponent of PEM are1. Clinical manifestations: unintentional poor

nutritional intake, unintentional BW loss, depleted energy (fat tissues) stores, and loss of somatic protein (low muscle mass).

2. Laboratory investigations: low level of visceral protein; s. albumin, prealbumin and transferrin and others.

3. Abnormal anthropometric measurements.

Readily utilizable criteria for the clinical diagnosis of PEM in CKD

Prevalence

Depending in part upon the method used and the population studied, up to 40 to 70 % of patients with end-stage renal disease are malnourished.

Potential causes of PEM in patients with non-dialysis dependent CKD

Factors contributing to malnutritionMalnutrition can be secondary to : 1- Poor nutritional intake:

Overzealous dietary restrictions.

Delayed gastric emptying and diarrhea.

Intercurrent illness .

Hospitalization.

Other medical cormorbidities.

Factors contributing to malnutritionMalnutrition can be secondary to :

1- Poor nutritional intakeMedication causing dyspepsia e.g. phos. binders, iron therapy .

Suppression of oral intake by PD load.

Inadequate dialysis

Decreased food intake on HD days

Monetary restriction

Depression

Altered taste sensation

2- Increased protein losses

Gastrointestinal blood loss: “100ml blood = 14-17g protein.”

Intradialysis nitrogen loss: “ HD : 6-8 g amino acid/ procedure” “PD : 8-12 g protein/day”

Factors contributing to malnutrition

3- Increased protein catabolism Intercurrent illness and hospitalizations. Metabolic acidosis. Catabolism associated with HD Catabolic effects of hormones “cortisol, PTH, glucagon”Dysfunction of GH and IGF endocrine axis.

Factors contributing to malnutrition

Squeals of PEM

Malaise, fatigue, poor rehabilitation

Increase susceptibility to infection.

Impaired wound healing.

Increase hospitalization rate.

Increase morbidity and mortality rate.

Agenda DefinitionPrevalence Factors contributing to malnutrition Nutritional assessment Nutritional therapy Conclusion and Recommendations

ASSESSMENT OF NUTRITIONAL STATUS

No single gold standard measurement. Therefore, a panel of measurements is recommended and including:

1. Assessment of dietary nutritional intake2. Assessment of body composition.3. Laboratory values 4. Scoring

I-Nutritional Intake

A- Patient’s interview• Often provides important clue to patients who might be

malnurished • Symptoms: nausea, vomiting, anorexia, fatigue, weight

loss or gain• Pharmacological therapy: steroid therapy, iron therapy

and phos. binder• Co-morbidity and non uremic diseases e.g. DM,

alcoholism, GI diseases.• Psychological issues.

I-Nutritional IntakePhysical Examination Should include anthropometry The patient's actual BW is estimated and should be

compared to the recommended “dry or peer” body weight.

The percentile change (if any) of the "dry weight" should also be assessed approximately every month.

I-Nutritional IntakeB- Assessment of food intake• Food questionnaire: the 24 h recall helps the patients to

remember food intake in the previous day and to quantate it.

• Food record: quantitative and qualitative data on food intake collected for an average 3 days including 2 two week day and one week end day (3 days should include dialysis and non-dialysis day).

• A food diary is very useful, especially if the patient weighs the portions of food. The intake of protein, fat and carbohydrate can then be calculated from standard food tables.

I-Nutritional Intake

B- Assessment of food intake: The semi-quantitative food–frequency questionnaire

(SFFQ): is used to assess the frequency of consumption of food items and groups during a specific reference time period, which may or may not be the period the patient actually bases his(her) recalls on.

I-Nutritional IntakeC-Protein equivalent of total nitrogen

appearance (PNA) & nPNA Calculating the protein catabolic rate (PCR)

is a good indirect index for dietary protein intake, expressed g/day.

KDOQI guidelines prefers the name: protein equivalent of total nitrogen appearance (PNA), expressed g/day.

Normalized nPNA ,expressed g/Kg/day.

I-Nutritional IntakeC-Protein equivalent of total nitrogen

appearance (PNA) & nPNA Determination of nPNA: Calculated by

Formula Computer Program Target level =1.0-1.2 g/Kg/day. Best survival rate at level= 1.0-1.4 g/Kg/day. An increased overall mortality rate at level

<0.8 or>1.4 g/Kg/day.

Interpretation of nPNA

Observation Interpretation ConsiderationnPNA exceeds DPI or is unexpectedly high

Only tentative conclusions about protein intake possible

Catabolic state:-Inadequate energy intake-Presence of inflammation or inflammatory stressors (fever, infection)-Weight loss- Metabolic acidosis-Bioincompatible dialysis membrane.Inaccurate diet recordLow lean body mass

nPNA less than DPI or is unexpectedly low

Only tentative conclusions about protein intake possible

Anabolic state: -Corticosteroid use- Recovery from infection or illness- Pregnancy or growthInaccurate diet recordEdema or excess body weight

nPNA=DPI nPNA reflects protein intake

Conclude patient is in nitrogen balance and nPNA reflects intake if none of the above apply

II- Body composition

1- Body weight-based measures: BMI, weight for height, edema-free BW, fat-free BW.

2- Skin and muscle anthropometry: caliper, skin fold, extremity muscle mass.3- Total body elements: total body potassium.4- Energy-beam-based methods: total body N2,

DEXA, BIA, NIR.5- Other method: underwater weighting.

A-BMIThe international classification of adult underweight, overweight and obesity

according to BMI

Classification BMI (kg/m2)

Underweight < 18.5

Severe thinness < 16

Moderate thinness 16-16.99

Mild thinness 17-18.49

Normal average 18.5-24.99

Overweight ≥ 25

Pre-obese 25-29.99

Obese ≥ 30

Obese class I 30-34.99

Obese class II 35-39.99

Obese class III ≥ 40

B-Anthropometry

Aim: to compare peer (ideal or average) BW to the actual BW (special tables).

Anthropometry is practical, simple, rapid, non-invasive, non-expensive and reproducible technique for evaluating body fat and muscle mass.

It can be easily done by dietitian.

B-AnthropometryK/DOQI guidelines :The anthropometric measurement that are valid for assessing

nutritional status:1. For body fat : triceps (or biceps) skin fold(TSF) .2. For muscle mass : mid arm muscle circumference (MAMC)

&mid arm circumference (MAC).3. For obesity : BMI4. % of usual body weight (UBW) and % of standard body

weight (SBW).This measures should be taken immediately post-dialysis at right side of the body; best carried out by the same observer

As a general rule, the percentile values/normal

limitation to the use of anthropometry is that serial measurements are best carried out by the same observer

adequate nutrition Values >95 %

risk of malnutrition values 75 % and 95 % significant malnutrition

values <75 %

More sophisticated measures of body composition include :

Bioelectric impedance analysis (BIA) Dual-energy x-ray absorptiometry (DEXA)

A major drawback of these techniques is the difficulty in distinguishing between fat mass and body water.

At present, anthropometry is the only method that can be readily performed in most units.

BIA or DEXA should be reserved for selected patients.

III-Laboratory evaluation

1. Visceral protein: negative acute phase reactants; albumin, prealbumin, transferrin and amino acids.

2. Lipids: chlosterol, TG and other lipids.3. Somatic protein and nitrogen surrogates: BUN

and serum creatinine.4. Growth factors: IGF-1 and liptin.5. Peripheral CBC, lymphocyts.6. Others.

III-Laboratory evaluationI-Plasma protein measurements

Serum albumin Transferrin Prealbumin Amino acids

I-Plasma protein measurements

Serum albumin Transferrin Prealbumin Amino acids

I-Plasma protein measurementsSerum Albumin Clinical practice guidelines for nutrition were published by a working group for the NKF/DOQI recommended that the serum albumin concentration (obtained either predialysis or when stable) should be measured monthly.


Serum Albumin Impact of Low serum albumin level: It is strong predictor of mortality and

hospitalization; risk rises dramatically and logarithmically as levels decline below 4.0 g/dL.

It has been shown to predict coronary calcification.


Serum transferrin: Serum transferrin is not good indicator of nutritional

status; perhaps due to fluctuations in iron stores, presence of inflammation and changes in volume status.


Prealbumin

The plasma concentration of prealbumin (has a shorter half-life than albumin) provides a consistent assessment of visceral protein and can be used to assess the response to nutritional interventions begun for presumed malnutrition as it.

This protein is normally excreted and metabolized by the kidney and tends to accumulate in renal failure.

I-Plasma protein measurements PrealbuminValue < 30 mg/dL is indicative of malnutrition in the patients on maintenance hemodialysis.

I-Plasma protein measurements Amino acids

There is a variable plasma amino acid pattern in ESRD.

In general, the levels of the essential and branched chain AA are decreased, while the nonessential AA are either within the normal range or increased.

III-Laboratory evaluationII-Plasma cholesterol

concentration The plasma cholesterol concentration is reduced in

malnourished patients with normal renal function.

Cholesterol levels are also lower in patients with ESRDs. In this setting, there is an inverse relationship between mortality and the cholesterol concentration.

III-Laboratory evaluationIII-Blood urea nitrogenReflects the balance between urea generation and removal Malnourished patients often show a gradual reduction in

BUN and become wasted.Low levels commonly seen in dialyzed patients (well

dialyzed or inadequately dialyzed) with poor nutrition. Low predialysis BUN levels have also been associated with

increased mortality. It is for this reason, protein catabolic rate is monitored in

dialysis patients, since this parameter can estimate protein intake in the stable patient.

III-Laboratory evaluationIV-Creatinine productionSince creatinine is produced from nonenzymatic

creatine metabolism in skeletal muscle, estimating the rate of creatinine production has been used to assess lean body mass in stable patients.

Estimated lean body mass was below normal in 47 and 66 % of hemodialysis and peritoneal dialysis patients, a presumed reflection of inadequate nutrition.

III-Laboratory evaluation V- C-Reactive protein A positive acute phase reactant protein. It correlates negatively with visceral protein

concentration. Help to uncover potential covert

inflammation especially if serum level of albumin or prealbumin is low.


No gold standard measurement. Therefore, a panel of measurements is recommended and including:


Subjective global assessment (SGA)

• Conventional SGA is a simple method depends on the experience of clinician to make an overall evaluation of nutritional status.

• Advantages: includes objective data and several manifestations of poor nutritional status.

• Limitation: heavy reliance on the clinical judgment and the inability to tailor a specific nutritional therapy.


This is a clinical method for evaluation of nutritional status; including:-

A- History and symptoms:1- % of weight loss in the last 6 months2- Dietary nutrient intake3- Presence of anorexia, nausea, vomiting, diarrhea or

abdominal pain4- Functional capacity5- Metabolic demands in the view of activity


B-Physical parameters focus on:• Assessment of subcutanous fat.• Assessment of muscle wasting in the temporal

area, deltoid and quadriceps.• Presence of sacral or ankle odema.• Presence of ascites.

Subjective global assessment (SGA) The SAG has good reproducibilty and correlates

well with outcome in ESRD.

Indices of malnutrition in HD patients

1. S. albumin concentration < 4.0 gm/dl.2. Low s.prealbumin concentration (<30 mg/ dl)3. Low b. urea & s. creatinine level in patients

with residual renal function.4. PCR < 0.8gm/Kg/day.5. Chol. concentration<150mg/dl(3.9mmol/L).6. Transferrin <150 mg/dl.

Indices of malnutrition in HD patients

7. IGF-1 concentration < 300 µg/L.8. Low predialysis serum K (and possibly

phosphororus) concentration. 9. Marked reduction in anthropometric

measurement 10. Continuous decline in estimated dry weight.11. BW < 80% of ideal weight.

Agenda• Definition• Factors contributing to malnutrition• Disorders of nutrient metabolism in CKD• Nutritional assessment • Nutritional therapy• Conclusion and Recommendations

Nutritional therapy Why malnutrition should be corrected? Many studies documented that poor

nutritional status increases the morbidity and mortality CKD patients.

Specifically; low s. creatinine ,albumin concentration and % of ideal dry BW at time of initiation of maintenance dialysis are associated with increased risk of morbidity and mortality during sub sequent years of HD.

Why malnutrition should be corrected? PEM is one of the strongest predictors of mortality and morbidity and is the third of the killing triad in CKD and HD patients

1. CV accidents2. Infection

3. PEM

Nutritional therapy

Interventions to prevent and/or treat malnutrition in advanced kidney failure

CKD patients:1- Close supervision and nutritional counseling (especially for patients on protein-restricted diets).2- Initiation of dialysis or kidney transplant in advanced CKD patients with apparent uremic malnutrition despite vigorous attempts to rectify it.

Maintenance dialysis patients:1- Appropriate amount of dietary protein (> 1.2 g/kg/day) and calorie (> 35 kcal/kg/day) intake.2- Optimal dose of dialysis (urea reduction ratio > 70%). Use of biocompatible hemodialysis membranes.3-Nutritional support in chronic dialysis patients who are unable to meet their dietary needs:a-Oral supplements.b-Tube feeds (if medically appropriate).c-Intradialytic parenteral nutritional supplements for HD patients.d-Amino acid dialysate for peritoneal dialysis patients.e-TPN

Nutritional therapyStrategies for correction of malnutrition I. Dietary counseling, support and optimization.II. Adequate dialysis.III. Nutritional support in chronic HD patient who are

unable to meet their dietary needs: 1- Oral supplementation. 2- Tube feeding(if medically appropriate). 3- IDPN supplements for HD patients. 4- AA dialysate for PD patients. 5-Continuos total parenteral nutrition(TPN)

Nutritional therapy

Other interventions 1. Correction of anemia, metabolic acidosis and SHPT.2. Anabolic agents :insulin, growth factor, or

androgenic anabolic steroid.3. Exercise.4. Treatment of inflammation :statin, vit E.5. Social work.6. Pharmacy support.7. Transplantation.

Nutritional therapyDietary requirement The recommended average level of nutritional

intake are listed in the following table.

These recommendations are consistent with NKF ,KDOQI and EBP guidelines for nutrition for CKD patient.

Recommended intakes of protein, energy, and minerals in kidney failure

Protein Energy Phosphorus Sodium

Chronic kidney disease-Stages 1-3 (GFR > 30 ml/min)-Stages 4-5 (GFR < 30 ml/min)

No restriction

0.60-0.75 g/kg/day

No restriction

35 kcal/kg/day

600-800 mg/day

600-800 mg/day

< 2 g/day

< 2 g/day

End-stage renal disease-Hemodialysis

- Peritoneal dialysis

> 1.2 g/kg/day

> 1.3 g/kg/day

35 kcal/kg/day

35 kcal/kg/day

600-800 mg/day

600-800 mg/day

< 2 g/day

< 2 g/day

Acute renal failure-No dialysis

- Dialysis

1-1.2 g/kg IBW/day1-1.2 g/kg IBW/day

35 kcal/kg/day

35 kcal/kg/day

600-800 mg/day

600-800 mg/day

< 2 g/day

< 2 g/day

74

Recommended vitamin intake for patients receiving maintenance hemodialysis

Thiamine (B1) 1.1–1.2 mg/day Riboflavin (B2) 1.1–1.3 mg/day Niacin 14–16 mg/day Pantothenic Acid 5 mg/dayVitamin B6 10 mg/day Vitamin B12 2.4 mg/day Biotin 30 mcg/day Vitamin C 75–90 mg/dayFolic acid 1 mg/dayZinc 15 mg/day

Nutritional therapyNeeds for individualizationAdherence to the renal diet is difficult & stressful.Prescribed diet should be individualized to help every patient

in the terms of: cost, palatability, comorbidities and cultural eating habits.

Too many restriction should be avoided as they may lead to poor intake.

Reinforcement by all members of the family and medical stuff.

Compliance should be assessed on regular basis even monthly .

Strategies to enhance oral intake

Adequacy of dialysis

Early referral to dialysis is very crucial. Optimal dose of dialysis(URR>70%). Use of biocompatible HD membrane. Keep KT/V =1-1.2 An important consensus: Adequate dialysis coupled with good nutrition is

the main pillar for best quality of life.Adequate dialysis corrects uremia & anorexia which

enhance nutrition.

Peer rather than actual BW

Protein and caloric recommendation should be based on the peer BW for healthy subjects of the same age, sex, height and body frame size as the patients.

Recommendation

• Understanding and application of the nutritional principles.

• Periodic assessment of nutritional status (once/ month) should be part of the routine care of CKD and dialysis patients to permit early recognition.

• Providing and institution of appropriate therapy for the best improvement of nutrition status .

• Renal dietitian should be a member of the medical personals.

Take home message

• PEM is underappreciated, although it largely preventable and completely curable.

DهDلDلDا DمDكDاDزDجخDيDرDاً

Recommended intakes of protein, energy, and minerals in kidney failure

Protein Energy Phosphorus Sodium

Chronic kidney disease-Stages 1-3 (GFR > 30 ml/min)-Stages 4-5 (GFR < 30 ml/min)

No restriction

0.60-0.75 g/kg/day

No restriction

35 kcal/kg/day

600-800 mg/day

600-800 mg/day

< 2 g/day

< 2 g/day

End-stage renal disease-Hemodialysis

- Peritoneal dialysis

> 1.2 g/kg/day

> 1.3 g/kg/day

35 kcal/kg/day

35 kcal/kg/day

600-800 mg/day

600-800 mg/day

< 2 g/day

< 2 g/day

Acute renal failure-No dialysis

- Dialysis

1-1.2 g/kg IBW/day1-1.2 g/kg IBW/day

35 kcal/kg/day

35 kcal/kg/day

600-800 mg/day

600-800 mg/day

< 2 g/day

< 2 g/day

88

Recommended vitamin intake for patients receiving maintenance hemodialysis

Thiamine (B1) 1.1–1.2 mg/day Riboflavin (B2) 1.1–1.3 mg/day Niacin 14–16 mg/day Pantothenic Acid 5 mg/dayVitamin B6 10 mg/day Vitamin B12 2.4 mg/day Biotin 30 mcg/day Vitamin C 75–90 mg/dayFolic acid 1 mg/dayZinc 15 mg/day

Recommended daily dietary intake for adultpatients on maintenance hemodialysis

VitaminsEBPG nutrition, NDT 2007

A conceptual model for etiology of PEW inCKD and direct clinical implications.

Response to reduced dietary protein andenergy intake.

Response to reduced dietary protein andenergy intake.

• (A) Normal response. Reduced dietary protein and energy drive an increase in hunger and

• a fall in REE, loss of protein preferentially from the visceral organs, and increased insulin sensitivity of muscle.The liver and kidney provide glucose, and serum albumin is maintained at a normal level.

• (B) Response with PEW. During PEW, the adaptations to increase hunger and lower REE are blunted in part by an increased half-life of leptin and ghrelin and in part by inflammation and dialysis. The loss of protein occurs preferentially from muscle because of the effects of metabolic acidosis, glucocorticoids, and inflammation, leading to increased insulin resistance. Dialysis results in the loss of amino acids, stimulating muscle protein breakdown. Under the influence of inflammation and metabolic acidosis, the liver makes glutamine for deamination in the kidney, increases acute-phase reactants, and reduces serum albumin. The kidney increases glucose production from glutamine under the influence of metabolic acidosis.

Potential causes of frailty and protein-energy wasting in elderly patients with end stage kidney disease.

Clinical consequences of frailty and protein-energy wasting in elderly patients with end stage kidney disease.

Potential preventive and therapeutic strategies for frailty and PEW in elderly ESRD patients

Readily utilizable criteria for the clinical diagnosis of protein energy wasting in chronic kidney disease criteria

Selected nutritional parameters for varying levels of kidney disease

Strategies to enhance oral intake

Potential causes of protein-energy wasting in patients with non-dialysis dependent chronic kidney disease

Potential causes of PEM in patients with non-dialysis dependent CKD

Methods of evaluation for diagnosis of PEM in patients with non-dialysis- dependent CKD

Schematic representation of the development of protein-energy wasting with advancing stages of CKD

Selected nutritional parameters for varying levels of kidney disease (K/DOQI guidelines)

Nutritional Parameters

Stages 1-4 CKD Stage 5 Hemodialysis

Calories (kcal/kg/d) 30 – 35 35 - 60Protein (g/kg/d) 0.6 – 0.75 1.2Fat (% total kcal) For patients at risk for CVD, < 10% saturated

fat, 250-300 mg cholesterol/dSodium (g/d) < 2 2Potassium (g/d) Match to laboratory

values2 - 3

Calcium (g/d) 1.2 2 from diet and medicines

Phosphorus (mg/d) Match to laboratory values

800 – 1000

Fluid (ml/d) Unrestricted with normal urine output

1000 + urine

protein energy malnutrition in ckd

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