Assessment of the Nutritional Status of Pediatric … of the Nutritional Status of Pediatric...

Assessment of the Nutritional Status of Pediatric Patients on Regular Hemodialysis

THESIS

Submitted for Fulfillment of

master degree in pediatrics

By

SAMER AHMED ABED

(MB.,Bch.)

Supervised

by

Dr. HALA MOHAMMED LOTFY MA'AROF

Assistant professor of Pediatrics

Faculty of Medicine, Cairo University

Dr. SAMAR MOHAMMED SABRY

Assistant professor of Pediatrics


Dr. EMAD EMIL GHOBRIAL

Lecturer of Pediatrics


Faculty of medicine Cairo University

2012

Abstract

I

ABSTRACT

Poor nutritional intake is a common concern in children with CKD, and

this often leads to severe growth retardation. Maintaining adequate

nutrition and normal body composition is important for patients with

chronic kidney disease (CKD) as well as those with end-stage renal

disease (ESRD). These needs are further enhanced in children because of

the added requirements for maintaining growth.

This study was carried out to assess the nutritional status in 50 Egyptian

children with end stage renal disease on regular Hemodialysis at the

Hemodialysis unit of the Center of Pediatric Nephrology and

Transplantation of Cairo University. Their age ranged from 3 – 16 years.

Results revealed their height was the most affected anthropometric

parameter, as (78%) of the patients were shorts (height SDS below -3)

and ranged between 0.0 – -9.2 (mean -4.6 ± 2.1), body weight is less

affected than height, as body weight SDS of (34%) of the patients were

less than -3 SDS, ranged from 1.6 – -13.8 (mean -2.84 ± 2.38). in addition

the body mass index of 16% of the patient were < 3rd percentile , while

only 4% of the patient were > 97th percentile. The BMI ranged from 8.9 –

23.4 (mean 17.1 ± 2.84).

Key words: nutrition status, children, chronic kidney disease, growth retardation

Acknowledgment

Ii

ACKNOWLEDGMENT

First and foremost, I thank Allah who have granted me the ability to accomplish this work.

I would like to express my deepest gratitude and deep thanks to Dr Hala Mohammed Lotfy Ma'arof, Assistant Prof. of pediatrics, Cairo University, faculty of medicine for her encouragement and valuable instruction

I wish to express my profound gratitude and heavy thanks to Dr. Samar Mohammed Sabry, Assistant Prof. of pediatrics, faculty of medicine, Cairo University for her generous supervision, valuable advice, and constant support throughout the whole work.

I am deeply grateful to Dr Emad Emil Ghobrial, lecture of pediatrics, faculty of medicine, Cairo University for his kind supervision and constant help.

I am also extremely grateful to all the team of hemodialysis unit of the Center of Pediatric Nephrology and Transplantation of Cairo University for their great help and cooperation.

Words can never express my sincere appreciation to my family for their encouragement and unlimited support.

INDEX

Iii

Index

Content Page List of tables iv

List of figures v

List of abbreviations vi

Introduction and aim of the work viii

Review of literature Chapter (1): Chronic Renal FailureChapter (2): HemodialysisChapter (3): Nutritional Assessment in Chronic kidney disease

12445

Patients and methods 75

Results 81

Discussion 91

Summery 99

Conclusion and Recommendation 101

References 102

Arabic summary 117

List of tables

IV

LIST OF TABELS

Number and title of the tables Page1. Criteria for definition of CKD. 12. NKF-K/DOQI Classification of the stages of CKD. 23. Classification according to the decrease in GFR. 24. The pathophysiologic manifestation of CKD. 45. Markers of kidney damage. 96. Summarizes the advantage and disadvantage of peritoneal dialysis. 227. Criteria for performing living related donor or cadaver renal transplantation in pediatrics patients.

23

8. Summarize post – transplantation complication in pediatrics patients. 239. Causes of hemolysis in dialysis patients. 4110. Vaccination needs during Hemodialysis. 4411. Recommended energy and protein intake in children by age. 4712. Recommended calcium and phosphorus intake at different ages. 5513. Causes of kidney disease wasting. 6014. Recommended parameter and frequency of nutritional assessment for children with CKD stages 2 to 5 and 5D.

73

15. Biochemical & hematological data. 8316. caloric intake 8417. caloric intake frequency and percentage 8418. protein intake 8419. protein intake frequency and percentage 8420. anthropometric measurements 8521. Height and Weight standard deviation percentage 8522. BMI percentile and percentage 8623. Anthropometric measurement range and mean ± SD 8624. mid arm anthropometric frequency and percentile 8725. mid arm anthropometric measurement frequency and percentage 8726. caloric intake correlations 8827. protein intake correlations 8828. duration of HD correlations 88

List of figures

V

List of figures

Number and title of the tables Page1. A bell-shaped vessel 242. Hemodialysis machine 253. Male to female ratio 814. The original renal disease in our study 825. The vascular access used in our study group 826. The serum albumin in our study group 857. Correlation between caloric intake/kg/day and BMI 888. Correlation between caloric intake/kg/day and TSF 899. Correlation between DurHD and Ht.SDS 89

List of abbreviations

vi


ACEIs: Angiotensin – converting Enzyme Inhibitors ALS: acid – labile subunit.

AMDR: Acceptable Macronutrient Distribution Range

ARAs: Angiotensin receptor antagonists

ARF: Acute Renal Failure

AVF: Arterio – Venous Fistula BDI: Beck Depression Inventory

BIA: Bioelectrical Impedance Analysis

BMI: Body Mass Index

BUN: Blood Urea Nitrogen

Ca: Serum Calcium CAD: Cadaveric

CAPD: Continuous Ambulatory Peritoneal Dialysis

CCPD: Continuous Cyclic Peritoneal Dialysis

CERA: Continuous Erythropoiesis Receptor Activator

CKD: Chronic Kidney Disease CRF: Chronic Renal Failure

CRI: Chronic Renal Insufficiency

CT: Computed Tomography

CVD: Cardio Vascular Disease

DPI: Dietary Protein Intake DRI: Dietary Reference Intake

DXA: Dual energy X-ray Absorptiometry

ECF: Extra Cellular Fluid

EDS: Excessive Day time Sleepiness

EER: Estimated Energy Requirement ESRD: End Stage Renal Disease

FSH: Follicle Stimulating Hormone

FT3: Free Triiodothyronine

GFR: Glomerular Filtration Rate

GH: Growth Hormone GHR: Growth Hormone Receptors

GI: Gastro – Intestinal

HBV: Hepatitis B Virus

HD: Hemodialysis

HDL: high Density Lipoprotein HIF: Hypoxia Inducer Factor

HIV: Human Immunodeficiency Virus

ICF: Intra Cellular Fluid


vii

IDPN: Intra-Dialytic Parenteral Nutrition

IGF – 1: Insulin like Growth Hormone – 1.

IGF – D: Insulin like Growth Factor – Displacer IGF: Insulin – Like Growth Factor

IGF1 – R: Insulin like Growth Factor 1 – Receptor

IL – 6: Interleukin 6

IPD: Intermittent Peritoneal Dialysis

IRF: Impaired Renal Function IV: Intravenous

K/DOQI: Kidney Disease Outcomes Quality Initiative.

KDW: Kidney Disease Wasting

LH: Luteinizing Hormone

LRD-RT: Living Related Donor - Renal Transplantation MAC: Mid Arm Circumference

MAMA: Mid Arm Muscle circumference Area

MAMC: Mid Arm Muscle Circumference

NIPD: Nocturnal Intermittent Peritoneal Dialysis

NKF – K/DOQI: The National Kidney Foundation – Kidney Disease Outcomes Quality Initiative.

NKF: The National Kidney Foundation nPCR: Normalized Protein Catabolic Rate

nPNA: Normalized Protein equivalent of Nitrogen Appearance

PAL: Physical Activities Level

PO4: Serum Phosphorus

PTH: Parathyroid Hormone RAS: Renin – Angiotensin System

RDA: Recommended Dietary Allowances

rhGH: Recombinant Human Growth Hormone

rhIGF-1: Recombinant Human Insulin like Growth Factor - 1

rhIGFBP-3: Recombinant Human Insulin like Growth Factor Binding Protein -3 RT: Renal Transplantation

SDS: Standard Deviation Score

STAT: Signal Transducer and Activator of Transcription

T3: Triiodothyronine

T4: Thyroxine TBW: Total Body Water

TNF – α: Tumor Necrosis Factor Alpha

TSH: Thyroid Stimulating Hormone

TT3: Total Triiodothyronine

TT4: Total Thyroxine URR: Urea Reduction Rate

UTI: Urinary Tract Infection

VA: Vascular Access

Introduction and aim of the work

viii


Malnutrition is recognized to be a serious and common complication of

chronic kidney disease (CKD) and is associated with increased morbidity

and mortality (Foster and Leonard, 2004). Contributing factors to this

malnutrition include poor appetite, various co-morbidities, dietary

restrictions, inflammation and infection, metabolic acidosis and oxidative

stress (Morais et al, 2005).

Nutritional status is particularly important in children as it influences

growth, sexual development and neurocognitive development, thus its

accurate and regular assessment is highly recommended in patients on

regular hemodialysis (HD). (Cameron, 1996)

Malnutrition includes several aspects. One of the important aspects is the

state of decreased body protein mass and fuel reserves (body protein and

fat mass), now better known as protein- energy wasting (PEW) (Fouque

et al, 2008). Given the complexity of the pathogenesis and clinical

picture of PEW, no single measure, but rather panels of nutritional

measures are necessary to diagnose the condition (Edefouti et al, 2009).

The Kidney Disease Outcome Quality Initiative (K/DOQI) recommended

the following measures for evaluation of protein-energy nutritional status

for children receiving maintenance HD: Dietary intake (interview or


ix

diary), serum albumin, height or length, head circumference (for children

< 3 months), estimated dry weight, Height standard deviation score (SD),

weight/height index / midarm anthropometric measures and skin fold

thickness (National Kidney foundation, 2000).

Aim of the work

The aim of this study is to assess the growth and the nutritional status in

children with CKD and to correlate their caloric and protein intake with

different variables (anthropometric measurements, serum alb and duration

of hemodialysis).

Chronic Kidney Disease

1


Definition

Chronic kidney diseases (CKD) is defined as kidney damage or

glomerular filtration rate (GFR) < 60ml/min/1.73m² for 3 months or

more, regardless of the underlying etiology .The current definition of

CKD encompasses all of the patients who were classified as having

chronic renal failure (CRF) and chronic renal insufficiency (CRI).

Table 1: Criteria for the definition of CKD:

Criteria for the Definition of CKD1.Kidney damage for ≥ 3 mo, as defined by structural or functional abnormalities of the kidney, with or without decreased GFR, manifested by 1 or more of the followingfeatures:• Abnormalities in the composition of the blood or urine• Abnormalities in imaging tests• Abnormalities on kidney biopsy2. GFR < 60 mL/min/1.73 m² for ≥ 3 mo, with or without the other signs of kidney damage.

(NKF-K/DOQI, 2002)

Kidney damage is defined as structural or functional abnormalities of the

kidney, initially without decreased GFR, that can lead to a future decrease

in kidney function; and is identified by abnormalities in the blood, urine,

imaging tests, and renal biopsy .The broader implications of this common

definition for CKD is that patients are identified earlier with their kidney

disease, which may prolong their native kidney function and improve

their long-term health.

CKD staging: To achieve these aims, a CKD staging system has been

developed, with an associated action plan for each stage (Table 2). It is

important to note that the CKD stages only apply to children 2 years old

and above. (Wong and Mak.2007)


2

Table 2: NKF-K/DOQI Classification of the Stages of CKD

Stage GFR (mL/min/1.73 m²) Description Action Plan*1 ≥90 Kidney damage with normal

or increased GFRTreat primary and co-morbid conditionsSlow CKD progression, CVD risk reduction

2 60–89 Kidney damage with mildreduction of GFR

Estimate rate of progression of CKD

3 30–59 Moderate reduction of GFR Evaluate and treat complications

4 15–29 Severe reduction of GFR Prepare for kidney replacement therapy

5 <15 (or dialysis) Kidney failure Kidney replacement therapy

(NKF-K/DOQI, 2002)

According to the decrease in GFR, the loss of renal function may also classify into the following stages as shown in (table 3):

Table 3: classification according to the decrease in GFR

Stage Residual renal function

Symptoms or metabolic abnormalities

Impaired renal function(IRF)

50-80% Free of symptom &signs except for slight increase in serum urea nitrogen & creatnine

Chronic renalinsufficiency (CRI).

25-50% Changes in plasma ions. Impaired calcium absorption Retarded growth rate Major stress as dehydration can lead to acute

renal failure (ARF).

Chronic renal failure (CRF).

<25% Metabolic acidosis, renal osteodystrophy, hypertension, anemia, ect.

End stage renal disease(ESRD)

<10% Chronic dialysis or transplantation is needed to maintain quality of life

(Chan et al., 2002)

Etiology

In children, CKD may be the result of congenital, acquired, inherited, or

metabolic renal disease and the underlying cause correlates closely with

the age of the patient at the time when the CKD is first detected. CKD in

children younger than 5 yr is most commonly a result of congenital


3

abnormalities such as renal hypoplasia, dysplasia, and/or obstructive

uropathy. Additional causes include congenital nephrotic syndrome,

prune belly syndrome, cortical necrosis, focal segmental

glomerulosclerosis, polycystic kidney disease, renal vein thrombosis, and

hemolytic uremic syndrome.

After 5 yr of age, acquired diseases (various forms of glomerulonephritis

including lupus nephritis) and inherited disorders (familial juvenile

nephronophthisis, Alport syndrome) predominate. CKD related to

metabolic disorders (cystinosis, hyperoxaluria) and certain inherited

disorders (polycystic kidney disease) may present throughout the

childhood years.

Pathogenesis

In addition to progressive injury with ongoing structural/metabolic

genetic diseases, renal injury may progress despite removal of the

original insult. Although the precise mechanisms that result in

progressive deterioration of renal function are unclear, putative factors

include hyperfilteration injury, persistent proteinuria, systemic or intra

renal hypertension, renal calcium-phosphorus deposition, and

hyperlipidemia. (Vogt and Avner, 2007)

The pathophysiology of CKD

CKD may be viewed as a continuum of disease with increasing

biochemical and clinical manifestations as renal function deteriorate.

(Vogt and Avner, 2007)


4

TABLE 4: the pathophysiologic manifestations of CKD

MANIFESTATION MECHANISMSAccumulation of nitrogenous waste products / Acidosis

Decrease in glomerular filtration rate Decreased ammonia synthesis Impaired bicarbonate reabsorption

Decreased net acid excretionSodium retention Excessive renin production

OliguriaSodium wasting Solute dieresis

Tubular damageUrinary concentrating defect Solute dieresis

Tubular damageHyperkalemia Decrease in glomerular filtration rate

Metabolic acidosis Excessive potassium intake

Hyporeninemic hypoaldosteronismRenal osteodystrophy Impaired renal production of 1, 25-

dihydroxycholecalciferol Hyperphosphatemia Hypocalcemia

Secondary hyperparathyroidismGrowth retardation Inadequate caloric intake

Renal osteodystrophy Metabolic acidosis Anemia

Growth hormone resistanceAnemia Decreased erythropoietin production

Iron deficiency Folate deficiency Vitamin B12 deficiency

Decreased erythrocyte survival

Bleeding tendency / Infection Defective platelet function Defective granulocyte function Impaired cellular immune functions

Indwelling dialysis cathetersNeurologic symptoms (fatigue, poor concentration, headache, drowsiness, memory loss, seizures, peripheral neuropathy)

Uremic factor(s) Aluminum toxicity

Hypertension

Gastrointestinal symptoms (feeding intolerance, abdominal pain)

Gastroesophageal reflux

Decreased gastrointestinal motility

Hypertension Volume overload

Excessive renin productionHyperlipidemia Decreased plasma lipoprotein lipase activityPericarditis/cardiomyopathy Uremic factor(s)

Hypertension

Fluid overloadGlucose intolerance Tissue insulin resistance (Vogt and Avner, 2007)


5

Clinical manifestations

Many children with CKD do not manifest clinically until their renal

failure is advanced. In many patients the diagnosis is first made during an

emergency room visit for a complication of CKD, such as bone pain,

anemia, or vomiting resulting from uremic gastritis.

Clinical manifestations of CKD are the consequence of metabolic

derangements that accompany failure of kidney functions, and

accumulation of known and unknown ‘uremic toxins’. Poor linear growth

and short stature are the well-recognized clinical features of long-

standing CKD. While renal osteodystrophy may remain asymptomatic in

some children with CKD, bone pain, difficulty in walking, and skeletal

deformities may be prominent symptoms in others. Poor tolerance of

usual activity, being tired, poor attention span, and congestive cardiac

failure can be the manifestations of anemia. High urine output is a

common manifestation in patients with congenital urinary abnormalities

or tubulointerstitial disorders. New onset of enuresis can be an early

manifestation of concentrating defect seen in CKD, and should always be

investigated. Oliguria is generally present in those with underlying

glomerulonephritis or nephrotic syndrome. Poor nutritional intake,

resulting in calorie-protein malnutrition, is a prominent manifestation in

some patients with CKD. Need for a large volume of nutrition-poor free

water to compensate for high urine output can further compromise the

nutritional state in some patients. Uremic encephalopathy, gastritis,

Pericarditis, and neuropathy can develop in the advanced uremic state.

These complications are especially common if dialysis therapy is delayed,

or clearance of uremic ‘toxins’ in dialysis is inadequate. As noted above,

some patients present for the first time with such advanced complications.

(Wong and Mak, 2007)


6

Anemia: Erythropoietin synthesis is decreased (potentially leading to

anemia, which causes fatigue).Anemia is a frequent complication of CKD

in children. Warady and Ho determined that a hematocrit less than 33% at

dialysis initiation was not only associated with a greater mean number of

hospitalization days within the initial year of dialysis but was also

associated with a significantly greater probability for a hospitalization of

30 days or more during that year In addition, there was an estimated 52%

greater risk of death in association with the presence of anemia.

(Warady et al., 2003)

Cachexia is a common problem in patients with CKD. It is characterized

by loss of lean body mass and high metabolic rate despite inadequate

dietary intake. The term malnutrition, which implies that abnormalities

can be reversed by provision of appropriate nutrition, inadequately

describes the pathologic state of cachexia in CKD. The etiology is

multifactorial. Metabolic acidosis, insulin resistance, and increased

cytokine expression stimulate muscle protein loss by mechanisms that

work independent of the impact of anorexia. (Mitch et al., 2002)

Anorexia is commonly seen in patients with CKD and ESRD, and has

been attributed to the presence of ‘middle molecules’ in patients with

renal dysfunction. Although the identity of these anorexigenic molecules

in uremic serum is unknown, (Mitch, 2005)

Other potential causes of anorexia in CKD include an inability to

distinguish flavors, gastric irritation caused by medications,

hemodynamic instability as a result of antihypertensive therapies, a

sensation of fullness during peritoneal dialysis, and psychologic and

economic factors. (Mitch, 2005)


7

Elevated circulating levels of leptin, which mediate its effects through

the central melanocortin system, may be an important cause of cachexia

in CKD. (Cheung et al., 2005)

Growth failure has long been recognized as one of most common and

profound clinical manifestations of CKD in infants, children, and

adolescents. Multiple factors that contribute to growth retardation are age

at onset of CKD, type of primary renal disease, concomitant metabolic

acidosis, malnutrition from calorie deprivation, anemia, renal

osteodystrophy, and perturbations of the growth hormone (GH) and

insulin-like growth factor (IGF) axis. (Tonshoff et al., 1997)

GH resistance seen with CKD may be caused by a combination of (1)

down-regulation of GH receptors (GHR) in liver and the growth-plate and

(2) defective GH post-receptor signaling involving impaired

phosphorylation of signal transducer and activator of transcription (STAT

5) in the skeletal muscles. Furthermore, increased levels of IGF binding

proteins may limit the bioavailability of IGF-I. Proinflammatory

cytokines, such as tumor necrosis factor alpha (TNF-α) and interleukin 6

(IL-6), can also cause GH resistance by down-regulating GHR and

impairing GH signaling at the same step of STAT 5 phosphorylation. The

precise role of these cytokines in abnormalities in GH metabolism and

their impact on growth is not entirely clear at this time. (Schaefer et al.,

2001)

Insulin resistance is common in children with CKD. The major site of

this resistance is the peripheral tissues; mainly the skeletal muscle.

Circulating toxins in CKD may be responsible for the insulin resistance,

which has been shown to improve after the initiation of dialysis.

Correction of acidosis, (Mak, 1998) anemia, and hyperparathyroidism, as


8

well as low protein diets, may improve insulin resistance and correct

glucose tolerance. (Mak, 1986)

Peritoneal dialysis is more effective than hemodialysis in improving

insulin resistance with ESRD (Mak, 1996)

Metabolic acidosis due to CKD may stem from a number of

abnormalities: reabsorption of filtered bicarbonate, reduction in ammonia

synthesis, decreased excretion of titratable acid, and decreased

acidification of tubular luminal fluid by the distal nephron. Type IV renal

tubular acidosis, as a result of loss or insensitivity of aldosterone

receptors in the renal tubules, is also common in advanced stages of

CKD. (Craig, 2007)

Renal osteodystrophy encompasses a spectrum of high- to low-turnover

skeletal lesions. The impact of therapy may change the histologic pattern.

As CKD progresses, secondary hyperparathyroidism develops as a result

of several factors: phosphate retention, impaired renal 1, 25(OH) 2D3,

alterations in PTH secretion, hypocalcemia, skeletal resistance to the

calcemic actions of PTH, and alterations in the calcium-sensing receptor.

Phosphorus retention increases the secretion of PTH indirectly by

lowering serum ionized calcium levels and also by reducing renal

synthesis of1, 25(OH) 2D3 through inhibition of the enzyme 1 α-

hydroxylase in the proximal tubules. Normal serum phosphorus

concentration is maintained in mild to moderate CKD by increasing PTH

levels, thus attempting to increase urinary phosphate excretion.

Hyperphosphatemia usually develops in CKD stages 4 to 5.

(Craig, 2007)


9

Table 5: Markers of kidney damage

Blood:

Serum creatinine elevation Blood urea nitrogen (BUN) elevation Hypoalbuminemia Hyperuricemia Hypo- or hypernatremia Hypo- or hyperkalemia Hypo- or Hyperphosphatemia Metabolic acidosis

Urine: Microalbuminuria Proteinuria Hematuria RBC casts Pyuria WBC casts Tubular cells Granular casts Lipid

Imaging:

Increased echogenicity Small, ‘hyperechoic’ kidneys Absence of one kidney Acute pyelonephritis Kidney scarring Large kidneys Kidney size disparities Hydronephrosis Urinary obstruction Renal artery stenosis Nephrocalcinosis Urinary calculus disease Cystic kidney diseases Medullary sponge kidney

(Craig, 2007)

Assessment of the Nutritional Status of Pediatric … of the Nutritional Status of Pediatric...

Documents

Transcript of Assessment of the Nutritional Status of Pediatric … of the Nutritional Status of Pediatric...