Article nephrology

Chronic Kidney Disease in Children and

Adolescents
Susan F. Massengill, MD,*
Educational Gap
Maria Ferris, MD, MPH,
PhD† Chronic kidney disease (CKD) is a devastating diagnosis with many co-morbidities, in-
creasing the risk of mortality 30 to 150 times that of the general pediatric population.
Recognition of at-risk children can lead to earlier screening and risk reduction. Primary
Author Disclosure care clinicians are often unaware of the comorbid conditions and long-term consequen-
Drs Massengill and ces of CKD, particularly with respect to cardiovascular disease, nutrition and growth,
Ferris have disclosed neurocognitive development, and burden of disease.
no financial
relationships relevant
Objectives After completing this article, readers should be able to:
to this article. This
commentary does not 1. Be aware of the life course of CKD and its co-morbidities.
contain a discussion of 2. Recall the risk factors and complications of pediatric CKD.
an unapproved/ 3. Discuss measures to prevent or delay the progression of pediatric CKD.
investigative use of 4. Optimize the communication between the primary care clinician and nephrologist in
a commercial product/ treating children, adolescents, and young adults with CKD.
device.
Case 1
A 13-month-old toddler new to your practice presents for his 1-year health maintenance
visit with poor growth and developmental delay. He is just now sitting without support
and appears to have occasional leg pain. He is pale, weighs 7.9 kg, and has a normal blood
pressure. The results of laboratory studies are remarkable for anemia (hemoglobin,
9 g/dL [90 g/L]), profound acidosis (carbon dioxide, 12 mEq/L [12 mmol/L]), azotemia
(urea nitrogen, 117 mg/dL [41.8 mmol/L]; creatinine, 2.44 mg/dL [216 mmol/L]), and
profound hypocalcemia (calcium, 5.6 mg/dL [1.40 mmol/L]), prompting further evalu-
ation where hypocalcemia was confirmed. Urinalysis revealed a specific gravity of 1.005 and
proteinuria (1þ). Renal ultrasonography revealed bilateral renal hypoplasia. Renal replace-
ment therapy was initiated with peritoneal dialysis, and the patient is on the renal transplan-
tation waiting list.

Case 2
A previously healthy, 14-year-old, African American girl
Abbreviations presents with a 3-month history of facial and lower-extremity
1,25(OH)2 D: 1,25-dihydroxyvitamin D rash and a 4.5-kg weight loss. Her medical history is unre-
ACE: angiotensin-converting enzyme markable for contributing conditions. She denies sexual ac-
CKD: chronic kidney disease tivity, travel, pet ownership, or tick exposure. Her family
CKiD: Chronic Kidney Disease in Children history is positive for type 1 diabetes mellitus in a younger
CVD: cardiovascular disease brother and hypothyroidism in her mother. On physical ex-
eGFR: estimated glomerular filtration rate amination, she is hypertensive (blood pressure, 150/90
ESKD: end-stage kidney disease mm Hg), with a malar erythematous rash and palpable pur-
GFR: glomerular filtration rate pura on the lower extremities. Laboratory studies reveal the
HCT: health care transition following: serum creatinine, 2.5 mg/dL (221 mmol/L); esti-
MBD: metabolic bone disease mated glomerular filtration rate (eGFR), 34 mL/min/1.73 m2;
urea nitrogen, 75 mg/dL (26.8 mmol/L); and positive

*Director, Pediatric Nephrology, Levine Children’s Hospital, Adjunct Associate Professor of Pediatrics, University of North Carolina
School of Medicine, Charlotte, NC.
†
Director, Pediatric Dialysis and Transplant Programs, UNC Kidney Center, Founder and Director, The UNC Children’s Hospital
TRxANSITION Program, University of North Carolina at Chapel Hill, Chapel Hill, NC.

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antinuclear antibody and anti–double-stranded DNA re-
sults. Urinalysis reveals blood (3þ), proteinuria (4þ), 10
to 20 red blood cells per high-power field, and 1 red
blood cell cast. Urine protein to creatinine ratio is 2.5
(reference range, <0.2). Renal biopsy reveals a crescentic
diffuse proliferative glomerulonephritis (World Health
Organization class IV systemic lupus erythematosus
nephritis).
Introduction
In 2002, the National Kidney Foundation established
evidence-based clinical practice guidelines entitled the
Kidney Disease Outcomes Quality Initiatives, which
were designed to define chronic kidney disease (CKD)
based on the presence or absence of markers of kidney
damage and the level of kidney function (glomerular filtra-
tion rate [GFR]) irrespective of the type of kidney disease
(kidney.org/professionals/kdoqi/guidelines_commentaries.
cfm). The 2 independent criteria for CKD are as follows:
1. Kidney damage for 3 months or longer as defined
by structural or functional abnormalities of the kidney,
with or without decreased GFR, manifested by either
pathologic abnormalities or markers of kidney dam-
age, including abnormalities in the composition of
the blood or urine or abnormalities in imaging studies.
2. GFR less than 60 mL/min/1.73 m2 for 3 months or
longer, with or without kidney damage.
In addition, a common nomenclature was proposed
for stages of CKD (Table 1) to improve communication
between primary care clinicians and nephrologists.
Chronic Kidney Disease
Table 1.
Classification
Stage Description
1 Kidney damage with a normal or increased
GFR (>90 mL/min/1.73 m2)
2 Mild reduction in the GFR
(60-89 mL/min/1.73 m2)
3 Moderate reduction in the GFR
(30-59 mL/min/1.73 m2)
4 Severe reduction in the GFR
(15-29 mL/min/1.73 m2)
5 Kidney failure GFR
(<15 mL/min/1.73 m2 or dialysis)
GFR¼glomerular filtration rate.
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nephrology chronic kidney disease
The Chronic Kidney Disease in Children (CKiD)
study (a longitudinal cohort study of children with mild
to moderate CKD) observes the risk factors related to dis-
ease progression, neurocognition and quality of life
changes, cardiovascular morbidity, and the growth failure
in patients with CKD. (1) From this study, a more precise
and accurate estimated glomerular filtration rate (eGFR) us-
ing serum creatinine, height, and a constant (k) (eGFR ¼ k
[height in centimeters]/serum creatinine) was developed.
An updated constant (k) of 0.413 is used (eGFR ¼
0.413[height in centimeters]/serum creatinine) with chil-
dren with mild to moderate CKD (http://nephron.com/
peds_nic.cgi).
Epidemiology and Etiology of Pediatric CKD
National Health and Nutrition and Examination Survey
data from 1999 to 2006 estimated the incidence of CKD
among adults at 26,000,000 of a population base of 200
million, with millions more at risk. The prevalence of
CKD in children is unknown, but it is estimated at 82
cases per million per year. Conversely, national registries
have determined the incidence of pediatric end-stage
kidney disease (ESKD), the worst form of CKD, at 15
cases per million per year. The 10-year survival rate for
adolescent-onset ESKD is 80%, although lower rates
are seen in adult-onset ESKD. This represents a 30-fold
increase in mortality compared with the general US ado-
lescent population. In this survey, survival was better for
younger adolescents, males, whites, Asians, and trans-
plant recipients. (2)
The cause of ESKD varies by age. Younger patients
have increased rates of structural anomalies of the kidneys
and urinary tract, whereas older children and adolescents
are more likely to have glomerular diseases. (2) The most
frequent acquired and congenital forms of CKD include
glomerulopathies (33%); vesicoureteral reflux, obstruc-
tion, or infections (25%); hereditary nephropathies
(16%); hypoplasia or dysplasia (11%); and vascular disor-
ders (5%). African Americans and Latinos are dispro-
portionately affected by CKD in part due to a higher
incidence of glomerular conditions. With the increasing
incidence of obesity and type 2 diabetes mellitus in youth,
the incidence of CKD in adult life is expected to increase.
The pediatric ESKD population is only 2% of all patients
with this condition, making the transition to adult-
focused care difficult because adult nephrologists are un-
familiar with pediatric diagnoses (ie, the most common
cause of CKD among adults is diabetes mellitus). The life
course of CKD in children and adolescents are discussed
in the following sections and summarized in Table 2.
Pediatrics in Review Vol.35 No.1 January 2014 17
nephrology chronic kidney disease

Table 2. Life Course and Co-Morbidities of Chronic Kidney Disease

Co-Morbidities Events or Sequelae
Traditional cardiovascular Arrhythmias
Hypertension Valvular heart disease
Dyslipidemia Cardiomyopathy (dilated)
Abnormal glucose metabolism Acute cardiac death
Obesity
Tobacco use
Sedentary lifestyle
Nontraditional cardiovascular
Anemia
Volume overload
Abnormal calcium and phosphorus metabolism
Left ventricular hypertrophy
Chronic inflammation
Malnutrition
Metabolic
Hypokalemia and hyperkalemia Arrhythmias
Hyponatremia
Hyperphosphatemia and hypocalcemia Metabolic bone disease
Urinary concentrating defects Diurnal or nocturnal enuresis

g
Acidosis Poor growth
Mineral metabolism
Impaired phosphate excretion
Metabolic bone disease
Decreased vitamin D formation

g
Secondary hyperparathyroidism
Anemia
Erythropoietin deficiency
Blood loss Fatigue
Iron deficiency Impaired cognition
Bone marrow suppression Sleep disturbances
Malnutrition Decreased exercise tolerance
Chronic inflammation Depression
Uncontrolled hyperparathyroidism Poor appetite
Inadequate dialysis

g
Ongoing systemic disease
Nutrition
Acidosis
Anemia
Anorexia
Volume overload
Endocrine disorders Malnutrition
Chronic inflammation Cachexia
Low nutrient intake Protein-energy wasting
Taste disturbances
Nausea and vomiting
Impaired gastric emptying

g
Nutrient loss during dialysis
Growth
Early-onset CKD
Acidosis
Decreased linear growth
Treatment modalities
Poor health-related quality of life
(corticosteroids)
Associated genetic conditions
Protein-calorie malnutrition
Continued

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 nephrology chronic kidney disease

Table 2. (Continued)

g
Co-Morbidities Events or Sequelae
Neurocognitive
Hypertension
Lower IQ Poor school performance
Impaired memory and executive functioning
Sleep disturbances
School absenteeism and grade retention

g
Learning disabilities and ADHD
Disease burden
Number of medications Decreased quality of life
Medication dosing schedule Depression
Medication route (oral, injections, infusions) ADHD
Monitoring (blood pressure, urine) Poor self-esteem
Dietary restrictions Family stress
Need for dialysis Financial burden
Depression Frequent school absences
Frequent parental work absences
Marital discord
Sibling(s) feeling neglected
Immunologic
Immunosuppressed or underimmunization Susceptibility to infections by common
and opportunistic organisms
Reproductive
Impaired fertility Infertility and/or fetal loss
Pregnancy-related events Prematurity, teratogenicity
Psychosocial
School absences Underemployment
Dysmorphic features Few romantic relations, bullying, low self-esteem
Medication adverse effects Nonadherence (high risk in adolescents)
Psychiatric
Depression Depression
Sleep disturbances Anxiety
Posttraumatic stress disorder
Family related
Economic burden Poverty
Parental work or health insurance loss Maladjustment
Divorce Poor family function
Healthy siblings
ADHD¼attention-deficit/hyperactivity disorder.

Pathogenesis of CKD before diagnosis, timing of therapeutic intervention, hyper-

CKD progression is influenced by the severity of the ini-
tial renal damage, extent of nephron loss, and the age of
nephron loss, which limits renal reserve. An increased risk
of progressive structural damage occurs when there is
superimposed acute kidney injury from infections, dehy-
dration, drugs, or toxins. The extent of injury can result
from a single episode, as seen with acute glomerulone-
phritis; continuous injury from vesicoureteral reflux,
chronic infections, obstructive uropathies; or recurrent
injuries from diabetes, lupus, or chronic glomerulopathies.
Additional factors that influence progression include host
susceptibility, genetic susceptibility, and duration of disease
tension, and proteinuria. Periods of rapid growth, such as
with infancy and puberty when body mass increases, may
result in deterioration of renal function due to the increased
filtration demands on the remaining nephron units.
Understanding the presentation of clinical and labora-
tory features of CKD assists in the early diagnosis. Hypo-
plastic and dysplastic nephropathies often present with
fluid and electrolyte losses and growth failure. Glomeru-
lopathies typically present with hypertension, hematuria
(microscopic and macroscopic), edema, and alterations
in urine output. In contrast, tubular and interstitial ne-
phropathies present with significant losses of electrolytes

Pediatrics in Review Vol.35 No.1 January 2014 19

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nephrology chronic kidney disease
(hypokalemia and hypophosphatemia), polyuria, polydip-
sia, urinary concentrating defects, enuresis, metabolic ac-
idosis, and no clinical edema or hypertension. Despite
these factors, progression of CKD is modifiable with
the use of angiotensin-converting enzyme (ACE) inhibi-
tion. The Effect of Strict Blood Pressure Control and
ACE Inhibition on the Progression of Chronic Renal
Failure in Pediatric Patients trial was a randomized con-
trolled trial that involved 385 children, ages 3 to 18 years,
with CKD who were treated with ramipril, an ACE inhib-
itor. This trial found that intensified blood pressure con-
trol and early decreases in proteinuria effectively slowed the
progression of renal disease in those children with CKD
due to primary glomerulopathies or renal hypoplasia-
dysplasia. (3)
Immunizations and CKD
Children with CKD or ESKD, including those undergo-
ing dialysis or those with kidney transplants, are likely to
have reduced responses or reduced duration of immunity
after immunizations, placing them at increased risk for vaccine-
preventable diseases. (4) Either specific disease states
(lupus nephritis, nephrotic syndrome, dialysis, or kidney
transplant) or their consequent therapies lead to subop-
timal immunization rates from delayed or missed im-
munizaions. Children with CKD should receive the
recommended childhood immunizations as published by
the Centers for Disease Control and Prevention (www.
aap.org/immunization; http://www.cdc.gov/vaccines/
schedules/index.html), with the exception of live viruses
in those receiving immunosuppressive medications. Spe-
cial attention is necessary for immunization against hep-
atitis B and pneumococcus. Patients undergoing dialysis,
particularly hemodialysis, are at risk for hepatitis B infec-
tion from suboptimal vaccination responses or a rapid de-
cline in immune response. If postvaccination monitoring
does not reveal protective antibody levels after the pri-
mary series, then reimmunization should be instituted.
If the patient remains nonimmune, then further attempts
at immunization are not recommended. Patients with ne-
phrotic syndrome and those with CKD are at risk for in-
vasive disease from Streptococcus pneumoniae, and all
should receive the recommended dosages of the 13-valent
pneumococcal conjugate vaccine and coverage for addi-
tional pneumococcal serotypes with the 23-valent poly-
saccharide pneumococcal vaccine administered after age
2 years and at least 8 weeks after they have received
the 13-valent pneumococcal conjugate vaccine. Annual im-
munization against influenza is now recommended for
all children older than 6 months, with only the inactivated
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influenza vaccine recommended for those with CKD receiv-
ing immunosuppressive therapies. Finally, immunization
with live-attenuated vaccines, such as measles-mumps-
rubella, varicella zoster virus, and rotavirus, should be
avoided in those children with CKD or transplants who
are receiving immunosuppressive medications, including
corticosteroids.
Cardiovascular Disease in CKD
The long-term survival of children with CKD remains
low compared with the general population. Specifically,
the lifespan of a pediatric patient undergoing dialysis is
shortened by 50 years compared with age- and race-
matched controls. Even after successful renal transplanta-
tion, their lifespan is reduced by 25 years. As in adult
patients, cardiovascular disease (CVD) accounts for most
deaths in patients with pediatric-onset CKD, but unlike
adults, pediatric-onset CKD patients rarely demonstrate
symptomatic atherosclerosis or diabetes mellitus. (5)
The prevalence of cardiovascular events with ESKD is
24.3% and 36.9% in children ages 0 to 4 years and 15
to 19 years, respectively. The most common events included
arrhythmias (19.6%), valvular heart disease (11.7%), cardio-
myopathy (9.6%), and acute cardiac death (2.8%). In a sep-
arate analysis, CVD and cardiac death represented 40% and
20%, respectively, of all deaths in pediatric patients with
ESKD. In addition, cardiovascular alterations that lead to
these terminal events begin in the early stages of CKD pos-
sibly as an adaptation to the hemodynamic and biochemical
derangements present in CKD.
Pediatric patients with CKD have a high prevalence of
traditional risk factors for CVD. One of the most com-
mon risk factors in this population is hypertension. It is
also recognized that high-risk populations, including pa-
tients with diabetes mellitus and CKD, may have normal
office-based blood pressures but significant elevations
outside the office. Termed masked hypertension, these el-
evations are associated with development of end-organ
damage. Recent data from the CKiD study demonstrate
that masked hypertension is prevalent and hypertension is
observed in 54% of patients in the early stages of CKD.
Furthermore, the prevalence of hypertension increases
in patients undergoing long-term dialysis (75%) and re-
mains high after transplantation. The development of hy-
pertension in pediatric CKD is multifactorial. These
patients also demonstrate a high prevalence of dyslipide-
mia and abnormalities in glucose metabolism. Studies
have elucidated several nontraditional risk factors that
perpetuate CVD in these patients, including anemia, al-
tered calcium-phosphorus metabolism, chronic inflammation,

and oxidant stress. Aggressive control of blood pressure,
lipid metabolism, and anemia may be critical in these pa-
tients. Additional therapeutic options, such as exercise,
and anti-inflammatory agents, such as statins, ACE in-
hibitors, and angiotensin receptor antagonists, must also
be examined to enhance the efficacy of traditional car-
dioprotective agents.
Metabolic Derangements
Fluid and Electrolyte Disturbances
Patients with CKD secondary to congenital anomalies of
the kidneys and urinary tract are at risk for hypokalemia,
hyponatremia, and urinary concentrating defects. Primary
care clinicians need to pay particular attention when these
patients develop dehydration because the normal tubular
response to antidiuretic hormone (vasopressin) is im-
paired. Patients with early CKD can present with a non-
gap metabolic acidosis, but as the disease progresses this
metabolic derangement becomes an increased anion gap
acidosis. Hyperkalemia may become worse with progres-
sion of renal disease or in patients receiving ACE inhib-
itors or angiotensin-receptor blockers for hypertension.
Mineral Metabolism and Vitamin D
One of the most common complications of CKD is met-
abolic bone disease (MBD) (previously known as renal
osteodystrophy). CKD-MBD is caused by the inability
of the kidneys to excrete phosphorus and synthesize ac-
tive 1,25-dihydroxyvitamin D (1,25[OH]2 D). The de-
creased 1,25(OH)2 D formation was hypothesized to be
due to loss of functioning renal tissue or a direct result of
hyperphosphatemia. More recently, the role of fibroblast
growth factor 23, a bone-derived regulator of phosphate
metabolism, has been recognized. With the retention of
phosphate, fibroblast growth factor 23 increases and fur-
ther suppresses 1,25(OH)2 D formation by the kidney.
With dysregulation of calcium, phosphorus, and vitamin
D, the parathyroid glands are stimulated and secondary
hyperparathyroidism occurs. Until the CKD becomes se-
vere, the serum levels of calcium and phosphorus remain
normal, but parathyroid levels increase.
The treatment of CKD-MBD begins with restriction
of phosphorus intake. This approach is difficult in chil-
dren without severely affecting their choice of foods.
Phosphorus absorption can be blocked by phosphate
binders, which can be calcium-based compounds or
non–calcium-containing compounds. The role of cal-
cium as phosphate binders is balanced by the newly rec-
ognized dangers of vascular calcification as a result of
elevated calcium and phosphorus in the blood.
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nephrology chronic kidney disease
Hyperparathyroidism can be treated by administration
of active vitamin D metabolites, such as 1,25(OH)2 D,
which may raise the serum levels of calcium and phospho-
rus. Newer artificial vitamin D metabolites, which selec-
tively suppress parathyroid secretion without increasing
absorption of calcium and phosphorus, are often used
in patients with more severe renal failure. Finally, in chil-
dren undergoing dialysis who have uncontrolled hyper-
parathyroidism, activators of the calcium receptors on
parathyroid cells have been found to be effective agents
to control severe CKD-MBD when all other treatment
agents have proven to be ineffective. As result of the avail-
ability of these most recent agents, the need for parathy-
roidectomy in children receiving dialysis has become rare.
Hematologic Complications
Anemia is a common complication of CKD and increases
in prevalence with progression of CKD. Although eryth-
ropoietin deficiency is the primary cause of anemia, other
contributing factors include blood loss, iron deficiency,
bone marrow suppression, malnutrition, inflammation,
uncontrolled hyperparathyroidism, inadequate dialysis,
or ongoing systemic diseases. Aluminum toxicity, a com-
mon cause of anemia in the past, is now extremely uncom-
mon unless water supplies at home or in dialysis units are
contaminated or when aluminum phosphate binders are
used. Chronic anemia in children has significant effects
on the child, including fatigue, impaired cognition, sleep
disturbances, decreased exercise tolerance, depression,
and poor appetite. The Kidney Disease Outcomes Quality
Initiatives recommend targeting hemoglobin levels be-
tween 11 and 13 g/dL (110-130 g/L) to reduce the
need for transfusions; to lessen cardiovascular complica-
tions, such as left ventricular hypertrophy; and to enhance
overall quality of life. Anemia is best managed with re-
combinant human erythropoiesis-stimulating agents and
iron supplementation. After kidney transplantation, ane-
mia may persist from continuing degrees of CKD, ad-
verse effects of the immunosuppressive medications, or
viral infections, such as parvovirus.
Nutrition and Growth
Provision of adequate calories, particularly in infants and
young children with CKD, is paramount given the effect
of nutritional status on growth and neurocognitive devel-
opment. (6)(7) Although cachexia and protein-energy
wasting are well described among adult patients with ad-
vanced CKD, data concerning the prevalence in children
with CKD are limited. Anorexia, increased energy expen-
diture despite adequate caloric intake, and muscle wasting
Pediatrics in Review Vol.35 No.1 January 2014 21
nephrology chronic kidney disease
are 3 major pathophysiologic features. Other contributing
factors implicated are systemic inflammation, endocrine
disturbances, and maladaptive neuropeptide signaling.
Hypoalbuminemia and malnutrition in dialysis patients
are predictors of mortality in this patient population. An-
orexia, particularly in infants, may be related to altered
tastes, oral food aversions, gastroesophageal reflux, de-
layed gastric emptying, elevated cytokine levels, and alter-
ations in appetite-regulating hormones, such as leptin and
ghrelin. Aggressive nutritional management with the guid-
ance of qualified dieticians is critical. Dietary modifications
should be individualized and may include alterations to
calories, protein, fat, sodium, potassium, calcium, phospho-
rus, and fluid intake (http://kidney.org/professionals/
KDOQI/guidelines_ped_ckd/cpr1.htm). Acknowledg-
ment of cultural food preferences may improve adherence
to dietary changes. If nutrition cannot be maximized
through the addition of carbohydrate or fat sources, then
placement of gastrostomy tubes, particularly in infants
and small toddlers, is often necessary to provide adequate
nutrition, fluids, and/or medications via bolus or contin-
uous infusions.
Decreased linear growth is one of the most apparent
effects of CKD in children. The mean height of children
with CKD is 1.5 SDs below the mean. Factors that con-
tribute to impaired growth include age at the onset of
CKD, duration of CKD, metabolic acidosis, treatment
modalities for primary renal disease (corticosteroids), as-
sociated genetic disorders, protein-calorie malnutrition,
residual urine volume, and hormonal disturbances of the
gonadotropic axis (luteinizing hormone and follicle-
stimulating hormone) and somatropic axis (growth hor-
mone, insulinlike growth factor 1, and thyroid hormone).
Short stature is the most common concern associated
with low health-related quality of life among survivors
of pediatric-onset CKD. Optimization of growth can be
achieved with appropriate caloric intake and the use of
growth hormone replacement.
Neurologic and Neurocognitive Effects of CKD
Children, adolescents, and young adults with CKD are
at risk for neurocognitive function impairment. This is
particularly true for patients with CKD who also have
hypertension because they have a lower IQ score com-
pared with patients in similar age groups who have
CKD without hypertension. (8) When compared with
healthy controls, children and adolescents with CKD
are at higher risk for grade retention, absenteeism,
and impairments on measures of intelligence and read-
ing. In-depth neurocognitive tests, memory, and
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executive function impairment are both directly associ-
ated with the level of renal function, especially in patients
undergoing dialysis.
Burden of Care, Quality of Life Issues, and
Psychosocial Issues in CKD
The burden of care for children and adolescents with
CKD correlates directly with the level of kidney damage
and requires time and attention by patients and their fam-
ily. An example of this care includes the number of med-
ications (mean [SD], 5.7 [4.8]) patients take once to
several times per day, with dialysis and transplant patients
requiring the largest number (particularly the first 6-12
months after transplantation). (9) The complexity of care
also includes procedures such as self-catheterization sev-
eral times per day, fluid and dietary restrictions, blood
pressure measurements daily, injections (erythropoiesis-
stimulating agents once to thrice weekly, growth hor-
mone daily, or insulin several times per day), and/or
home peritoneal (daily) or hemodialysis (thrice weekly)
in ESKD cases.
Compared with healthy children and adolescents, pa-
tients with CKD have significantly lower health-related
quality of life in the physical, school, emotional, and so-
cial domains. Interestingly, in a longitudinal national co-
hort of pediatric CKD patients, longer disease duration
and older age were associated with higher quality of life
scores in the physical, emotional, and social functioning
domains, but older age was associated with lower school
domain scores, likely related to prolonged neurocogni-
tive abnormalities. Maternal education of 16 years or
more was associated with higher Pediatric Quality of Life
scores in the domains of physical, school, and social func-
tioning. Short stature has been associated with lower
quality of life. Moreover, patients with CKD and those
with anemia have greater limitations in physical function-
ing, school work or activities with friends as a result of
physical health, and parental effect on time and family
activities.
On the basis of a sleep questionnaire in a Canadian co-
hort, sleep disorders occur in approximately 30% of chil-
dren and adolescents with CKD (including dialysis and
transplant), particularly restless leg syndrome and periodic
limb movements. (10) In a regional US multi-institution
study, 58.5% of patients with CKD had symptoms of
a sleep disturbance (restless leg syndrome, periodic limb
movements, excessive daytime sleepiness, or sleep disor-
dered breathing), correlating with a decrease in quality
of life, independent of the level of kidney function. (11)
In the North American CKiD cohort, parents of children

and adolescents with lower levels of renal function were
more likely to report low energy, severe weakness, or day-
time sleepiness and, consequently, overall poorer quality of
life.
Depression and attention-deficit/hyperactivity disor-
der are common comorbidities in patients with CKD.
Screening for these conditions and referral to psycholog-
ical services are paramount in ensuring adjustment to the
diagnosis of CKD. Families with a child with CKD expe-
rience emotional, physical, and financial stress; 2-parent
households have better adaptation to this family chal-
lenge. Additional psychological burdens to the family in-
clude increased school absences for patients and their
siblings and missed opportunities for family activities. Pa-
rental distractions related to the patient’s chronic condi-
tion can lead to feelings of neglect by siblings and affects
the family’s financial well-being. Financial burdens result
from interrupted work schedules, insurance copayments
for medical visits or medications, and poor reimburse-
ment for travel costs, meals, or parking. In general, par-
ents of a chronically ill child have higher marital distress
and decreased marital harmony when compared with pa-
rents of healthy children. The primary care clinician can
help CKD families adapt to their child’s diagnosis and
treatment by performing periodic screening of family
health and encouraging communication during periods
of family distress.
Health Care Transition, Disease Self-
Management, and Treatment Adherence
The survival of patients with pediatric-onset CKD neces-
sitates a coordinated health care transition (HCT) prep-
aration from pediatric- to adult-focused health services
and coordination between the primary care and nephrol-
ogy teams. HCT is a process that should begin between
ages 12 and 14 years, considering patient characteristics
(cognition, developmental stage, culture, and literacy
level), family factors, and health-related resources within
the clinical and community settings. (12) Parental or
caregiver willingness to relinquish responsibilities for dis-
ease management requires reassurance that the children
will be successful health self-managers. Patient and family
education with learning tools that meet health literacy
standards is fundamental for successful HCT preparation.
Measuring transition readiness to guide HCT prep-
aration is critical to ensure guided patient education
strategies. Our pediatric nephrology practices are us-
ing a clinician-administered clinical tool termed the
TRxANSITION Scale, developed among pediatric pa-
tients with CKD and ESKD. (13) Preliminary work with
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nephrology chronic kidney disease
this tool suggests that older age is significantly associated
with greater acquisition of HCT skills and disease self-
management. A self-administered HCT readiness tool
has also been created for patients with CKD and is termed
The STARx Transition-readiness survey, and our prelimi-
nary data reveal that older age and female sex appear to be
associated with greater transition readiness. (13)
To ensure a successful HCT process, an interdisciplin-
ary collaboration among the patient, family, and primary
and subspecialty pediatric clinicians must occur. Commu-
nication between the pediatric- and adult-focused health
care teams and the patient is paramount to ensure conti-
nuity of care, optimized health outcomes, health-related
quality of life, and continuous quality improvement. An
example of a tool that can assist with this communication
is the TRxANSITION Passport, a patient portable med-
ical summary with information on diagnoses and medica-
tions in the form of a wallet-size identification card. (12)
Transition preparation is optimized with the services of
a dedicated transition coordinator.
Adherence to medical treatment among pediatric pa-
tients with CKD and ESKD is multifactorial and a major
challenge, particularly in the adolescent and young adult
populations. CKD can be silent, and the consequences of
nonadherence are not palpable to patients who have such
complex medical and dietary regimens. In fact, despite
medical advances, kidney transplant loss in adolescents
exceeds that of any other population. (14) Adherence
among adolescents is also compromised by poor under-
standing and poor consequence recognition, leading to
an inconsistent commitment to the treatment regimens.
In our practice, low parental and child literacy has been
correlated with lower adherence to medical appoint-
ments, greater emergency department use, and greater
morbidity (peritonitis and transplant rejection). A prob-
lem with measuring treatment adherence is the lack of
a standardized definition of what constitutes adherence
and how to measure adherence consistently. The primary
care clinician and subspecialists can confirm adherence in
patients who have biomarkers, such as drug levels. In
CKD patients, phosphorus levels, prescription refill rates,
or medical appointment attendance can be used to deter-
mine adherence.
Discussion of Cases
Case 1
Prenatal ultrasonography may have identified small kid-
neys, leading to an earlier diagnosis and medical interven-
tion. His poor growth is attributable to metabolic acidosis,
fluid and electrolyte losses, inadequate nutritional intake,
Pediatrics in Review Vol.35 No.1 January 2014 23
nephrology chronic kidney disease

Primary Care Clinician’s Activities as Comanager of Pediatric-

Table 3.

Onset Chronic Kidney Disease

Activity Action Plan Monitoring
Identify at risk LBW infant, history of prior acute kidney Yearly BP, urinalysis, periodic serum
individuals injury, obesity, diabetes, HTN chemical analyses
History of HUS, HSP, lupus, or other Yearly BP, urinalysis, serum chemical
glomerulopathies analyses
History of urologic disorders (UTI, High index of suspicion for UTI, stones,
obstructive uropathy) obstruction, monitor BP
Positive family history for CKD, PKD, ESKD Yearly BP, urinalysis
History of HTN Monitor BP at routine health screenings
(http://www.nhlbi.nih.gov/guidelines/
hypertension/child_tbl.htm), annual
echocardiogram, and 24-hour ABPM
Immunizationsa Routine www.aap.org/immunization,
Pneumococcal (23-valent Pneumovax and http://www.cdc.gov/vaccines/schedules/
Prevnar 13) index.html
HPV
Influenza
Counseling/prevention Tobacco, alcohol, drugs Inquire about substance use at each clinic
visit in private
Nutrition, adequate dietary calcium Show the growth chart to patients and
Avoidance of physical inactivity, obesity families, establishing ideal anthropometric
measurements and discuss physical activity
at each visit
Sexual practices Discuss healthy sexual behavior at each
Self-examinations (breast, testicular) adolescent visit
Sun exposure Yearly: skin cancer prevention
School absenteeism and social isolation Yearly: school performance and need for
individualized education
Screen for depression, anxiety, ADHD Each visit: screen for psychosocial distress
and coping
Screen for ability to read prescription or Each visit: reconcile medications and ask the
food labels and patient education material patient to read labels to you and use the
teach-back method when patient
education takes place
Monitor adherence Each visit: discuss adherence strategies
(eg, alarms, pill-boxes)
ABPM¼ambulatory blood pressure monitoring, ADHD¼attention-deficit/hyperactivity disorder; BP¼blood pressure; ESKD¼end-stage kidney disease;
HPV¼human papillomavirus; HSP¼Henoch-Schönlein purpura; HTN¼hypertension; HUS¼hemolytic uremic syndrome; LBW¼low birth weight;
PKD¼polycystic kidney disease; UTI¼urinary tract infection.
a
Note vaccine response may be reduced in dialysis or transplant population.

and MBD. The leg pains are likely due to hypocalcemic-
induced cramps. The developmental delay that resulted
from progressive, unrecognized kidney failure places him
at risk for poor school performance and neurocognitive ab-
normalities. He will require aggressive nutritional moni-
toring and likely a gastrostomy tube to meet caloric
demands. Early intervention programs and individualized
education plans will optimize vocational milestones. The
likelihood of high urinary output from renal tubular dam-
age impairs urinary concentrating ability regardless of hy-
dration status. This high urinary output translates into
constant thirst and frequently daytime and nighttime in-
continence, with its psychosocial effect of adjustment dis-
order. Thorough family history is indicated because this is
a congenital anomaly. He needs to get to a weight of ap-
proximately 10 kg to physically be able to receive a kidney
transplant. If this child’s diagnosis were posterior urethral
valves, many of these complications would also apply. Al-
though posterior urethral valves can be diagnosed prena-
tally, in many instances and despite surgical valve
ablation, patients are still at risk for CKD or ESKD,
particularly during adolescence.

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 nephrology chronic kidney disease

Pediatric CKD: Health Maintenance Activities by Primary Care

Table 4.

Clinicians
Diagnosis and Reduce Negative Effect of
Surveillance and Treatment of Comorbid Conditions and
Conditions Risk Reduction Comorbid Conditions Treat Complications
Stages of CKD
1 (GFR >90) Urinalysis and BP Monitor growth Modify CVD risk
measurement factors
2 (GFR 60-89) If low birth weight Monitor for
or other factors proteinuria
for Y renal mass Normalize BP
3 (GFR 30-59) BP measurement Monitor growth Growth hormone as
4 (GFR 15-29) Monitor proteinuria, needed, modify
normalize BP CVD risk factors
5 (Transplant) Growth, nutrition Viral infection Rapid fluid resuscitation
Urinalysis and BP surveillance in dehydration
measurement (CMV, EBV):
Exercise lymphadenopathy,
Encourage adherence enlarged tonsils,
and hydration fever, bone
marrow
suppression
Peritoneal dialysis Growth, nutrition Monitor for signs of Encourage living donor
peritonitis, optimize transplantation
protein intake
Hemodialysis Growth, maintain High index of
fluid restriction suspicion
for infection
Selective conditions or
psychosocial issues
Congenital anomalies Teratogen avoidance and Postnatal Surgical correction as
of the kidney and prenatal vitamins in ultrasonography, needed, healthy
urinary tract future pregnancies high index of toilet habits
suspicion for UTI Psychosocial support of
long-term enuresis
Voiding history not reliable
during dehydration
(poor ADH response)
Acute kidney injury Urinalysis and BP Encourage hydration, Nephrology referral for
recovery measurement avoid nephrotoxic abnormal growth or
Serum chemical agents laboratory values
analyses
Monitor growth
Hypertension Encourage healthy Monitor serial BP Annual echocardiogram,
diet and exercise urinalysis, eye
examination; modify
CVD risk factors
Universal medical services, Screen for modifiable CVD factors: normal BP, hyperlipidemia, exercise, and healthy
universal literacy and weight and diet
numeracy appropriate Provide immunizations
services Assume low functional and health literacy and numeracy and provide patient
education and counseling at a fourth grade or below level. Monitor parent and
patient’s ability to read prescription and food labels. Use teach-back method to
ensure comprehension of education sessions and material.
Universal Psychosocial Services Monitor: psychosocial evaluation, health-related quality of life, individualized
education plan
Encourage: therapeutic camp participation
Continued

Pediatrics in Review Vol.35 No.1 January 2014 25

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nephrology chronic kidney disease

Table 4. (Continued)

Diagnosis and Reduce Negative Effect of

Surveillance and Treatment of Comorbid Conditions and
Conditions Risk Reduction Comorbid Conditions Treat Complications
Health care transition and Assess patient and parent literacy to customize patient and family
treatment adherence education efforts;
Monitor ability to read prescriptions and food labels; prescription refill rate or
drug levels (when applicable) and support the health care transition process;
adherence and successful disease self-management
ADH¼antidiuretic hormone; BP¼blood pressure; CKD¼chronic kidney disease; CMV¼cytomegalovirus; CVD¼cardiovascular disease; EBV¼Epstein-Barr
virus; ESKD¼end-stage kidney disease; UTI¼urinary tract infections.

Case 2 identification of pediatric CKD in patients at risk is par-

This patient has been diagnosed as having CKD at a cru-
cial developmental age. She is at risk for psychological dis-
tress and must adjust to her life-changing diagnosis and
the medical treatment. This form of nephritis will need
aggressive immunosuppression (corticosteroids and cy-
clophosphamide), which has many adverse effects, some
of which can affect appearance, placing her at risk for
treatment nonadherence. Her hypertension with protein-
uria will require the use of ACE inhibitors or angiotensin-
receptor blockers for their renoprotective effect. She
needs to know that if she becomes pregnant the fetus
is at risk for ACE fetopathy, affecting the fetal kidneys.
Cases 1 and 2
Both patients are at risk for early cardiovascular events dur-
ing young adulthood. They would benefit from participat-
ing in therapeutic camps and psychosocial services. Both
families will need to receive counseling and support to
optimize family function. Living kidney donation for
transplantation by family members of friends needs to
be encouraged because this type of donation has better
outcomes. The HCT preparation will need to start be-
tween ages 12 and 14 years to ensure successful disease
self-management when they transfer to adult-focused
health care clinicians. Both patients are at greater risk
of nonadherence during the adolescent years, and pre-
scription refill rate or therapeutic drug levels will assist
the primary care clinician’s team to counsel these patients
and encourage treatment concordance.
Primary Care Clinician Activities to Overcome
the Challenges in the Diagnosis and
Management of Pediatric-Onset CKD
The 2 major barriers for early diagnosis and treatment of
CKD are low awareness by the patient, family, and health
care clinicians of risk factors for this condition and the si-
lent nature of this condition in its initial stages. Early
amount to optimize patient outcomes. We suggest activ-
ities to achieve this goal in Table 3. Patients often present
to emergency departments with CKD or ESKD in its late
stages, and adjustment to the diagnosis is a major chal-
lenge for both the patients and their families. Regular
screening for CKD factors as suggested in Table 3 and
Table 4 will ensure early diagnosis and referral for pre-
vention of unnecessary complications. As soon as CKD
is diagnosed, referrals for psychosocial and educational-
related services will help with adjustment to this condi-
tion. We find that if we refer all patients and families with
a new diagnosis of CKD to obtain a baseline psycholog-
ical evaluation there is less resistance by these families
when a future need for these services arise. Establishing
a relationship between the psychology team and the pa-
tient and family decreases the anxiety and stigma effect
that this type of referral may create.
Starting HCT-related activities in the early stages of ad-
olescence will ensure successful disease self-management
on transferring to adult-focused health care clinicians.
Monitoring and encouraging adherence to treatment
and medical appointments prevents CKD complications
(transplant rejection, volume overload, and hypertensive
crisis) along with optimizing the longevity of renal trans-
plants. Once the diagnosis of CKD or ESKD is estab-
lished, finding a living donor among the family members
or friends is difficult in part due to public misconceptions
about donation. The primary care clinician can assist with
patient education and identification of potential donors.
Ensuring close collaboration between the medical home
(primary care clinicians) and medical neighbors (sub-
specialty clinicians, educators, community workers, and
agencies) can be difficult given that electronic medical re-
cords are not readily available to all, but close communi-
cation among health care clinicians that includes the
patient and family will positively affect the long-term out-
comes of youth with pediatric-onset CKD.

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ACKNOWLEDGMENTS. We thank Wallace Brown, MD,
Andrew Wallace, MS4, William Primack, MD, and Keisha
Gibson, MD, MPH, from the University of North
Carolina School of Medicine and Donald Jack Weaver, MD,
PhD, and Charles McKay, MD, from Levine Children’s
Hospital for their insightful comments.
Summary
On the basis of evidence, children, adolescents, and
young adults with chronic kidney disease or end-stage
kidney disease may have:
• Great morbidity in other organ systems, affecting their
long-term survival. (1)(2)(3)(5)(6)(7)(8)
• Lower immunization rates, placing them at risk for
preventable conditions. (4)
• Psychosocial and neurocognitive issues, affecting
their self-esteem and school or job performance. (1)
(8)(10)(11)
• Psychiatric conditions, such as depression, anxiety,
attention-deficit/hyperactivity disorder,
maladjustment, and posttraumatic stress disorder. (1)
(10)(11)
• Nonadherence (14) and great treatment burden, (9)
particularly in adolescence and young adulthood,
placing these patients at risk for transplant loss and
hospitalizations.
On the basis of research evidence and expert consensus,
health care transition preparation to self-manage their
condition will ensure successful outcomes and im-
proved health-related quality of life. (12)(14)
References
1. Copelovitch L, Warady BA, Furth SL. Insights from the Chronic
Kidney Disease in Children (CKiD) study. Clin J Am Soc Nephrol.
2011;6(8):2047–2053
Parent Resources From the AAP at HealthyChildren.org
• English: http://www.healthychildren.org/English/family-life/health-management/pediatric-specialists/Pages/What-is-a-
Pediatric-Nephrologist.aspx
• Spanish: http://www.healthychildren.org/spanish/family-life/health-management/pediatric-specialists/paginas/what-is-a-
pediatric-nephrologist.aspx
• English: http://www.healthychildren.org/English/health-issues/conditions/genitourinary-tract/Pages/Children-with-a-Single-
Kidney.aspx
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nephrology chronic kidney disease
2. Ferris ME, Gipson DS, Kimmel PL, Eggers PW. Trends in
treatment and outcomes of survival of adolescents initiating end-
stage renal disease care in the United States of America. Pediatr
Nephrol. 2006;21(7):1020–1026
3. Wühl E, Trivelli A, Picca S, et al; ESCAPE Trial Group. Strict
blood-pressure control and progression of renal failure in children.
N Engl J Med. 2009;361(17):1639–1650
4. Neu AM. Immunizations in children with chronic kidney
disease. Pediatr Nephrol. 2012;27(8):1257–1263
5. Shroff R, Weaver DJ Jr, Mitsnefes MM. Cardiovascular compli-
cations in children with chronic kidney disease. Nat Rev Nephrol.
2011;7(11):642–649
6. Mak RH, Cheung WW, Zhan J-Y, Shen Q, Foster BJ. Cachexia
and protein-energy wasting in children with chronic kidney disease.
Pediatr Nephrol. 2012;27(2):173–181
7. Foster BJ, McCauley L, Mak RH. Nutrition in infants and very
young children with chronic kidney disease. Pediatr Nephrol. 2012;
27(9):1427–1439
8. Lande MB, Gerson AC, Hooper SR, et al. Casual blood
pressure and neurocognitive function in children with chronic
kidney disease: a report of the children with chronic kidney
disease cohort study. Clin J Am Soc Nephrol. 2011;6(8):
1831–1837
9. So TY, Layton JB, Bozik K, et al. Cognitive pharmacy services at
a pediatric nephrology and hypertension clinic. Ren Fail. 2011;33
(1):19–25
10. Sinha R, Davis ID, Matsuda-Abedini M. Sleep disturban-
ces in children and adolescents with non-dialysis-dependent
chronic kidney disease. Arch Pediatr Adolesc Med. 2009;163
(9):850–855
11. Davis ID, Greenbaum LA, Gipson D, et al. Prevalence of sleep
disturbances in children and adolescents with chronic kidney
disease. Pediatr Nephrol. 2012;27(3):451–459
12. Ferris ME, Mahan JD. Pediatric chronic kidney disease and the
process of health care transition. Semin Nephrol. 2009;29(4):
435–444
13. Ferris ME, Harward DH, Bickford K, et al. A clinical tool to
measure the components of health-care transition from pediatric
care to adult care: the UNC TR(x)ANSITION scale. Ren Fail.
2012;34(6):744–753
14. Kiley DJ, Lam CS, Pollak R. A study of treatment compliance
following kidney transplantation. Transplantation. 1993;55(1):
51–56
Pediatrics in Review Vol.35 No.1 January 2014 27
nephrology chronic kidney disease

PIR Quiz Requirements

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1. A 5-year-old child presents with short stature and anemia. Growth parameters have indicated that he has
a downward trend on his percentile curves for age from the 25th percentile for weight and height at age 1 year
to below the third percentile at present. He weighs 14 kg, and his height is 100 cm. Physical examination
reveals heart rate of 100/min, respiratory rate of 26/min, and blood pressure of 120/80 mm Hg. Laboratory
studies are as follows: hemoglobin, 9 g/dL; hematocrit, 27; serum sodium, 134 mEq/L; serum potassium, 4.2
mEq/L; serum chloride, 104 mEq/L; serum bicarbonate, 18 mEq/L; serum calcium, 7.0 mg/dL; serum
phosphorous, 6.8 mg/dL; serum creatinine, 1.1 mg/dL; and blood urea nitrogen, 22 mg/dL. Abdominal
ultrasonography reveals small kidneys bilaterally. In addition to his serum creatinine concentration which of
the following is most helpful in determining his estimated glomerular filtration rate?
A. Blood urea nitrogen.
B. Fractional excretion of phosphorous.
C. Height.
D. Mean blood pressure.
E. Weight.

2. A 13-year-old boy with reflux nephropathy and hypertension has been treated since age 5 years with an
angiotensin-converting enzyme (ACE) inhibitor and dietary salt restriction. His vesicoureteral reflux was
successfully repaired surgically. He is being followed up regularly by his pediatrician in consultation with
a pediatric nephrologist. His blood pressure has been well controlled in the past. He has been in the 50th
percentile for height and weight. Two years ago his serum calcium and phosphorous levels were normal, and his
serum creatinine level was 1.1 mg/dL. On his visit today, he says that he has been tired and not able to sleep
well at night. He also has had a runny nose and sore throat for the last 2 days. He has gained 10 cm in height
and 10 kg in weight in the last 2 years and he remains in the 50th percentile for his age. His blood pressure and
other vital signs are normal. Physical examination reveals pubic hair and genital development consistent with
Tanner stage IV. His serum creatinine level is 1.7 mg/dL. Which of the following is the most likely reason for
increase in his serum creatinine?
A. ACE inhibitor nephropathy.
B. Expected increase according to age.
C. Growth spurt.
D. Intercurrent infection.
E. Recurrence of vesicoureteral reflux.

3. A 9-year-old girl presents with fever, facial rash, and joint pains. On examination she appears ill, with a heart
rate of 124/min, axillary temperature of 39˚C, respiratory rate of 28/min, and blood pressure of 146/90 mm Hg.
Physical examination reveals erythematous rash in the malar area and petechial rash on extremities. Spleen is
enlarged 2 cm below the costal margin. Laboratory studies are remarkable for the following: platelets, 70 3
103/mL (70 3 109/L); serum creatinine, 2.5 mg/dL; urea nitrogen, 54 mg/dL; and positive antinuclear antibody
and anti–double-stranded DNA. Urinalysis reveals 3D blood, proteinuria (4D), and 20 red blood cells per
high-power field. The urine protein to creatinine ratio is 2.5. Renal biopsy specimen reveals crescentic
proliferative glomerulonephritis. The patient responds favorably to appropriate treatment with
corticosteroids and cyclophosphamide. Which of the following antihypertensive medication for strict
control of blood pressure will result in maximum protection from progression of chronic renal failure?
A. Darusentan (endothelin receptor antagonist).
B. Hydralazine (vasodilator).
C. Nifedipine (calcium channel blocker).
D. Propranolol (b blocker).
E. Ramipril (ACE inhibitor).

28 Pediatrics in Review Vol.35 No.1 January 2014

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 nephrology chronic kidney disease

4. A 5-year-old girl who underwent renal transplantation a year ago for dysplastic kidneys is under your care as
her primary pediatrician. She is receiving corticosteroids and cyclosporine to prevent graft rejection. She is
doing well and now is scheduled to enter kindergarten. If administered, which of the following vaccines poses
the greatest risk to her health?
A. Diphtheria, tetanus, and acellular pertussis.
B. Hepatitis B.
C. Inactivated influenza.
D. 23-valent polysaccharide pneumococcal vaccine.
E. Varicella zoster.

5. A 14-year-old girl is awaiting renal transplantation for end-stage renal disease from focal segmental
glomerulosclerosis. She is receiving hemodialysis 3 times a week and is taking multiple medications to control
her hypertension. She was doing well until 6 months ago, when she started to feel constantly tired and was not
able to sleep well at night. She has daytime somnolence and loss of appetite. She complains of frontal
headaches in the morning and often refuses to go to school. Her school grades have fallen from A’s and B’s to
mostly D’s. Last week her mother caught her smoking marijuana in her bedroom. Evaluation by a neurologist
has revealed no abnormality. Referral to psychology services is required to evaluate her for which of the
following conditions?
A. Chemical dependency.
B. Childhood-onset schizophrenia.
C. Depression.
D. Munchausen syndrome.
E. Oppositional defiant disorder.

Corrections
In the November 2013 article ”Cephem Antibiotics: Wise Use Today Preserves Cure for Tomorrow“ Parker S, Mitchell M,
Child J. Pediatr Rev. 2013;34(11):510–524, doi: 10.1542/pir.34-11–510), in Table 3, under the Cefotaxime column, in the
Escherichia coli row, the missing value should be S: £1.
Also, in the print version of that article, in the Selected References introduction, the link to the complete reference list
should be: http://pedsinreview.aappublications.org/content/34/11/510/suppl/DCSupplementary_Data. The link is correct in
the online version of the journal.
In the October 2013 article ”Pneumonia“ (Gereige, RS, Laufer, PM. Pediatr Rev. 2013;34(10):438–456), ampicillin dosing
in the first paragraph of ”Empiric Therapy“ should read, ”If this dose is desired, a combination of ampicillin-sulbactam at 300
mg/kg daily (dosing ampicillin at 200 mg/kg daily) and regular ampicillin at 100 to 200 mg/kg daily is a recommended
regimen.“ The online version of the article was resupplied with correct dosage.
The journal regrets this errors.

Pediatrics in Review Vol.35 No.1 January 2014 29

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 Chronic Kidney Disease in Children and Adolescents
Susan F. Massengill and Maria Ferris
Pediatrics in Review 2014;35;16
DOI: 10.1542/pir.35-1-16

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 Chronic Kidney Disease in Children and Adolescents
Susan F. Massengill and Maria Ferris
Pediatrics in Review 2014;35;16
DOI: 10.1542/pir.35-1-16

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