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NEPHROLOGY NURSING JOURNAL ■ May-June 2004 ■ Vol. 31, No. 3 287

Challenges for Nephrology Nurses inthe Management of Children withChronic Kidney Disease

Deborah Miller, MSN, RN, CNN, is ClinicalNurse Specialist in Pediatric Nephrology, InovaFairfax Hospital, Falls Church, VA. She is a memberand past president of the Capitol Chapter of ANNA.

Dina Macdonald, BSN, RN, CNN, is ClinicalNephrology and Renal Transplant Coordinator,UCSD Medical Center/Children’s Hospital, SanDiego, CA. She is a member of the ANNA PediatricSIG and member and past president of NephrosSouth Chapter of ANNA.

Ken Kolnacki, BSN, RN, CNN, isCoordinator/Staff Nurse in the Pediatric DialysisUnit, Albany Medical Center Hospital, Albany, NY.He is a member of the ANNA Pediatric SIG and amember of ANNA Northeast Tri-State Chapter.

Teresa Simek, MSN, CPNP, CDE, CNN, is theNephrology and Hypertension Case Manager, MaryBridge Children’s Hospital and Health Center,Tacoma, Washington. She currently is a member ofthe ANNA Pediatric SIG Committee and willassume the leadership position in April 2004. She isa member of ANNA’s Greater Puget Sound Chapter.

For 3 decades, considerableresources have been directedtoward the effective manage-ment of patients with end stage

renal disease (ESRD). As a result,attention is now being focused onidentifying those patients with earli-er stages of kidney disease to slow orinterrupt disease progression(Compton, Provenzano, & Johnson,2002). Since children may notexhibit signs and symptoms ofchronic kidney disease (CKD) untilsignificant progression has occurred,nephrology experts have establishedclinical guidelines to promote earlieridentification of patients at risk andto provide recommendations foroptimizing prevention and treatmentstrategies (National Kidney Foundation[NKF], 2002). These and other educa-tional efforts are critical in promotingappropriate referral to nephrologycare and improving health outcomesin children with CKD.

This article reviews the complica-tions associated with CKD and thechallenges they present in nephrologynursing care. These important clinicalchallenges include the management ofanemia, metabolic acidosis, malnutri-tion, hyperparathyroidism and associ-

ated bone disease, and ultimately,impaired growth and development.Nephrology nurses caring for childrenwith CKD should be knowledgeableregarding these issues so that appro-priate intervention can be initiatedand growth and development are notsignificantly compromised.

EpidemiologyAlthough ESRD is the most

severe stage of CKD, early stages ofCKD are more common and can alsosignificantly impact the health andwell-being of affected children (U.S.Department of Health and HumanServices, 2000). In 2001, the NorthAmerican Pediatric Renal TransplantCase Study (NAPRTCS) reportedthat 4,666 patients under 20 years ofage with CKD were registered in itsdatabase (Seikaly, Ho, Emmett, Fine,& Tejani, 2003). Although the prima-ry etiologies of CKD vary with age,congenital structural anomalies pre-

dominate in pediatric patients (seeTable 1). Inflammatory, infectious, orimmunologic processes that damagethe structures of the kidney, such asglomerulonephritis, may also beinvolved in the etiology of CKD. Incontrast, hypertension and diabetesare the primary etiologies for CKD inthe adult population.

Identifying Pediatric Patientswith CKD

Since patients with early-stage CKDare often asymptomatic, delayed diag-nosis is common (Kaskel, 2003;Szromba, Thies, & Ossman, 2002).Additionally, CKD has been under-diagnosed and undertreated because ofa lack of agreement on definition andclassification of disease stage. As aresult, a series of guidelines have beendeveloped by the NKF Kidney DiseaseOutcomesQuality Initiative (K/DOQI)to improve the detection and manage-ment of CKD (NKF, 2002). As stated in

An important treatment goal for pediatric nephrology caregivers is the optimization of a child’scapacity for normal growth and development. However, the physiologic and metabolic derange-ments associated with chronic kidney disease (CKD) significantly alter these processes, creat-ing important challenges in the care of affected children. Evidence-based clinical practice guide-lines support early recognition and treatment of CKD-related complications to improve growthand development and, ultimately, quality of life for children with this chronic condition.

Goal:Describe the complications of chronic kidney disease (CKD) in affected children and emphasize theimportance of early and optimal medical management to improve treatment outcomes.

Objectives:1. Identify the primary etiologies of CKD in children.2. Describe the physiologic and metabolic changes that affect growth and development in children

with CKD.3. Discuss recommendations for evaluation, assessment, and treatment of children with growth

failure related to CKD.

Deborah Miller, Dina Macdonald, Ken Kolnacki, and Teresa Simek

This offering for 2.0 contact hours is being provided by the American Nephrology Nurses’ Association(ANNA), which is accredited as a provider of continuing nursing education by the American Nurses’Credentialing Center-Commission on Accreditation (ANCC-COA). ANNA is an approved provider of continuingeducation in nursing by the California Board of Registered Nursing, BRN Provider No. 00910.

The Nephrology Nursing Certification Commission (NNCC) requires 60 contact hours for eachrecertification period for all nephrology nurses. Forty-five of these 60 hours must be specific to nephrologynursing practice. This CE article may be applied to the 45 required contact hours in nephrology nursing.

NEPHROLOGY NURSING JOURNAL ■ May-June 2004 ■ Vol. 31, No. 3288

these guidelines, CKD is established bythe presence of kidney damage or aglomerular filtration rate (GFR) < 60ml/min/1.73 m2 (see Table 2). This clas-sification has recently been updated toinclude suggested action plans for eachstage of CKD, focusing on preventiveinterventions (Hogg et al., 2003). Theterm “chronic renal insufficiency” hastraditionally been used to define thestage of CKD associated with a GFR <75 ml/min/1.73 m2 (Fine, Kohaut,Brown, & Perlman, 1994).

Since major health consequencesof kidney disease may be improvedor prevented by early intervention,efforts should be directed towardscreening and identifying patientswho are at risk. Patients at risk forCKD include those with a family his-tory of renal disease, congenital oracquired renal anomalies, or otherpredisposing chronic diseases suchas diabetes or hypertension (see

Table 3). Previously, there was littleconsensus on which tests should bedone to screen for kidney disease inchildren. For individuals consideredto be at risk for CKD, early-stage dis-ease may be detected by relativelysimple tests, such as blood pressure,urine protein, and serum creatininemeasurements. The NKF guidelinesemphasize persistent proteinuria asan important marker of kidney dam-age (NKF, 2002). Proteinuria refers toan increase in urinary excretion ofalbumin or total protein. Urine pro-tein can be measured with standardurine dipstick testing. Additionally,kidney damage can be detected byexamining the urine sediment or bydipstick methods to identify the pres-ence of red blood cells (RBC) andwhite blood cells in the urine. Resultsof kidney imaging or biopsy studiesmay also be used to support a diag-nosis of CKD.

An estimate of GFR is the bestoverall indicator of the level of kidneyfunction. In children and adolescents,it is recommended that GFR bedetermined by using prediction equa-tions including the patient’s height,

gender, and serum creatinine concen-tration (Hogg et al., 2003). Of the var-ious equations currently available, theSchwartz formula has gained wide-spread use and provides a practicalmethod for estimating GFR in child(Schwartz, Haycock, Edelmann, &Spitzer, 1976) (see Table 4).

Managing the Complicationsof CKD

In addition to screening for early-stage disease, optimal care for patientswith CKD includes recognition andeffective management of related com-plications, such as anemia, metabolicacidosis, malnutrition, bone and min-eral abnormalities, and growth failure.Major therapeutic interventions forthese complications of CKD are dis-cussed in the following sections.

Anemia. Anemia may develop inthe early stages of CKD and has beenconsistently associated with anincreased risk of cardiac morbidityand mortality (Szromba et al., 2002).Anemia associated with CKD inadults is a well-known condition forwhich effective management is avail-able. In children, recognition and

Challenges for Nephrology Nurses in the Management of Children with Chronic Kidney Disease

Congenital

Structural (59%)• Obstructive uropathy• Aplasia/hypoplasia/dysplasia• Reflux nephrology• Polycystic kidney disease• Prune belly syndrome

Inherited (3%)

• Familial nephritis• Cystinosis• Primary oxalosis

Acquired

Inflammatory/immunologic (14%)• Focal segmental glomeru-

losclerosis• Systemic lupus erythematosus• Renal infarct• Chronic glomerulonephritis

Infectious (4%)

• Pyelonephritis• Hemolytic uremic syndrome

Table 1Primary Etiologies of Kidney

Disease in Children

Note: Adapted from NAPRTCS (2003).

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

Stage

1

2

3

4

5

GFR(ml/min/1.73 m2)

90

60-89

30-59

15-29

< 15 (or dialysis)

Description

Kidney damage withnormal or increasedGFR

Kidney damage withmild reduction of GFR

Moderate reduction ofGFR

Severe reduction ofGFR

Kidney failure

Action Plan*

Treat primary andcomorbid conditions

Slow CKD progression,CVD risk reduction

Estimate rate of pro-gression of CKD

Evaluate and treatcomplications

Kidney replacementtherapy

Notes:* CVD indicates cardiovascular disease.The actions that are listed in the more severe stages of CKD also include actionsfrom less severe stages.Adapted from Hogg et al. (2003).


treatment of anemia is also important;if left untreated, anemia may be alsoassociated with impairments in cogni-tive function, immune response, qual-ity of life, and growth (NKF, 2001).The appropriate treatment of anemiaincludes: (a) correction of iron defi-ciency (6 mg elemental iron/kg/dayorally; intravenous iron is recom-mended if a hemoglobin of 11 g/dLcannot be attained with oral therapy)(NKF 2001); (b) stimulation of ery-thropoiesis (erythropoietin 150units/kg/wk in 3 divided doses, withdose adjustments based on weight)(Eschbach, 1989); (c) vitamin supple-ments (e.g., folic acid, vitamin B6,ascorbic acid) to assist in RBC forma-tion (NKF, 2001); and (d) RBC trans-

fusions as indicated for acute bloodloss associated with hemodynamicinstability or for chronic blood loss inepoetin-resistant patients (NKF, 2001).The nephrology nurse’s role in CKDscreening and anemia prevention iskey to avoiding other cardiovasculareffects as well as impaired growth anddevelopment (Szromba et al., 2002).Additionally, nurses are challengedwith providing routine educationalsupport to patients and their families.It is important to emphasize the ben-efits of complying with anemia thera-pies, although improvements may notoccur for approximately 4 weeks(Szromba et al., 2002).

Metabolic acidosis. Acid-basehomeostasis is regulated primarily by

the kidneys and involves proximaltubular reabsorption of bicarbonateand distal tubular secretion of acids. Asrenal function declines, metabolic aci-dosis develops as a result of bicarbon-ate wasting and the reduced ability ofthe kidneys to excrete ammonia andother acids. Children with CKD com-monly develop metabolic acidosis, par-ticularly when GFR decreases to below50% of normal (Chan, Goplerud,Papadopoulou, & Novello, 1981).

Metabolic acidosis is known to bea profound contributor to poor nutri-tional status and growth in childrenwith CKD due to increased proteincatabolism, decreased albumin syn-thesis, bone loss, and resistance to thy-roid and growth hormones (Adrogue& Madias, 1998; Kuemmerle et al.,1997). Close attention to serum bicar-bonate levels is required at every stageof CKD and should be monitored ateach visit. Correction of metabolic aci-dosis with alkali therapy increasesappetite, decreases protein degrada-tion, and increases lean body mass,and is recommended when serumbicarbonate levels fall below 22mmol/L (Kovacic, Roguljic, &Kovacic, 2003). Initial treatmentinvolves the oral administration ofsodium bicarbonate or sodium citratein a dose of 2 mEq/kg/day (Holliday,1994).

Malnutrition. Progression ofCKD in adults and children has a sig-nificant impact on nutritional status.Outcomes such as morbidity, mortal-ity, and quality of life are correlatedclosely with nutritional status (Brady& Hasbargen, 2000). For all patientswith CKD, dietary recommendationschange as the patient’s degree of kid-ney function declines and must beclosely monitored to prevent malnu-trition. In children, dietary recom-mendations vary based on the etiolo-gy of the kidney disease and stage ofgrowth. Restriction of calories, pro-tein, and fluids is rarely recommend-ed. For most children, protein restric-tion should not be lower than the rec-ommended daily intake (RDI) for age(Nelson & Stover, 1994). Ongoingeducational efforts require collabora-tion of health care providers, patients,

· Family history of polycystic kidney disease or other genetic kidney disease· Low birth weight infants· Children with a history of acute kidney failure resulting from perinatal hypox-

emia or other acute insults to the kidneys· Renal dysplasia or hypoplasia· Urologic disorders—especially obstructive uropathies· Vesicoureteral reflux associated with recurrent urinary tract infections and

scars in the kidneys· Prior history of acute nephritis or nephrotic syndrome· Prior history of hemolytic uremic syndrome· Prior history of Henoch-Shönlein purpura· Diabetes mellitus· Systemic lupus erythematosus· Prior history of hypertension, e.g., from renal artery or renal vein thrombosis

in the neonatal period

Table 3Disorders that Increase the Risk of CKD

Note: Adapted from Hogg et al. (2003).

Table 4Estimating GFR in Children with CKD

Body Weight (kg)

< 10

≥10, ≤ 70

> 70

Formula

0.45 x height (cm)SCr (mg/dL)

0.55 x height (cm)SCr (mg/dL)

1.55 x age (yr) + 0.5 x height (cm)SCr (mg/dL)

Note: From Schwartz et al. (1976).


and family members with special con-sideration for cultural differences,socioeconomic status, and patient andfamily educational level (Wells, 2003).In early childhood, poor kidney func-tion may result in suboptimal caloricintake due to fatigue, anorexia, acido-sis, and gastroesophageal reflux dis-ease (GERD). GERD uncontrolled bydrug therapy may require a surgicalprocedure such as a Nissen fundopli-cation to wrap the esophagus aroundthe stomach to prevent reflux and sub-sequent vomiting. Malnutrition maybe exacerbated by the increased pro-tein catabolism that occurs in uremicpatients (Kaskel, 2003) and by the pro-teinuria that occurs in patients withnephrotic syndrome. The combina-tion of reduced energy and proteinintake along with urinary protein loss-es may have a negative impact ongrowth and development. Therefore,patients identified as high-risk or cur-rently malnourished should bereferred to a pediatric renal nutrition-ist for a comprehensive nutritionalassessment and follow- up. This assess-ment should include a detailed recordof protein, caloric, and fluid intake forthe previous 3 days. In addition,nephrology nurses should be attunedto recognizing signs of malnutritionincluding weight loss (or loose-fittingclothes), decreased strength andendurance, and loss of muscle mass(which may be evident during bloodpressure monitoring). Anthropometricmeasurements such as head circumfer-ence, skinfold thickness, and mid-armmuscle circumference are also clinical-ly useful indicators of protein-energynutritional status (NKF, 2000).

Bone disease. CKD is associatedwith abnormal calcium and phospho-rus metabolism and a variety of bonedisorders. Bone disorders can be clas-sified into those associated with highparathyroid hormone (PTH) levelsand those with low or normal PTHlevels (NKF, 2000). Increases inserum phosphate and decreases in1,25-dihydroxycholecalciferol (vitaminD3) lead to a reduction in calciumabsorption and disruption of the phos-phorous-calcium balance. These factorsstimulate the production of PTH, lead-

ing to secondary hyperparathyroidism,and if left untreated, secondary hyper-parathyroidism may cause metabolicbone disease (i.e., renal osteodystro-phy). The development of bone diseasemay manifest as pain, bone fractures,and impaired growth.

Although bone biopsy remainsthe gold standard for histologicallyclassifying renal bone disease, it is noteasy to perform and is currently indi-cated only for patients with sympto-matic disease (NKF, 2002). Indices ofbone/mineral metabolism should bemeasured at all stages of CKD. Intactparathyroid hormone (iPHT), phos-phorus, and ionized calcium levelsare the most commonly used bio-markers. These biomarkers should befollowed longitudinally in individualpatients, as it is expected that abnor-malities may develop or becomemore severe as kidney function dete-riorates (NKF, 2002).

The challenge for nephrologycaregivers includes not only restoringthe calcium-phosphate homeostasis inthe child with CKD but also achiev-ing optimal somatic growth and bonemass. The current standard of care formanaging bone disease related toCKD includes dietary phosphaterestriction, administration of oralphosphate-binders (with the caveatthat aluminum- based binders shouldnot be used), oral calcium supple-ments, and vitamin D analogs as indi-cated. The pediatric renal nutritionistcan be helpful in identifying less obvi-ous sources of dietary phosphorus(e.g., preservatives in processedfoods) and calcium (e.g., HawaiianPunch with “added calcium” containsadditional hidden phosphorus).

Growth failure. A unique physicaland psychosocial burden for childrenwith CKD is the impact of the diseaseand its complications on growth anddevelopment. Growth failure is com-mon in children with CKD and is asignificant cause of morbidity andmortality (Wong et al., 2000). It maybe helpful to use height z-scores (thenumber of standard deviations fromthe mean value for a reference popu-lation) to closely monitor trends in anindividual patient’s height and

weight. The Centers for DiseaseControl offer computer software thatcalculates and graphs Z-scores forheight, weight and weight/height(Centers for Disease Control &Prevention [CDC], 2004).

A peripubertal onset of renal fail-ure is associated with an average 2-year delay in puberty as well as apotentially irreversible loss of malereproductive capacity (Phadke,MacKinnon, & Dossetor, 1970;Schaefer et al., 1990). Despite aggres-sive management, 62% of male and41% of female CKD children (age<15 years) demonstrate an adultheight more than 2.5 standard devia-tion scores (SDS) below the mean fornormal adults (Rizzoni et al.,1985).The degree of renal failure, and par-ticularly a GFR < 25 mL/min/1.73m2,is an important factor influencingpoor growth (Kaskel, 2003); however,growth failure can occur at any stageof CKD (NAPRTCS, 2003).

Normally, the greatest longitudi-nal growth occurs during the first 2years of life (Schaefer, Haffner, Wuhl,& Mehls, 1999). This phase accountsfor one third of the final adult staturewhen nutritional and metabolic pro-files are favorable. Thus, the risk forgrowth failure is highest in patientsdeveloping CKD at birth or early ininfancy. Early nutritional interventionand prevention of metabolic deficitsassociated with congenital renal failurecan preclude severe stunting of growthin the first 2 years of life (Van Dyck,Bilem, & Proesmans, 1999). Low elec-trolyte formulas may not provideenough sodium, potassium, and phos-phorus in the rapidly growing infant.Therefore, electrolyte panels should beclosely monitored and infant formulasadjusted as needed.

To better understand the manage-ment of growth failure in childrenwith CKD, it is useful to brieflyreview normal growth hormone (GH)physiology and the derangementsoccurring in the CKD child. TheGH–insulin-like growth factor-I (IGF-I) axis plays a critical role in promot-ing linear growth and development(see Figure 1) (Roelfsema & Clark,2001). GH is secreted by the soma-



totrophs of the anterior pituitarygland and is regulated by stimulatoryand inhibitory hypothalamic hor-mones; neurotransmitters and neu-ropeptides related to factors affectingGH secretion (such as sleep, stress,exercise, and nutrition); and feedbackby circulating levels of GH and IGF-I. Circulating GH stimulates hepatic(but also bone and muscle) productionof IGF-I, the primary mediator of GH-related effects. IGF-I is primarilybound to IGF-binding protein(IGFBP)-3, with smaller amountsbound to other IGFBPs or circulatingin the free (active) form. UnboundIGF-I exerts its growth-promotingeffects by stimulating expansion andmaturation of chondrocytes, increasingprotein synthesis, and promoting glu-cose uptake by muscle tissue. Of inter-est, IGF-I also acts in the kidney toincrease renal plasma flow and GFR.

In children with CKD, anemia,metabolic abnormalities, poor nutri-tional status, and renal osteodystro-phy all contribute to the developmentof growth failure. However, perturba-tions of the GH–IGF-I axis have beendocumented and are believed to beimportant contributing factors as well(Roelfsema & Clark, 2001). In thesepatients, GH levels are elevated dueto impaired feedback mechanismsand reduced renal clearance. Despiteincreased GH levels, the bioavailabil-ity of IGF-I is reduced due todecreased liver production, increasedIGFBP-3 degradation, and increasedconcentrations of other inhibitoryIGFBPs. Overall, these derange-ments result in relative GH and IGF-I resistance and impaired growth anddevelopment.

Alterations in normal growth pat-terns may have a significant psy-chosocial impact on adolescents. It isreported that children with CKDexhibit an increased risk for thedevelopment of social phobias, anxi-ety attacks, and depressive disorders(Stabler, Siegel, & Tancer, 1993).Nephrology nurses play an importantrole in the identification of issuesrelated to delayed growth and devel-opment in adolescents and children.In young people struggling to attain

autonomy in the face of chronic ill-ness, as well as with issues of treat-ment noncompliance, collaborationwith social work and psychology col-leagues may be indicated.

GH Treatment in Childrenwith CKD

Recombinant technology has sig-nificantly increased the availability ofGH treatment for all growth-impairedchildren. Several clinical trials havedemonstrated the efficacy of GHtreatment in improving staturalgrowth (Fine et al., 1994; Fine,Kohaut, Brown, Kuntze, & Attie,1996; Hertel et al., 2002; Hokken-Koelega et al., 1991; Vimalachandra,Craig, Cowell, & Knight, 2001) andrestoring previously disproportionateextremities to normal size (Zivicnjak,Franke, Ehrich, & Filler, 2000) in chil-dren with CKD. GH therapy is mosteffective in promoting growth when it

is initiated at an early age in childrenwith adequate nutrition and whenappropriate doses are employed(Haffner et al., 2000; Vance &Mauras,1999). After the child hasachieved a target height, discontinua-tion of GH treatment may result in adecelerated growth velocity; so care-ful follow-up is required to determinethe need for long-term treatment(Fine et al., 1996). Although concernshave been raised regarding the poten-tial for deterioration of renal functionduring GH therapy, studies to datehave not shown significant changes inrenal parameters in GH-treated chil-dren with CKD (Brewer et al., 1995;Fine et al., 1996; Schaefer et al., 1999;Wuhl et al., 1998).

The nephrology nurse plays a vitalrole in the early identification ofpatients with CKD and growth fail-ure. Accurate measurement alongwith careful attention to monitoring

Figure 1GH–IGF-I axis. In children with CKD, the primary abnormalities

involve reduced IGF-I production by the liver and increased levels of binding proteins, except for IGFBP-3,

which undergoes enhanced proteolysis.


of patient status may be associatedwith improved therapeutic outcomes(see Figure 2). Evaluation of renal lab-oratory values and GFR should beaccompanied by a growth assess-ment, including height and weightmeasurements at least every 3months, in order to identify changesin linear growth and height velocity.Before the patient is started on GHtherapy, effective management ofcomplications associated with CKD(e.g., anemia, metabolic acidosis, andrenal osteodystrophy) should be initi-ated, as described (NKF, 2002).

Treatment with GH should be con-sidered in children who have (a) aheight or height velocity more than 2standard deviations below the meanfor age- and sex-matched children, (b)growth potential documented by openepiphyses, and (c) no other contraindi-cation for recombinant human growth

hormone use (NKF, 2002). GH thera-py is currently indicated for childrenwith growth failure associated withCRI (GFR < 75 mL/min/1.73 m2) upuntil the time of renal transplantation.

Before GH treatment is initiated, abaseline physical examination shouldbe performed, including Tanner stag-ing to determine pubertal status. Inaddition, baseline bone x-rays, labo-ratory values (BUN, Cr, iPTH, TFTs),and a funduscopic exam should beobtained. GH dose calculations arebased on body weight, but require-ments are higher in children withCKD compared to patients with GHdeficiency due to the GH–IGF-I resis-tance described. At each visit, growthand renal assessments should berepeated. GH dose increases shouldbe considered with weight increasesand for compliant patients not exhibit-ing acceptable growth. On a semian-

nual basis, Tanner staging and boneage x-rays should be repeated to mon-itor pubertal growth and advance-ment of bone development. GH treat-ment should also be discontinued atthe time of renal transplant, closure ofthe epiphyses, or if neoplasia occurs.

Posttransplant GH Therapy Optimizing growth following renal

transplant can be challenging in thepresence of corticosteroid use orabnormal graft function. A review ofclinical studies shows that GH therapysignificantly increases height andgrowth rate in children who haveundergone renal transplantation(Acott & Pernica, 2003). Importantly,GH therapy was not associated with anincreased rate of acute rejection; how-ever, some patients may be more sus-ceptible to rejection than others. A sep-arate analysis of patients under 19 years


Figure 2A nursing algorithm for the evaluation and treatment of growth failure in children with CKD.


of age at the time of transplant did notidentify GH treatment as an additionalrisk factor for the development of renalcarcinoma (Mehls et al., 2002).

Although the development of treat-ment-associated neoplasms andreduced renal function are often citedas potential side effects, current evi-dence indicates the contrary. In a con-trolled study by Fine and colleagues(2002), no difference in the incidenceof malignancies was observed in chil-dren who received GH posttransplantversus nontreated patients. A landmarkEuropean study following 40,000 chil-dren treated with GH between 1987and 2003 also found no increase incancer frequency as compared tountreated children (Wilton, 2003).

Given the need for corticosteroidadministration following renal trans-plantation and the relative insulinresistance noted in children withCKD, the risk for glucose intoleranceand potential exacerbation by GHtherapy is a concern. To date, somestudies have noted transient eleva-tions in fasting serum glucose and/orinsulin levels (Maxwell & Rees, 1998;Tonshoff et al., 1993;), while othershave shown no change in these para-meters (Benfield, Parker, Waldo,Overstreet, & Kohaut, 1993; Broyer,1996; Guest et al., 1998). Until moredata from long-term studies are avail-able, careful monitoring of glucosemetabolism is recommended in thesepatients.

Barriers to GH TreatmentDespite advances in GH therapy,

many children with CKD-relatedgrowth failure do not receive treat-ment (Seikaly et al., 2003). Barriers totreatment include parental fear ofadverse effects, perceptions aboutlack of efficacy, fear of injections, andcost issues. In addition, family mem-bers, medical personnel, and third-party payers may erroneously viewCKD-related growth failure as a cos-metic condition. Nephrology nursescan be instrumental in educatingpatients and their families about theseimportant issues and ensuring thatappropriate assessment and monitor-ing are performed to ensure third-

party reimbursement and long-term,uninterrupted GH treatment.

Conclusion As the incidence of CKD contin-

ues to rise, there is an increased needfor earlier screening and intervention.There is evidence that it may be pos-sible to slow the progression of CKDif intervention is initiated early.Similarly, complications related toCKD, such as anemia, malnutrition,osteodystrophy, and metabolic acido-sis, must be recognized and managedeffectively to reduce further morbidi-ty, including growth failure. Growthfailure is a unique challenge fornephrology clinicians caring for chil-dren with CKD, requiring carefulassessments to determine eligibilityfor GH treatment. Nurses must beknowledgeable about issues in chil-dren with CKD, as they play a vitalrole in monitoring and treatingcomorbidities, optimizing GH thera-py, educating patients, and providingsupport to patients and families.

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Hokken-Koelega, A.C., Stijnen, T., deMuinck Keizer-Schrama, S.M., Wit,J.M., Wolff, E.D., de Jong, M.C., et al.(1991). Placebo-controlled, double-blind, cross-over trial of growth hor-mone treatment in prepubertal chil-dren with chronic renal failure. Lancet,338, 585-590.

Holliday, M. (1994). Fluid and nutritionsupport. In M. Holliday, M.T. Barrat,& E.D. Avner (Eds). Pediatric nephrology(3rd ed, pp. 287-311.) Baltimore:Lippincott, Williams and Wilkins.

Kaskel, F. (2003). Chronic renal disease: Agrowing problem. Kidney International,64, 1141- 151.

Kovacic, V., Roguljic, L., Kovacic, V.(2003). Metabolic acidosis of chroni-cally hemodialyzed patients. AmericanJournal of Nephrology, 23, 158-164.

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Deborah Miller, MSN, RN, CNN; Dina Macdonald, BSN, RN, CNN; Ken Kolnacki, BSN, RN, CNN; Teresa Simek, MSN, CPNP, CDE, CNN

Posttest — 2.0 Contact Hours Posttest Questions

(See posttest instructions on the answer form, on page 296.)

1. Primary causes for CKD in chil-dren include

A. diabetes and hypertension.B. congenital structural abnormali-

ties.C. immune-mediated diseases

and glomerulonephritis.D. diseases secondary to infec-

tion.

2. What formula is recommendedfor estimating creatinine clear-ance in children?

A. There is no formulaB. Cockroft-Gault formulaC. MDRD formulaD. Schwartz formula

3. Metabolic acidosis contributes topoor growth in children due to

A. increased catabolism only.B. increased catabolism and

bone loss only.C. increased catabolism, bone

loss and resistance to growthhormone only.

D. increased catabolism, boneloss, resistance to growth hor-mone and anemia.

4. The risk for growth failure ishighest in children developingCKD during which period?

A. Infancy to age 2B. School-ageC Peri-pubertalD. Adolescent

5. Which factor is a cause for growthfailure in children with CKD?

A. Low levels of circulating GHB. Resistance to GH and IGF-IC. Decreased concentration of

inhibiting IGFD. Insufficient somatotroph

receptors

6. The role of IGF-I in growth is critical in

A. synthesizing GH in the soma-totrophs.

B. increasing renal plasma flow.C. binding ingested proteins to

IGFBP-3.D. stimulating expansion of chon-

drocytes.

7. For children with CKD, every visitto the renal clinic should include

A. bone x-rays.B. detailed diet history.C. accurate height and weight

measurements.D. anthropometric measurements.

8. Growth hormone should be con-sidered in children with CKD when

A. height is more than 1 standarddeviation below the mean forage and sex-matched children.

B. weight is more than 2 standarddeviations below the mean forage and sex matched children.

C. height velocity is more than 2standard deviations below themean for age and sex-matched children.

D. growth potential is blocked by aclosed epiphyses.

9. Growth hormone dose calcula-tions and dose increases arebased on

A. body weight only.B. body weight and height veloci-

ty only.C. body weight, height velocity,

and glomerular filtration rate(GFR) only.

D. body weight, height velocity,glomerular filtration rate (GFR)and PTH level.

10. You are working in a pediatrictransplant clinic and meet Jerry, a7-year-old male with a 1-year histo-ry of kidney transplant. He meetsthe height recommendations forinitiation of growth hormone.Based on a literature review youshould monitor Jerry more closelyfor which of the following after ini-tiating growth hormone therapy?

A. Acute rejectionB. Renal carcinomaC. Glucose intoleranceD. Weight loss



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1. a b c d

2. a b c d

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6. a b c d

7. a b c d

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1. The objectives were related to the goal. 1 2 3 4 52. Objectives were met

a. Identify the primary etiologies of CKD in children. 1 2 3 4 5b. Describe the physiologic and metabolic changes

that affect growth and development in children with CKD. 1 2 3 4 5

c. Discuss recommendations for evaluation, assessment, and treatment of children with growth failure related to CKD. 1 2 3 4 5

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ANSWER FORMChallenges for Nephrology Nurses in the Management of Children

with Chronic Kidney DiseaseDeborah Miller, Dina Macdonald, Ken Kolnacki, and Teresa Simek

Describe the complications of chronic kid-ney disease (CKD) in affected children andemphasize the importance of early andoptimal medical management to improvetreatment outcomes.

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