Overview of The Management of Chronic Kidney Disease in Children - UpToDate PDF

15.03.
2020 Overview of the management of chronic kidney disease in children - UpToDate
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Prezentare generală a managementului bolilor renale cronice la

copii
Autori: Tarak Srivastava, MD, Bradley A Warady, MD
Editor de secțiuni: Tej K Mattoo, MD, DCH, FRCP
Editor adjunct: Melanie S Kim, MD
Toate subiectele sunt actualizate pe măsură ce noi dovezi devin disponibile și procesul nostru de evaluare de la egal la egal .
Analiza literaturii curente până în: Feb 2020. | Acest subiect a fost actualizat ultima dată: 10 ianuarie 2020.
INTRODUCERE
Boala renală cronică (CKD) se referă la o stare de afectare renală ireversibilă și / sau reducere a funcției renale,
care poate fi progresivă. CKD este acum termenul acceptat în comunitatea de nefrologie pediatrică, înlocuind
termenii clinici insuficiență renală cronică (CRF) și insuficiență renală cronică (CRI), care descriu disfuncția renală
de diferite grade, de natură severă până la ușoară. CKD definește mai clar disfuncția renală ca un continuum, mai
degrabă decât o schimbare discretă a funcției renale și va fi utilizată pe parcursul acestei revizuiri a subiectului.
O prezentare generală a managementului CKD la copii va fi revizuită aici. Etiologia, epidemiologia, cursul natural,
prezentarea și evaluarea CKD la copii sunt discutate separat. (A se vedea „Boala renală cronică la copii: definiție,
epidemiologie, etiologie și curs” și „Prezentare clinică și evaluare a bolii renale cronice la copii” .)
DEFINIȚII
Boala renală: Îmbunătățirea rezultatelor globale (KDIGO) Ghidul practicilor clinice 2012 (CPG) pentru evaluarea și
gestionarea bolii cronice a rinichilor a revizuit clasificarea din 2002 a bolii renale cronice pediatrice (CKD) prin
practica clinică a rezultatelor bolii renale (KDOQI). Ghid pentru boala cronică a rinichilor [ 1,2 ]. Clasificarea
KDIGO include etiologia, funcția renală bazată pe rata de filtrare glomerulară (GFR) și prezența și viteza de
excreție urinară de albumină și este utilizată pe tot acest subiect. (A se vedea "Boala renală cronică la copii:
definiție, epidemiologie, etiologie și curs", secțiunea „Definiții și clasificări” ).
Diagnosticul KDIGO al CKD pediatric este bazat pe îndeplinirea unuia dintre următoarele criterii clinice:
● GFR mai mic de 60 ml / min pe 1,73 m 2 pentru mai mult de trei luni, cu implicații asupra sănătății, indiferent
dacă sunt prezenți alți markeri CKD.
● GFR mai mare de 60 ml / min per 1,73 m 2, care este însoțit de dovezi de deteriorare structurală sau de alți
markeri ai anomaliilor renale funcționale, inclusiv proteinurie, albuminurie, afecțiuni tubulare renale sau
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15.03.2020 Overview of the management of chronic kidney disease in children - UpToDate
anomalii patologice detectate de histologie sau deduse prin imagistică.
Stabilirea KDIGO CKD pentru copiii cu vârsta mai mare de doi ani stratifică riscul de progresie a CKD și
complicațiile sale pe baza GFR și este utilizat pentru a ghida managementul ( tabelul 1 ):
● G1 - Normal GFR (≥90 ml / min per 1,73 m 2 )

● G2 - GFR între 60 și 89 ml / min per 1,73 m 2
● G3a - GFR între 45 și 59 ml / min per 1,73 m 2
● G3b - GFR între 30 și 44 ml / min per 1,73 m 2
● G4 - GFR între 15 și 29 ml / min pe 1,73 m 2
● G5 - GFR mai mică de 15 ml / min pe 1,73 m 2 (insuficiență renală)
Copiii sub doi ani nu se încadrează în sistemul de clasificare de mai sus, deoarece în mod normal au un GFR
scăzut chiar și atunci când sunt corectate pentru suprafața corpului. La acești pacienți, GFR calculat pe baza
creatininei serice poate fi comparat cu valorile normative adecvate vârstei pentru a detecta insuficiența renală (
tabelul 2 ). Ghidul KDIGO sugerează că o valoare GFR mai mult de o abatere standard sub medie ar trebui să
trezească îngrijorarea și să promoveze monitorizarea mai intensivă. (A se vedea "Boala renală cronică la copii:
definiție, epidemiologie, etiologie și curs", secțiunea „Rata de filtrare glomerulară” ).
PRINCIPII GENERALE
Managementul general al pacientului cu boală renală cronică (CKD) include următoarele componente:
● Tratează disfuncția renală reversibilă

● Preveniți sau încetiniți evoluția bolilor renale
● Tratează complicațiile CKD
● Identificați și pregătiți în mod adecvat copilul / familia în care va fi necesară terapia de substituție renală
Momentul de punere în aplicare a acestor componente variază în primul rând pe baza gravității CKD.
În stadiile incipiente ale CKD, există posibilitatea de a trata orice cauză reversibilă a disfuncției renale și de a
preveni sau încetini evoluția bolii renale. Copiii cu boala G1 și G2 sunt asimptomatici și trebuie urmăriți
îndeaproape pentru deteriorarea funcției renale. Această perioadă ar trebui să fie utilizată și pentru educarea
copilului și a familiei despre CKD, evidențiind conștientizarea factorilor de risc care pot agrava insuficiența renală
(de exemplu, medicamente nefrotoxice, infecții recurente, deshidratare, obezitate și fumat la adolescenți) și
despre măsurile care pot încetini progresia insuficienței renale (de exemplu, controlul tensiunii arteriale și
reducerea proteinuriei).
Complicațiile asociate cu CKD încep să apară pe măsură ce CKD progresează în stadiul G3a și G3b. Acestea
includ tulburări ale fluidelor și ale electroliților, anemie, hipertensiune, dislipidemie, anomalii endocrine, tulburări
de creștere, tulburări minerale și osoase (MBD) și tulburări datorate scăderii clearance-ului substanțelor în mod
normal excretate din organism de către rinichi (uremie). La acești pacienți, managementul este axat pe
prevenirea și tratarea acestor complicații. (Vezi "Prezentare clinică și evaluare a bolilor renale cronice la copii",
secțiunea „Complicații ale BKC” ).

Pacienții care vor necesita terapie de înlocuire renală (RRT) ar trebui să fie identificați cu mult timp înainte de
timpul necesar RRT, astfel încât să fie asigurată o pregătire și educație adecvată atât pacientului, cât și familiei.
Acest lucru apare în general la pacienții cu CKD în stadiul G4. (A se vedea „Terapia de substituție renală” mai
jos.)
Discuția următoare va analiza managementul CKD pediatric și este în concordanță cu recomandările din Boli
renale: Îmbunătățirea rezultatului global (KDIGO) Ghid de practică clinică și a liniei directoare a inițiativei de
calitate a rinichilor de la Fundația Națională a rinichilor (KDOQI) [ 1,2 ]. (A se vedea "Link-uri directoare ale
societății: boli renale cronice la copii" .)
REVERSIBLE KIDNEY DYSFUNCTION
In children with chronic kidney disease (CKD), identification and treatment of reversible causes of acute or chronic
kidney dysfunction may result in some recovery of kidney function, if addressed early in the course.
The most common conditions with potentially recoverable kidney function are primarily due to decreased kidney
perfusion or the administration of nephrotoxic agents.
● Decreased kidney perfusion – Kidney hypoperfusion is produced by hypotension (eg, septic shock), volume
depletion from vomiting, diarrhea, diuretic use, burns, major surgeries (eg, cardiac surgery performed on
cardiopulmonary bypass, orthopedic spine surgeries), or bleeding, and the administration of drugs that lower
the kidney perfusion (such as nonsteroidal anti-inflammatory drugs, angiotensin-converting enzyme [ACE]
inhibitors, and angiotensin II receptor blockers [ARBs]). (See "Etiology and diagnosis of prerenal disease and
acute tubular necrosis in acute kidney injury in adults", section on 'Causes of prerenal disease'.)
The normal response to kidney hypoperfusion is to lower the urine sodium concentration and the fractional
excretion of sodium. However, the superimposition of a prerenal process among patients with CKD may not
result in the expected lowering of urinary sodium because the renal tubular sodium reabsorption is impaired.
As a result, patients with CKD who are unable to normally reabsorb sodium are less able to respond to
conditions associated with fluid loss or hypotension leading to an increased risk of reduced kidney perfusion
and glomerular filtration rate (GFR). These patients should be identified at the onset of an intercurrent illness
associated with hypovolemia or hypotension so that fluid repletion can be initiated prior to a significant
decrease in kidney blood flow. If significant hypovolemia accompanied by a reduction of GFR occurs, a
judicious trial of fluid repletion may result in the return of kidney function to the previous baseline. (See
"Acute kidney injury in children: Clinical features, etiology, evaluation, and diagnosis".)
● Administration of nephrotoxic drugs – Common nephrotoxic drugs include nonsteroidal anti-inflammatory

agents, diagnostic agents (eg, radiographic contrast materials), and others (eg, aminoglycosides,
amphotericin B, cyclosporine, and tacrolimus). The administration of such drugs, therefore, should be
avoided or used with caution in patients with underlying CKD, with the assistance of therapeutic drug level
monitoring. When drugs that have a narrow therapeutic index are used and precision in dosing is critical (eg,
cisplatinum in bone marrow transplant induction protocol) based on kidney function, measurement of GFR
should be made using iohexol or one of the radioisotopes (51Cr-EDTA, 125Iothalamate, or 99Tc-DTPA). In this

situation, drug dosing ideally should not be based on an estimated GFR using a regression equation. (See
"Manifestations of and risk factors for aminoglycoside nephrotoxicity" and "NSAIDs: Acute kidney injury
(acute renal failure)" and "Pathogenesis, clinical features, and diagnosis of contrast-induced acute kidney
injury" and "Assessment of kidney function", section on 'Measurement of GFR'.)
Certain drugs, such as cimetidine, trimethoprim, ciprofloxacin, and flucytosine, lead to an elevation in serum
creatinine but not blood urea nitrogen (BUN), as they interfere with either the tubular secretion of creatinine
or the laboratory assay for creatinine [3].
SLOWING CHRONIC KIDNEY DISEASE PROGRESSION
Interventions to slow CKD progression include blood pressure (BP) control, reducing protein excretion, correcting
anemia and maintaining normal 25-hydroxyvitamin D levels [4-6].
Blood pressure control — In adults and children with CKD, strict blood pressure control has been shown to slow
the progression of kidney disease and reduce the risk of cardiovascular disease [7,8]. In particular, angiotensin-
converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) have been suggested as
antihypertensive therapy to reduce proteinuria and control blood pressure in these patients. (See
"Antihypertensive therapy and progression of nondiabetic chronic kidney disease in adults".)
We recommend that hypertension be strictly controlled with antihypertensive therapy in children with CKD based
upon the beneficial effect that blood pressure control has in reducing the progression of CKD in both children and
adults. We agree with the 2017 AAP Clinical Practice Guideline for screening and management of high blood
pressure in children and adolescents, which recommends that an ACE inhibitor or ARB is preferred to treat
children with CKD who have hypertension and proteinuria [9]. There is good evidence that these agents are more
protective than other antihypertensive drugs in slowing the progression of CKD [7-12]. The management of
hypertension is discussed in more detail below. (See 'Hypertension' below.)
Other interventions — Additional interventions that have been studied in adults with CKD include dietary protein
restriction, lipid lowering therapy, acidosis, and correction of anemia. However, results are inconclusive with
respect to the impact of these interventions upon delaying the progression of CKD. In children, data have not
shown a benefit of a low protein diet upon the progression of kidney disease [13]. The current consensus by
pediatric nephrology experts is to provide children with CKD the age-appropriate recommended daily allowance
for protein (see 'Nutrition' below and "Dietary recommendations for patients with nondialysis chronic kidney
disease").
CHRONIC KIDNEY DISEASE COMPLICATIONS
A wide range of complications result as a consequence of the loss of kidney function. These include disorders of
fluid and electrolyte balance, mineral and bone disorder, hypertension, anemia, dyslipidemia, growth impairment,
malnutrition, and risk of poor neurodevelopmental outcome.

The management of these abnormalities in children will be discussed in this section. The pathophysiology,
evaluation, and monitoring of these abnormalities are discussed separately. (See "Clinical presentation and
evaluation of chronic kidney disease in children", section on 'Complications of CKD' and "Clinical presentation and
evaluation of chronic kidney disease in children", section on 'Evaluation at presentation' and "Clinical presentation
and evaluation of chronic kidney disease in children", section on 'Follow-up evaluation'.)
Sodium and intravascular volume
Salt and fluid overload — In the late CKD stages (ie, stages G4 and G5 disease), water and sodium retention
may result in volume overload. In general, a combination of dietary sodium restriction and diuretic therapy is used
to prevent fluid overload. (See "Clinical presentation and evaluation of chronic kidney disease in children", section
on 'Sodium and water homeostasis'.)
● Sodium – Although the current recommended daily sodium intake in healthy children is only 1.2 g/day for
four- to eight-year-old children and 1.5 g/day for older children, this amount is substantially lower than the
average intake in a heathy child in the United States [14]. .
In our practice, we work with the child and family to decrease the sodium intake to 2 to 3 g/day. This is often
a difficult task given the sodium content of the current favorite foods of children.
● Diuretic therapy includes either loop diuretics such as furosemide given at a dose of 0.5 to 2 mg/kg per day
or thiazide diuretics such as hydrochlorothiazide at 1 to 3 mg/kg per day. At our center, we typically use a
thiazide diuretic in the early stages of chronic kidney disease (CKD) and a loop diuretic in the more advanced
stages of disease when the thiazides are less effective. Both classes of diuretics become less effective with
decreasing GFR.
Salt wasting and poor urinary concentration — Some children with obstructive uropathy and/or dysplastic
kidneys have poor urinary concentrating capacity and exhibit urinary sodium wasting, resulting in a propensity for
hypovolemia and hyponatremia. In addition, poor growth may also occur in children with salt wasting without
adequate sodium supplementation, which can range from 1 to 5 mEq/kg/day.
One must be aware that these children may continue to have substantial urine output, despite fluid losses that
occur during episodes of vomiting and/or diarrhea, and require ongoing and close monitoring of fluid and sodium
replacement. Small children and infants who are unable to independently access or indicate the need for fluids
are totally dependent upon caretakers for fluid replacement. The need for fluid replacement should be
emphasized to the caretakers, especially when the child has an intercurrent illness that increases volume losses
(eg, diarrhea) or decreases fluid intake (eg, vomiting).
Hyperkalemia — Hyperkalemia develops primarily because of inadequate potassium excretion due to a reduced
GFR. Other factors that can contribute to elevated potassium levels include a high dietary potassium intake,
increased tissue breakdown, metabolic acidosis, hypoaldosteronism (due in some cases to administration of an
angiotensin-converting enzyme [ACE] inhibitor or an angiotensin II receptor blocker [ARB]), or an impaired cellular
uptake of potassium. (See "Clinical presentation and evaluation of chronic kidney disease in children", section on
'Potassium homeostasis'.)
Management to prevent hyperkalemia in children with CKD consists of the following:

● Low potassium diet.
● Administration of a loop diuretic (eg, furosemide) to increase urinary potassium loss.
● If there is metabolic acidosis, oral sodium bicarbonate to correct acidosis. (See 'Metabolic acidosis' below.)
● Infant formulas and/or nutritional supplements that are low in potassium should be used for children with
elevated serum potassium levels.
● In infants under selected circumstances, formula can be mixed with sodium polystyrene sulfonate and
decanted externally to decrease the potassium content of the formula prior to feeding [15]. The use of sodium
polystyrene sulfonate in this manner is a common practice, but should be used with caution. Use of sodium
polystyrene sulfonate also results in a decrease in calcium, magnesium, and copper, and an increase in the
iron, sodium, and aluminum content of the nutritional formula [16].
● Patiromer, a potassium-binding polymer, has been studied in adults with CKD Stage 3 or greater with
hyperkalemia resulting in a significant decrease in serum potassium and a reduction in recurrent episodes of
hyperkalemia. It resulted in a significant decrease in serum potassium level after four weeks of treatment
compared with placebo, a reduction in recurrence of hyperkalemia, and it remained efficacious throughout
the study period of 52 weeks. Pediatric data are not available, although studies are underway in children.
(See "Treatment and prevention of hyperkalemia in adults", section on 'Patiromer'.)
Renal replacement therapy must be considered if conservative management fails to control hyperkalemia.
The medical treatment of acute hyperkalemia in children is presented separately. (See "Management of
hyperkalemia in children".)
Hypokalemia — Hypokalemia is uncommon in children with CKD. However, it can be observed in children in the
early stages of CKD associated with Fanconi syndrome, renal tubular acidosis, or from excessive diuretic therapy.
(See "Overview and pathophysiology of renal tubular acidosis and the effect on potassium balance".)
Metabolic acidosis — In children, overt acidosis is characteristically present when the estimated GFR is less
than 30 mL/min per 1.73 m² (ie, stage G4 disease). Acidosis is associated with growth impairment because the
body utilizes bone buffering to bind some of the excess hydrogen ions.
Current guidelines by the Kidney Disease Outcomes Quality Initiative (KDOQI) and Kidney Disease: Improving
Global Outcomes (KDIGO) working groups are to maintain the serum bicarbonate level at or above 22 mEq/L
[1,17]. We suggest sodium bicarbonate therapy in patients with metabolic acidosis to achieve this targeted goal
[17]. Sodium bicarbonate therapy is started at 1 to 2 mEq/kg per day in two to three divided doses, and the dose
is titrated to the clinical target. Citrate preparations should, on the other hand, be used with caution in children
with CKD, as these preparations enhance aluminum absorption from the intestine and increase the risk of
aluminum toxicity. (See "Aluminum toxicity in chronic kidney disease".)
Bone metabolism and bone disease — Changes in mineral metabolism and bone structure are an almost
universal finding with progressive CKD due to abnormalities in the metabolism of calcium, phosphate, vitamin D,
parathyroid hormone (PTH), and fibroblast growth factor-23 (FGF-23) levels [17-19]. If these abnormalities are not

addressed, these changes result in mineral, skeletal, and vascular abnormalities, known as CKD-mineral and
bone disorder (CKD-MBD) and previously referred to as renal osteodystrophy. Significant morbidity may be
associated with CKD-MBD, including growth failure, avascular necrosis, skeletal fractures and deformities, and
vascular calcifications [20].
The goals for prevention and management of CKD-MBD in children are discussed in greater detail separately.
(See "Pediatric chronic kidney disease-mineral and bone disorder (CKD-MBD)".)
Hypertension
Prevalence — The prevalence of hypertension in children with CKD is high, even when the GFR is only mildly
reduced, and increases with further declines in GFR [21-24].
BP control and renal function — We recommend strict blood pressure control in all children with CKD as
aggressive blood pressure control slows the progression of CKD. Treatment of hypertension should include
specification of target blood pressure levels, nonpharmacologic therapy, and antihypertensive therapy. Based on
the available evidence, the preferred choice of an antihypertensive agent is one that targets the renin-angiotensin
system (angiotensin-converting enzyme [ACE] inhibitor or angiotensin II receptor blockers [ARBs]) and provides
the added benefit of reducing proteinuria, which also slows CKD progression. (See 'Slowing chronic kidney
disease progression' above.)
The impact of BP control on CKD progression was illustrated in the Effect of Strict Blood Pressure Control and
ACE Inhibition on CRF Progression in Pediatric Patients (ESCAPE) trial of 385 children with CKD (GFR between
15 and 80 mL/min per 1.73 m²) that randomly assigned patients to intensified (target: 24-hour mean arterial
pressure [MAP] below the 50th percentile) or conventional (target: MAP between the 50th and 90th percentiles)
blood pressure control [7]. All patients were treated with ramipril (an angiotensin-converting enzyme [ACE]
inhibitor) at a dose of 6 mg/m² per day. Other antihypertensive agents that did not target the renin-angiotensin
system were added to achieve targeted MAP goals, if needed. At five-year follow-up:
● Children in the intensified BP control group were less likely to reach the primary endpoint of a decline of 50
percent in the GFR or development of end-stage kidney disease (ESKD) compared with those in the
conventional BP control group (30 versus 41 percent, hazard ratio 0.65, 95% CI 0.44-0.94).
● An initial 50 percent reduction in proteinuria after initiation of ramipril therapy was predictive of a delay in the
progression of CKD (hazard ratio 0.46, 95% CI 0.27-0.79).
● Factors associated with an increased likelihood of progressive CKD included a low baseline GFR, greater
degree of proteinuria, higher 24-hour MAP, and age. After adjustment for these covariates, intensified BP
control was still associated with a lower risk of CKD progression. The subgroups that benefited the most from
intensified versus conventional BP control were children with an underlying glomerulopathy, baseline GFR
<45 mL/min per 1.73 m² and annualized reduction of GFR >3 mL/min per year, and a urine protein to
creatinine ratio >1.5 mg/mg.
● The mean number of antihypertensive agents per patient in addition to ramipril was greater in the intensified
versus conventional treatment groups (0.9 versus 0.5).

● The target 24-hour MAP <50th percentile was reached by 60, 73, 71, 72, and 74 percent of the intensive
group by 12, 24, 36, 48 and 60 months, respectively. However, more than 50 percent of the conventional
group also had a 24-hour MAP below the 50th percentile with a ramipril monotherapy during the course of the
study.
● Overall, the median urinary protein excretion was reduced during the first six months of the study, but
gradually increased over time and was similar at three years to baseline values. In a subsequent post-hoc
analysis, early antiproteinuric response to ramipril was predictive of improved renal outcome [25]. In this
cohort, the greater degree of proteinuria reduction in the first months of therapy correlated with a lower risk of
CKD progression.
● There was no difference in adverse events between the two groups.
Of note, these findings were based upon mean 24-hour BP measurements, which are not routinely performed in
all patients. However, an office auscultatory BP measurement performed as recommended by the American Heart
Association Council on High Blood Pressure Research has similar predictive value as ambulatory BP monitoring
(ABPM) for left ventricular hypertrophy and the risk for ESKD [26,27]. (See "Evaluation and diagnosis of
hypertension in infants between one month and one year of age", section on 'Blood pressure measurement'.)
Target blood pressure goals — It remains unclear what optimal target BP goals should be for children with
CKD. Guidelines from several professional societies have been published using both office BP measurement and
ambulatory blood pressure monitoring (ABPM) [9,28,29].
We use the following target BP goals for office measurements:
● In younger children with CKD, we use target systolic and diastolic BPs of less than 90th percentile for age,
gender, and height.
● In adolescents, we use a target BP of ≤120/80 mmHg.
If ABPM is available, we use a target goal of a 24-hour mean arterial BP (MAP) below the 50th percentile based
on pediatric ABPM normative data for gender and height as recommended by the 2017 AAP guidelines [9].
Ambulatory blood pressure monitoring (ABPM) — We perform ambulatory blood pressure monitoring
(ABPM) in children with CKD in the following settings:
● If consistent blood pressure data are difficult to obtain with office measurements
● To evaluate the efficacy of antihypertensive therapy, especially when hypertension is difficult to control
● If the patient is symptomatic with complaints that could be attributed to adverse effects from antihypertensive
therapy
● To evaluate for the presence of masked hypertension
In particular, data from the CKiD study has shown the value of ABPM in identifying children with CKD who have
masked hypertension, as well as those with white-coat hypertension and ambulatory hypertension [30-32]. (See
"Ambulatory blood pressure monitoring in children".)

Therapeutic interventions — Therapy includes both nonpharmacologic and pharmacologic interventions:
● Nonpharmacologic therapy – Treatment should be initiated with lifestyle changes including weight reduction
for children who are overweight, a regular aerobic exercise regimen, dietary measures (eg, diet rich in
fruit/vegetables, and reduced fat and salt), and avoidance of excess alcohol consumption, caffeine, energy
drinks, and smoke exposure. (See "Nonemergent treatment of hypertension in children and adolescents",
section on 'Nonpharmacologic therapy'.)
● Pharmacologic therapy – The preferred choice of an antihypertensive agent is one that targets the renin-
angiotensin system (angiotensin-converting enzyme [ACE] inhibitor or angiotensin II receptor blockers
[ARBs]) and that provides the added benefit of reducing proteinuria. ACE inhibitors or ARBS should be used,
if tolerated, for treatment of hypertension in the earlier stages of CKD. They are the preferred
antihypertensive agents as they appear to be more beneficial in slowing the progression of CKD compared
with other agents in patients with CKD [1,7,25,33-35]. (See 'Slowing chronic kidney disease progression'
above and 'BP control and renal function' above.)
In our practice, we prefer to initiate therapy with an ACE inhibitor as there are more data on the safety and
efficacy of this class of drugs compared with ARBs in children. We start with an initial dose of enalapril of 0.08
mg/kg per day (maximum of 5 mg/day), which is titrated to a maximum dose of 0.6 mg/kg per day (maximum of
40 mg/day) based upon the response of the patient's blood pressure and results of lab tests (eg, serum
potassium). We use enalapril because its long half-life allows once a day dosing. Alternative, long-acting ACE
inhibitors commonly used in children are lisinopril and ramipril, which are also administered once a day. (See
"Nonemergent treatment of hypertension in children and adolescents", section on 'ACE inhibitors'.)
The data in children regarding ARB usage are limited [36,37]. We use ARBs to replace ACE inhibitors in patients
who have difficulty tolerating an ACE inhibitor (mostly adolescents) to treat hypertension and decrease
proteinuria. We start with an initial dose of Losartan 0.7 mg/kg per day (maximum of 50 mg/day), which is titrated
to a maximum dose of 1.4 mg/kg per day (maximum of 100 mg/day). We avoid combination therapy of ACE
inhibitors and ARBs, as data from adults suggest an increased likelihood of adverse events. (See "Major side
effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers", section on 'Combination
of ACE inhibitors and ARBs'.)
Both ACE inhibitors and ARBs should be used cautiously if the GFR is less than 60 mL/min per 1.73 m² [35].
Since the decline in GFR induced by an ACE inhibitor/ARB typically occurs within the first few days after the onset
of therapy, the serum creatinine and potassium concentrations should be remeasured three to five days after the
institution of therapy to ensure that the therapy has not adversely affected the GFR resulting in a significant
elevation of serum creatinine and/or hyperkalemia.
The teratogenic potential of these drugs in women of childbearing age also should be discussed with any
postpubertal adolescent female when administration of either an ACE inhibitor or ARB is being considered. (See
"Major side effects of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers" and
"Adverse effects of angiotensin converting enzyme inhibitors and receptor blockers in pregnancy".)
A diuretic is also often recommended in the early stages of CKD. The thiazide diuretics, such as
hydrochlorothiazide (1 to 3 mg/kg per day to a maximum of 50 mg/day), become less effective as monotherapy as
the GFR declines. Thus, a loop diuretic is recommended for the treatment of hypertension and edema in patients
with more severe CKD. In our practice, we use the loop diuretic furosemide at a dose of 0.5 to 2 mg/kg per day in
one to two divided doses.
Anemia — Anemia due to reduced kidney erythropoietin production generally develops when the GFR is below
30 mL/min per 1.73 m². Data from the CKiD study suggests that hemoglobin (Hb) begins to decline significantly
when the iohexol-determined GFR is at 43 mL/min per 1.73 m², a value which equates with a Schwartz estimated
GFR of 58 mL/min per 1.73m² (when determined with a serum creatinine measured by Jaffe methodology) [38].
At the onset of dialysis, the presence of anemia in children is very common and has been associated with
excessive morbidity and an increased mortality risk [39].
Because anemia is a common complication of children with severe CKD (ie, stages G4 and G5), established
guidelines have been developed for the identification, evaluation, and treatment of anemia in children at all stages
of CKD [1,40]. The recommendations for the management of anemia presented here are based upon these sets
of guidelines.
Screening and evaluation of anemia — Annual testing of Hb should be performed in children with CKD,
regardless of stage or cause.
A diagnosis of anemia is made when the observed Hb result is below the 2.5th percentile of normal adjusted for
age and sex (table 3) (see "Approach to the child with anemia", section on 'Definition of anemia'). We perform the
following evaluation, which is focused upon eliminating causes of anemia other than CKD and determining the
iron status of the patient, in any child with CKD and anemia [41].
● Red blood cell indices

● Reticulocyte count
● Iron parameters (serum iron, total iron binding capacity, percent transferrin saturation [TSAT], and serum
ferritin)
● Test for occult blood in stool
Target hemoglobin goals — The optimal Hb for children with CKD who receive an erythropoiesis stimulating
agent (ESA) has not been established. In our practice, we use a target Hb between 11 and 12 g/dL as
recommended by published guidelines and based on consensus expert opinion and the following data [40,42,43]:
● Levels below 10 and 11 g/dL:
• In the International Pediatric Peritoneal Dialysis Network (IPPN), children on peritoneal dialysis observed
a significant increase in patient mortality associated with a mean achieved Hb <11 g/dl [44].
• Other data showed that children with CKD and an Hb less than 9.9 g/dL were at increased risk for
mortality, left ventricular hypertrophy, and/or decreased exercise capacity compared with those with an
Hb greater than 9.9 g/dL [40].
• Quality of life and neurocognitive function improved in patients treated with rHuEPO who experienced a
significant increase in Hb compared with a baseline Hb that was below 9.9 g/dL [40].
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● Levels above 12 g/dL:
• A retrospective analysis of a merged dataset from the Clinical Performance Measures project and the
USRDS found that an Hb value >12 g/dL was not associated with increased CV morbidity or mortality in
pediatric HD patients [45]. (See "Treatment of anemia in hemodialysis patients".)
• Data in adults have shown that Hb levels of 13 g/dL or higher are associated with an increased risk of
CV-related events. As a result, there is a general consensus among expert panels that adult targeted Hb
levels should not exceed 13 g/dL in patients treated with an ESA, and established guidelines
recommend an Hb goal between 10 and 11.5 g/dL. (See "Treatment of anemia in nondialysis chronic
kidney disease", section on 'Target hemoglobin value'.)
In children, there are currently no data demonstrating an increased risk of CV deaths or events with Hb levels
greater than 13 g/dL. However, given the evidence of increased risk of CV death in children and adults with
advanced stages of CKD and the detrimental effects of a level below 11 g/dL, we agree with the recommended
target of Hb between 11 and 12 g/dL in children with CKD who receive therapy with an ESA.
Treatment of anemia — The treatment of anemia in children with CKD includes iron supplementation and an
erythropoiesis stimulating agent (ESA).
Iron — Iron therapy (elemental iron 3 to 4 mg/kg per day) should be initiated if iron deficiency is detected.
Iron supplementation is targeted to maintain a transferrin saturation (TSAT) ≥20 percent and a serum ferritin ≥100
ng/dL in children with CKD. Our practice is consistent with the NICE guidelines, which recommend that children
with CKD who are not receiving hemodialysis should be treated with oral iron therapy, and if the child is intolerant
of oral iron or target Hb levels are not reached, then intravenous iron therapy should be considered [41]. All
patients receiving therapy with an ESA, such as recombinant human erythropoietin (rHuEPO) and darbepoetin
alfa, require iron supplementation to prevent the development of iron deficiency. Once the iron status is normal, it
should be monitored at least every three months or monthly following the initiation of and/or increase in ESA
dosing. (See "Diagnosis of iron deficiency in chronic kidney disease".)
Erythropoiesis stimulating agents — Although primarily used in patients with end-stage kidney disease
(ESKD), erythropoiesis stimulating agents (ESAs) (eg, rHuEPO and darbepoetin alfa) are also used to correct the
anemia in some children at earlier CKD stages. Increasing the Hb into an acceptable range in pediatric patients
with anemia may ameliorate anemia-induced symptoms (eg, fatigue and exercise intolerance), result in CV
improvement, and possibly delay progression of CKD and decrease mortality [4]. (See "Treatment of anemia in
nondialysis chronic kidney disease".)
The initial rHuEPO dose in older children not receiving dialysis is 80 to 120 units/kg per week, administered in two
to three divided doses. Children younger than five years of age or children receiving dialysis frequently require
higher doses (as much as 300 units/kg per week). In predialysis patients and in those who receive peritoneal
dialysis, rHuEPO should preferably be administered by the subcutaneous route and the site of injection should be
rotated. In patients who receive hemodialysis, rHuEPO is typically administered intravenously through their
vascular access.

The response to rHuEPO is monitored by measurement of the Hb every one to two weeks following the initiation
of treatment or following a dose change until a stable target Hb and a stable rHuEPO dose have been achieved; it
should then be monitored every four weeks. The expected increase in Hb after the initiation of rHuEPO therapy or
after a dose change is between 1 to 2 g/dL over a two to four week period.
Darbepoetin alfa is a long-acting erythropoietic agent and is the preferred ESA for adolescents to improve
compliance. Its threefold longer half-life and greater biological activity compared with epoetin-alfa or epoetin-beta
allows for less frequent dosing to effectively maintain a target Hb. Based upon limited pediatric data, darbepoetin
alfa can be given at a dose of 0.25 to 0.75 mcg/kg no more frequently than once weekly [46-48]. In a trial,
darbepoetin alfa was shown to be effective and safe in 116 children with CKD-related anemia when administered
either weekly or every two weeks to achieve Hb targets of 10 to 12 g/dL [49].
In a systematic review, continuous erythropoiesis receptor activator (CERA, methoxy polyethylene glycol-epoetin
beta), a longer-acting ESA, did not offer better patient-centered outcomes compared with rHuEPO or darbepoetin
in adults with CKD [50]. In a small study of 64 children on hemodialysis, CERA was found to be safe and
efficacious in maintaining Hb levels [51]. However, it remains uncertain whether CERA offers any advantage over
rHuEPO or darbepoetin in pediatric patients.
The most common cause of an incomplete response to an ESA is iron deficiency. However, other conditions in
the iron replete patient may cause an inadequate response to an ESA as well and include:
● Infection or inflammation (see "Inflammation in renal insufficiency")
● Chronic blood loss (see "Approach to the child with anemia")
● CKD-mineral and bone disorder [52] (see "Overview of chronic kidney disease-mineral and bone disorder
(CKD-MBD)")
● Aluminum toxicity (see "Aluminum toxicity in chronic kidney disease")
● Folate or vitamin B12 deficiency (see "Treatment of vitamin B12 and folate deficiencies")
● Malnutrition
● Hemoglobinopathies
● Hemolysis (see "Overview of hemolytic anemias in children")
● Carnitine deficiency (rare)
● Copper deficiency (rare)
For children who develop acquired ESA hyporesponsiveness, avoid repeated escalations in ESA dose beyond
double the dose at which the Hb had been stable because of concern for direct toxicity related to the elevated
ESA dosages [43]. A dose of ESA >6000 international units/m2 per week in children on peritoneal dialysis was
associated with an increased mortality risk [44].

Dyslipidemia — Abnormal lipid metabolism is common in patients with CKD and adds to the risk for
cardiovascular disease (CVD). The risk of CVD increases with progression of CKD, with the highest risk for those
with ESKD and following kidney transplantation (algorithm 1) [53]. Observational data in children have shown that
the risk of dyslipidemia (eg, abnormally high triglyceride and non-high-density lipid cholesterol [non-HDL-C] levels
and decreasing HDL-C level) is high in children with CKD and increases as the measured GFR declines [54-61].
As a result, the American Academy of Pediatrics, American Heart Association, Kidney Disease: Improving Global
Outcomes (KDIGO), and an expert panel sponsored by the United States National Heart, Lung, and Blood
Institute (NHLBI) recommend that all children greater than two years of age with one or more known
atherosclerotic risks or conditions associated with CVD (including CKD) be screened for dyslipidemia. The 2013
KDIGO clinical practice guidelines suggest that children with CKD (including those on chronic dialysis or with
kidney transplantation) should have a fasting lipid profile obtained at the time CKD is first identified and annually
thereafter. The annual assessment is recommended as growth and development in children may influence lipid
levels and also to assess for secondary causes of dyslipidemia [53]. (See "Society guideline links: Lipid disorders
and atherosclerosis in children".)
The risk of dyslipidemia increases in children who are overweight as defined by BMI >85th percentile and/or waist-
to-hip ratio (WHR) >0.49 [62]. As a result, in addition to determining BMI, WHR should also be measured in
children with CKD.
Interventions — In our practice, we use dietary guidelines from KDOQI and KDIGO based on severity of CKD
and whether dyslipidemia is present:
● Children with CKD stage G5 should receive a very restrictive diet (table 4) [17].
● Children with CKD who have hypertriglyceridemia (fasting level >500 mg/dL [>5.65 mmol/L]) should receive a
very low fat diet (fat content less than 15 percent of the total caloric intake) with the use of medium-chain
triglycerides and fish oil instead of long-chain triglycerides [63]. However, in children who are malnourished,
dietary changes should be made judiciously, if at all.
● Fibric acid derivatives or niacin should not be used as there is a paucity of evidence regarding their safety
and efficacy [63].
● Statin therapy may be considered only in older patients (males ≥10 years of age and post-menarchal female
patients) with severely elevated LDL-C levels despite nonpharmacologic therapy. The decision is made jointly
with the family and patient (if appropriate) after considering the currently available evidence and the potential
for adverse effects of statin therapy. (See "Dyslipidemia in children: Management", section on 'Statin
therapy'.)
The screening and management of pediatric dyslipidemia are discussed in greater detail separately. (See
"Dyslipidemia in children: Definition, screening, and diagnosis" and "Dyslipidemia in children: Management".)
Our approach — In our practice, we evaluate the fasting lipid profile of children with CKD (including dialysis
and kidney transplantation) on an annual basis. If a lipid abnormality is found on evaluation, we recommend
therapeutic lifestyle changes with dietary recommendations (table 5) made in concert with our pediatric renal

dietitian. We consider the use of statins only in cases of failed conservative therapy where the magnitude of
dyslipidemia is severe (eg, LDL >130 mg/dL).
Nutrition — Appetite and nutritional intake decreases with progression of CKD in children over time [64,65]. As a
result, malnutrition is common in children with CKD because of poor appetite, decreased intestinal absorption of
nutrients, and metabolic acidosis. Attention to nutrition is critical, as it affects the physical growth, neurocognitive
development, and overall health status (ie, fragility) [66]. In children with CKD, weight loss primarily occurs when
the GFR decreases to <35 mL/min per 1.73 m2, and this weight loss is associated with a higher risk for ESKD
[67].
The KDOQI pediatric guidelines for nutrition recommend that the nutritional status of children with CKD should be
evaluated on a periodic basis [17]. The frequency of monitoring is primarily dependent upon the age of the patient
and CKD stage as follows:
● 0 to 1 year of age:
• CKD stages G2 to G5: From 0.5 to 3 months
• Patients receiving dialysis: From 0.5 to 2 months
● 1 to 3 years of age for all stages including dialysis patients: From 1 to 3 months
● >3 years of age:
• CKD stage G2: From 6 to 12 months
• CKD stage G3: Every 6 months
• CKD stage G4 and G5: From 3 to 4 months
The following parameters are measured:
● Dietary intake (three-day diet record or three 24-hour dietary recalls)

● Estimated dry weight and weight for age percentile or standard deviation score (SDS)
● Length or height for age percentile or SDS
● Weight/height index
● Body mass index (BMI) for height age percentile or SDS
● In patients younger than three years of age, head circumference for age percentile or SDS
● Normalized protein catabolic rate in hemodialyzed adolescents
Nutritional therapy based upon growth parameters should be developed for each child with CKD and should
ideally be coordinated by a dietician with expertise in pediatrics and renal nutrition. Nutritional management
should address the energy, protein, vitamin, mineral, and electrolyte needs of the individual patient.
Energy — The initial prescribed energy (calorie) intake for children with CKD is based upon the estimated
energy requirement (EER) for chronological age (table 6) [17]. Further supplementation should be considered
when the initial intake fails to meet the child's energy requirements and he/she is not achieving expected rates of
weight gain and/or growth. Although supplementation by the oral route is preferred, one may have to resort to

tube feedings with a gastrostomy, transpyloric tube, or nasogastric tube to ensure adequate energy intake (see
"Overview of enteral nutrition in infants and children"). A trial of intradialytic parental nutrition may be considered
in children undergoing chronic hemodialysis therapy.
Protein — Protein intake should be between 100 and 140 percent of the Dietary Reference Intake (DRI) based
upon age and gender for children with CKD stage G3 and between 100 and 120 percent for those with CKD
stages G4 and G5 (table 7) [17]. For patients on peritoneal dialysis, protein intake should be higher (additional
average 0.15 to 0.3 g/kg per day) to compensate for dialytic protein loss. (See "Chronic peritoneal dialysis in
children", section on 'Nutritional and metabolic issues'.)
Protein restriction is not recommended in children as it has not been shown to influence the decrease in kidney
function in children with CKD and may impair growth [13,68,69]. Protein supplementation should be considered if
the oral and/or enteral protein intake is inadequate [13,17,70].
Vitamins and minerals — Children with CKD should receive 100 percent of the DRIs for the vitamins:
thiamine (B1), riboflavin (B2), pyridoxine (B6), vitamin B12, A, C, E, K, and folic acid (table 8 and table 9); and the
minerals: copper and zinc [17]. In the CKiD cohort, a serum 25-hydroxyvitamin D <20 ng/mL was observed in 28
percent of the children, which was associated with older age, non-white race, higher BMI, assessment during
winter, less daily milk intake, absence of nutritional vitamin D supplement, and proteinuria [71]. In a post hoc
analysis of the ESCAPE trial, serum 25-hydroxyvitamin D >20 ng/mL (>50 nmol/L) was associated with greater
preservation of kidney function in children with CKD [6]. (See "Pediatric chronic kidney disease-mineral and bone
disorder (CKD-MBD)", section on 'Vitamin D deficiency'.)
In children with advanced CKD (ie, stage G5), the loss of renal clearance of vitamin A metabolites places them at
risk for developing hypervitaminosis A; these children should receive a water-soluble vitamin supplement with the
addition of vitamin A only if they have very low dietary intake.
Growth — Growth failure has been long recognized in children with CKD. While the institution of recombinant
human growth hormone (rHuGH) therapy can have a profound effect on the height velocity of children with CKD
who are growing poorly, early recognition and management of malnutrition, CKD-MBD, acid-base abnormalities,
and electrolyte disturbances should take place prior to considering the institution of rHuGH. (See "Prevention and
management of growth failure in children with chronic kidney disease" and "Growth hormone treatment in children
with chronic kidney disease and postkidney transplantation" and "Pathogenesis, evaluation and diagnosis of
growth impairment in children with chronic kidney disease".)
Neurodevelopment — Uremia is associated with alterations in cognition and may impact neurodevelopment in
children. Neurologic findings can range from seizures and severe intellectual disability (mental retardation) to
more subtle deficits resulting in poor school performance [72,73]. Children with CKD have lower scores for
executive function, memory (verbal and visual), mathematics, reading, and spelling compared with the general
population [74]. Children on dialysis have lower scores on cognitive testing than those with milder CKD [75,76].
Poor academic performance is related in part to school absenteeism, a common problem for children with CKD
[73,77]. Other reported factors associated with cognitive impairment in children with CKD include high blood lead
level [78] and changes in regional cerebral blood flow [79].

Management — In infants and young children with CKD, frequent monitoring of head circumference and age-
appropriate developmental evaluations are necessary. A more formal neurodevelopmental assessment is needed
in older children, especially if they have poor school performance.
In patients with neurodevelopmental impairment or learning disabilities, assessment of the general CKD
management should be performed to identify modifiable risk factors that can negatively impact learning capacity.
Neurodevelopmental impairment can be minimized by optimizing nutritional, dialysis, and anemia management.
Early identification of genomic disorders may also provide an opportunity to mitigate the effect on neurocognitive
function in children with CKD by referral to early intervention programs [80]. Special education school services
may be beneficial for children with neurodevelopmental impairment. (See "Specific learning disabilities in children:
Educational management".)
Uremic bleeding — An increased tendency for bleeding is present in patients with severe CKD due primarily to
abnormalities in platelet adhesion and aggregation properties. In asymptomatic patients, no specific therapy is
required. (See "Platelet dysfunction in uremia".)
However, in patients who are actively bleeding or who are about to undergo a surgical or invasive procedure
(such as kidney biopsy), the platelet abnormality should be addressed. A number of different treatment options
can be considered in this setting. These include the following:
● Desmopressin (dDAVP), an analog of antidiuretic hormone that is the simplest and least toxic acute
treatment. It is administered intravenously or subcutaneously at a dose of 0.3 mcg/kg with an onset of effect
within one hour of administration; the effect lasts for six to eight hours.
● Cryoprecipitate (1 to 2 units/10 kg); the effect lasts for 24 to 36 hours, but there is an increased risk of
transmitted infectious diseases.
● Estrogen (0.6 mg/kg per day for 5 days); the onset of effect is over 6 to 24 hours, but the effect lasts for two
to three weeks.
● Correction of anemia; an improved Hb (hematocrit) is believed to facilitate increased interaction between

platelets and blood vessels.
Uremic pericarditis — Uremic pericardial disease (pericarditis and pericardial effusion) is seen only in the late
stages of CKD and is an indication to institute dialysis. Most patients with uremic pericarditis respond rapidly to
dialysis with resolution of chest pain as well as a decrease in the size of the pericardial effusion.
Immunization — All childhood vaccinations should be administered in children with CKD with the caveat that live
attenuated vaccines should NOT be administered to children on immunosuppressive therapy. As an example, live
attenuated influenza vaccine should not be given to children undergoing dialysis or with CKD, but instead, the
inactivated version should be given [1]. The pneumococcal vaccine should be given to all children with nephrotic
syndrome and those with CKD. In addition, hepatitis B vaccination should be provided to all children with CKD or
undergoing dialysis. Limited data have shown a robust and sustained response to human papillomavirus in
children with pre-dialysis CKD and children on dialysis, but not in kidney transplant recipients [81,82].

END-STAGE KIDNEY DISEASE
Renal replacement therapy — Once the estimated glomerular filtration rate (GFR) declines to less than 30
mL/min per 1.73 m² (stage G4 chronic kidney disease [CKD]), it is time to start preparing the child and the family
for renal replacement therapy (RRT) [2]. The family should be provided with information related to preemptive
kidney transplantation, peritoneal dialysis, and hemodialysis.
As in adults, some form of renal replacement therapy will generally be needed when the GFR falls below 10 to 15
mL/min per 1.73 m² (stage G5 CKD). However, renal replacement therapy is often initiated before children reach
these levels for the following reasons:
● Poor total calorie intake resulting in failure to thrive

● Clinical symptoms attributable to uremia
● Delay in psychomotor development and associated educational issues
Early initiation at a higher GFR does not provide a survival advantage, and in fact, two studies reported that
dialysis initiation at higher eGFR was associated with lower survival [83,84].
Choice of renal replacement therapy — The choice of RRT is discussed separately. (See "Overview of renal
replacement therapy (RRT) for children with chronic kidney disease".)
Pediatric mortality — Children with end-stage kidney disease (ESKD) have a shortened life expectancy
compared with children without CKD. Renal transplantation remains the treatment of choice to maximize survival
and growth. (See "Overview of renal replacement therapy (RRT) for children with chronic kidney disease", section
on 'Choice of RRT'.)
Almost three-quarters of children diagnosed with ESKD undergo dialysis in the United States and the mortality
rate for these children is reported to be at least 30 times higher than in the general pediatric population [85].
However, data from the United States Renal Data System (USRDS) and the North American Pediatric Renal
Trials and Collaborative Studies (NAPRTCS) database have shown a decrease in mortality for children who
received chronic dialysis [86-88]. The 2018 USRDS Annual Data Report, which includes all children who receive
RRT (both kidney transplant and dialysis), found that the one-year adjusted all-cause mortality had decreased
from 49 to 39 per 1000 patient years between 2006 to 2010 and 2011 to 2015 [89]. Based on the North American
Pediatric Renal Trials and Collaborative Studies (NAPRTCS) database, survival of infants who initiate chronic
peritoneal dialysis in the first year of life has improved over time from 2000 to 2012 compared with an earlier
cohort from 1992 to 1999 [90].
The leading causes of death are cardiovascular disease and infection. The authors speculate that the reduction in
mortality is probably due to improved predialysis care, advances in dialysis technology, and increased clinical
experience in caring for these patients.
Outcome in adulthood — Patients placed on RRT before 15 years of age have a greater mortality and morbidity
risk than age-matched controls. This was illustrated in a long-term Dutch follow-up study (median time 25.5 years)
that observed 30 times greater mortality risk for adults who began pediatric RRT (median time of RRT 25.5 years)

than age-matched peers [91]. These individuals were more likely to have motor disabilities, skin cancer, and
severe fatigue when they were >40 years old.
QUALITY OF LIFE
Chronic kidney disease (CKD), as is true for any chronic condition, impacts the quality of life (QOL) for both the
child and family [64,92-95]. In particular, psychological (eg, depression) and social stresses are found in children
with CKD and their families [94,95]. The normal progression of the child to independence is impeded, and
concerns about body composition and image are greatly magnified in children whose growth and pubertal
development are delayed or altered, especially those who undergo chronic dialysis [94]. The prospect of a lifetime
with renal replacement therapy (dialysis and/or transplant) and the potential for catastrophic complications and/or
death makes it difficult to achieve normal childhood and adolescent developmental goals.
This difficulty continues into adulthood. Compared with age-matched population normative data, patients who had
childhood end-stage kidney disease (ESKD) were more likely to be unemployed, and to have lower income and
scores on QOL surveys [96-99]. Whereas many adults with childhood ESKD are able to attain social autonomy,
employment remains challenging due to an inability to work because of medical issues and a lack of
understanding among teachers and employers about the medical burden of CKD/dialysis that these young adults
have to deal with [99,100]. This results in loss of self-esteem, social isolation, fatigue, and low mood [99].
The negative impact of chronic disease on the emotional status of the patient's siblings is also well recognized
[101]. These siblings frequently feel "neglected" because the parents must provide substantial physical and
psychological support to the sick child. Furthermore, the well child may simultaneously feel jealous of the attention
provided to the sick child, as well as guilt about being well while the sibling is severely ill.
Optimal comprehensive management of these issues involves a multidisciplinary approach that proactively
addresses these concerns. Key members of the team include social workers and mental health specialists.
When, on a rare occasion, parents of a child with Stage G5 CKD elect conservative management and death over
a lifetime of dialysis and transplantation for their child, this should be considered a choice that may, on occasion,
be medically, ethically, and legally acceptable. A host of factors need to be considered by the family, the
healthcare providers, and often the institution's ethics committee. When a decision to forego renal replacement
therapy is deemed acceptable, the family should be supported emotionally and provided with whatever care is
necessary to maintain the child in a pain-free state [102]. (See "Palliative care for patients with end-stage kidney
disease" and "Withholding and withdrawal of dialysis".)
SOCIETY GUIDELINE LINKS
Links to society and government-sponsored guidelines from selected countries and regions around the world are
provided separately. (See "Society guideline links: Chronic kidney disease in children" and "Society guideline
links: Chronic kidney disease-mineral and bone disorder".)

INFORMATION FOR PATIENTS
UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics
patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the
four or five key questions a patient might have about a given condition. These articles are best for patients who
want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education
pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade
reading level and are best for patients who want in-depth information and are comfortable with some medical
jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these
topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on
"patient info" and the keyword(s) of interest.)
● Basics topics (see "Patient education: Bone problems caused by kidney disease (The Basics)" and "Patient
education: Medicines for chronic kidney disease (The Basics)")
SUMMARY AND RECOMMENDATIONS
The general management of children with chronic kidney disease (CKD) includes treating any reversible kidney
dysfunction, preventing or slowing the progression of CKD, treating the complications associated with CKD, and
identifying and preparing patients and their families for whom renal replacement therapy will be required. (See
'General principles' above.)
In addition, comprehensive management includes addressing the psychological and social stresses on the family
and child in dealing with a chronic condition. (See 'Quality of life' above.)
Reversing kidney dysfunction and slowing CKD progression
● Most conditions with potentially recoverable kidney function are primarily due to decreased kidney perfusion
or the administration of nephrotoxic agents, which may be corrected with either volume repletion or
discontinuation of a nephrotoxic drug. (See 'Reversible kidney dysfunction' above.)
● In adults and children with CKD, strict blood pressure control has been shown to slow the progression of
kidney disease and decrease the risk of cardiovascular disease. (See "Antihypertensive therapy and
progression of nondiabetic chronic kidney disease in adults".)
● In children with CKD, there is no evidence that a low protein diet slows the progression of kidney disease.
There is also concern that such a diet may impair growth. We suggest that children with CKD be given a daily
diet containing at least 100 percent of the dietary reference intake for protein based upon age and gender
(table 7) (Grade 2C). (See 'Slowing chronic kidney disease progression' above and 'Nutrition' above.)
Complications

● Volume overload – In children with severe CKD and volume overload due to water retention, we suggest a
combination trial of dietary sodium restriction and diuretic therapy (Grade 2C). In our practice, we limit the
sodium intake to 2 to 3 g/day. Thiazide diuretics (eg, hydrochlorothiazide) are preferred in the early stages of
CKD, while furosemide or another loop diuretic is used in more advanced stages of CKD. (See 'Sodium and
intravascular volume' above.)
● Hyperkalemia – In children with moderate to severe CKD, we recommend a low potassium diet to prevent
hyperkalemia (Grade 1C). Other interventions include the use of loop diuretics (eg, furosemide) and
correction of metabolic acidosis. (See 'Hyperkalemia' above.)
● Metabolic acidosis – In children with CKD and metabolic acidosis, we suggest administering sodium
bicarbonate to maintain a serum bicarbonate level ≥22 mEq/L (Grade 2C). Citrate preparations should be
avoided, as these preparations enhance aluminum absorption. (See 'Metabolic acidosis' above.)
● CKD-mineral and bone disorder (CKD-MBD) – Management of CKD-MBD includes ongoing monitoring of
bone metabolism (measurements of serum concentrations of calcium, phosphorus, parathyroid hormone and
alkaline phosphatase levels) and appropriate therapeutic interventions including dietary phosphate restriction,
phosphate binders, vitamin D replacement therapy, active vitamin D analogues, and calcimimetic drugs. (See
"Pediatric chronic kidney disease-mineral and bone disorder (CKD-MBD)".)
● We recommend that high blood pressure (BP) in children with CKD be avoided, and BP be strictly controlled
(Grade 1B). In patients with hypertension and proteinuria, we recommend that an angiotensin-converting
enzyme (ACE) inhibitor or an angiotensin II receptor blocker (ARB) be used rather than other classes of
antihypertensive agents (Grade 1B). In our practice, we use target systolic and diastolic blood pressures of
less than 90th percentile for age, gender, and height based on office blood pressure measurements. If
ambulatory BP monitoring is used, target BP should be a 24-hour mean arterial pressure below the 50th
percentile for gender and height. (See 'Slowing chronic kidney disease progression' above and 'Hypertension'
above.)
● Anemia – In children with CKD, hemoglobin (Hb) testing should be performed at least yearly. Anemia is
defined as an Hb below the 2.5th percentile of normal adjusted for age and sex (table 3). After eliminating
other causes of anemia, treatment of anemia due to CKD includes iron supplementation and in patients with
severe CKD, erythropoietin therapy.
In children with CKD who receive therapy with an erythropoiesis stimulating agent (ESA), we suggest a target
Hb between 11 and 12 g/dL (Grade 2C). (See 'Anemia' above.)
● Dyslipidemia – In children with CKD, screening for dyslipidemia is performed by obtaining fasting lipid profiles
on an annual basis. In patients with dyslipidemia, we suggest an initial trial of nonpharmacologic therapy that
includes diet (table 4 and table 5) and daily exercise (Grade 2C). We suggest statin therapy be considered in
patients greater than 10 years old with a persistently elevated low density lipoprotein (LDL) cholesterol level
(Grade 2C). (See 'Dyslipidemia' above and "Dyslipidemia in children: Management".)
● Growth and nutrition – In children with CKD, ongoing monitoring of their nutritional status includes
measurement of growth parameters and dietary review. We suggest that the diet contain 100 percent of the

estimated energy requirement based upon age and gender (table 6), and appropriate protein requirement
based upon age and CKD stage (table 7) (Grade 2C). In some patients with growth impairment, recombinant
human growth hormone is an option to improve linear growth. (See 'Growth' above and "Growth hormone
treatment in children with chronic kidney disease and postkidney transplantation".)
● Children with CKD are at risk for neurodevelopmental impairment, which may be minimized by optimal
nutritional and anemia management. Ongoing neurodevelopmental assessment is necessary to determine
whether additional educational support is needed for school-age children. (See 'Neurodevelopment' above.)
Renal replacement options — As the patient reaches CKD stage G4 disease (glomerular filtration rate <30
mL/min per 1.73 m²), it is time to start preparing the child and family for renal replacement therapy (RRT). At this
time, information related to preemptive kidney transplantation, peritoneal dialysis, and hemodialysis is provided to
the family. Although renal transplant is the preferred RRT, the choice of RRT is dependent on technical, social,
and compliance issues, and family preference. (See 'Renal replacement therapy' above and "Overview of renal
replacement therapy (RRT) for children with chronic kidney disease", section on 'Choice of RRT'.)
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REFERENCES
1. KDIGO 2012 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease.
Kidney Int Suppl 2013; 3:136.
2. National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation,
classification, and stratification. Am J Kidney Dis 2002; 39:S1.
3. Andreev E, Koopman M, Arisz L. A rise in plasma creatinine that is not a sign of renal failure: which drugs
can be responsible? J Intern Med 1999; 246:247.
4. Warady BA, Abraham AG, Schwartz GJ, et al. Predictors of Rapid Progression of Glomerular and
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38. Fadrowski JJ, Pierce CB, Cole SR, et al. Hemoglobin decline in children with chronic kidney disease:
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39. Warady BA, Ho M. Morbidity and mortality in children with anemia at initiation of dialysis. Pediatr Nephrol
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44. Borzych-Duzalka D, Bilginer Y, Ha IS, et al. Management of anemia in children receiving chronic peritoneal
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48. Schaefer F, Hoppe B, Jungraithmayr T, et al. Safety and usage of darbepoetin alfa in children with chronic
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50. Saglimbene VM, Palmer SC, Ruospo M, et al. Continuous erythropoiesis receptor activator (CERA) for the
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52. Altemose KE, Kumar J, Portale AA, et al. Vitamin D insufficiency, hemoglobin, and anemia in children with

53. Kidney Disease: Improving Global Outcomes (KDIGO) Lipid Work Group. KDIGO Clinical Practice Guideline
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54. Saland JM, Kupferman JC, Pierce CB, et al. Change in Dyslipidemia with Declining Glomerular Filtration
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56. Saland JM, Ginsberg H, Fisher EA. Dyslipidemia in pediatric renal disease: epidemiology, pathophysiology,
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57. Saland JM, Ginsberg HN. Lipoprotein metabolism in chronic renal insufficiency. Pediatr Nephrol 2007;
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58. Bonthuis M, van Stralen KJ, Jager KJ, et al. Dyslipidaemia in children on renal replacement therapy.
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61. Drożdż D, Kwinta P, Sztefko K, et al. Oxidative Stress Biomarkers and Left Ventricular Hypertrophy in
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62. Sgambat K, Roem J, Mitsnefes M, et al. Waist-to-height ratio, body mass index, and cardiovascular risk
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63. Kidney Disease: Improving Global Outcomes (KDIGO) Lipid Work Group. KDIGO Clinical Practice Guideline
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64. Ayestaran FW, Schneider MF, Kaskel FJ, et al. Perceived appetite and clinical outcomes in children with
65. Chen W, Ducharme-Smith K, Davis L, et al. Dietary sources of energy and nutrient intake among children
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66. Sgambat K, Matheson MB, Hooper SR, et al. Prevalence and outcomes of fragility: a frailty-inflammation
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67. Ku E, Kopple JD, McCulloch CE, et al. Associations Between Weight Loss, Kidney Function Decline, and
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71:648.
68. Chaturvedi S, Jones C. Protein restriction for children with chronic renal failure. Cochrane Database Syst
Rev 2007; :CD006863.
69. Uauy RD, Hogg RJ, Brewer ED, et al. Dietary protein and growth in infants with chronic renal insufficiency: a
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71. Kumar J, McDermott K, Abraham AG, et al. Prevalence and correlates of 25-hydroxyvitamin D deficiency in
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72. Lawry KW, Brouhard BH, Cunningham RJ. Cognitive functioning and school performance in children with
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73. Harshman LA, Johnson RJ, Matheson MB, et al. Academic achievement in children with chronic kidney
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Topic 6085 Version 48.0

GRAPHICS
Stages of chronic kidney disease for children based on the KDIGO 2012 clinical practice
guideline
GFR
GFR category Terms
(mL/min/1.73 m 2)
G1 ≥90 Normal or high
G2 60 to 89 Mildly decreased*
G3a 45 to 59 Mildly to moderately decreased
G3b 30 to 44 Moderately to severely decreased
G4 15 to 29 Severely decreased
G5 <15 Kidney failure
In the absence of evidence of kidney damage, neither GFR category G1 nor G2 fulfill the criteria for CKD.
KDIGO: Kidney Disease: Improving Global Outcomes; GFR: glomerular filtration rate; CKD: chronic kidney disease.
* Relative to young adult level.
Reprinted with permission from: Macmillan Publishers Ltd: Kidney International Supplements. KDIGO 2012 Clinical Practice Guideline for the
Evaluation and Management of Chronic Kidney Disease. Chapter 1: Definition and classification of CKD. Kidney Int Suppl 2013; 3:19.
Copyright © 2013. www.nature.com/kisup.
Graphic 89808 Version 2.0

Plasma creatinine reference intervals (2.5 th to 97.5 th percentiles)
Enzymatic creatinine Jaffe creatinine
Age group mg/dL micromol/L Age group mg/dL micromol/L
0 to 14 days 0.32 to 0.92 28 to 81 0 to 14 days 0.42 to 1.05 37 to 93
15 days to <2 years 0.10 to 0.36 9 to 32 15 days to <1 year 0.31 to 0.53 27 to 47
2 to <5 years 0.20 to 0.43 18 to 38 1 to <4 years 0.39 to 0.55 34 to 49
15 to 19 years 0.62 to 1.08 55 to 95 12 to 15 years 0.57 to 0.80 50 to 71

(male)
15 to <19 years 0.49 to 0.84 43.3 to 74 15 to <17 years 0.65 to 1.04 57 to 92

(female) (male)
15 to <17 years 0.59 to 0.86 52 to 76

(female)
17 to <19 years 0.69 to 1.10 61 to 97

(male)
17 to <19 years 0.60 to 0.88 53 to 78

(female)
Creatinine pediatric reference values measured by two different laboratory assays: enzymatic reaction by isotope dilution mass
spectrometry (IDMS) and the Jaffe reaction. Creatinine values are based on age; and for adolescent patients, reference values are
also based on sex.
Data from: Colantonio DA, Kyriakopoulou L, Chan MK, et al. Closing the gaps in pediatric laboratory reference intervals: a CALIPER database
of 40 biochemical markers in a healthy and multiethnic population of children. Clin Chem 2012; 58:854.

Hemoglobin, hematocrit, red blood cells, mean corpuscular volume, and white blood cells in
children 1 to 14 years of age, by age group and sex: The Third National Health and Nutrition
Examination Survey (1988 to 1991)
Male* (n = 5070) Female* (n = 5175)

Characteristic
Mean SD 95% CI Mean SD 95% CI
Hemoglobin, g/dL ¶
1 to 2 years 12.01 0.82 10.37 13.65 12.02 0.8 10.42 13.62
3 to 5 years 12.35 0.77 10.81 13.89 12.39 0.77 10.85 13.93
6 to 8 years 12.88 0.8 11.28 14.48 12.82 0.77 11.28 14.36
9 to 11 years 13.28 0.84 11.6 14.96 13.1 0.78 11.54 14.66
12 to 14 years 14.14 1.08 11.98 16.3 13.29 1 11.29 15.29
15 to 19 years 15.07 1.03 13.01 17.13 13.15 1 11.15 15.15
Hematocrit, percent
1 to 2 years 36 2 32 40 36 2 32 40
3 to 5 years 37 2 33 41 37 2 33 41
6 to 8 years 38 2 34 42 38 2 34 42
9 to 11 years 39 2 35 43 39 2 35 43
12 to 14 years 42 3 36 48 40 3 34 46
15 to 19 years 45 3 39 51 39 3 33 45
Red blood cells, 10 12 cells per liter
1 to 2 years 4.55 0.34 3.87 5.23 4.5 0.34 3.82 5.18
3 to 5 years 4.51 0.34 3.83 5.19 4.49 0.32 3.85 5.13
6 to 8 years 4.6 0.29 4.02 5.18 4.56 0.31 3.94 5.18
9 to 11 years 4.71 0.32 4.07 5.35 4.62 0.3 4.02 5.22
12 to 14 years 4.93 0.39 4.15 5.71 4.59 0.32 3.95 5.23
15 to 19 years 5.06 0.37 4.32 5.8 4.47 0.35 3.77 5.17
Mean corpuscular volume (femtoliters)
1 to 2 years 79.2 4.5 70.2 88.2 79.8 4.5 70.8 88.8
3 to 5 years 81.8 4.3 73.2 90.4 82.3 4 74.3 90.3
6 to 8 years 83.2 4 75.2 91.2 83.6 3.6 76.4 90.8
9 to 11 years 83.9 3.7 76.5 91.3 84.2 3.9 76.4 92
12 to 14 years 85.3 4 77.3 93.3 86.2 4.2 77.8 94.6
15 to 19 years 88.3 3.9 80.5 96.1 87.8 4.7 78.4 97.2
White blood cells, 10 9 cells per liter
1 to 2 years 8.74 2.53 3.68 13.8 8.66 2.41 3.84 13.48
3 to 5 years 7.68 2.26 3.16 12.2 7.9 2.12 3.66 12.14
6 to 8 years 7.45 2.02 3.41 11.49 7.63 2.1 3.43 11.83
9 to 11 years 7.01 2.07 2.87 11.15 7.2 1.98 3.24 11.16
12 to 14 years 7.02 2.07 2.88 11.16 7.3 2.06 3.18 11.42
15 to 19 years 7.15 2.11 2.93 11.37 7.58 2.18 3.22 11.94
The 95% confidence interval (+/– 2 SD) defines the normal range, and corresponds to the 2.5 th through 97.5 th percentiles.
SD: standard deviation; 95% CI: 95 percent confidence interval.

* Includes all race/ethnic groups.
¶ Hemoglobin is sometimes reported as grams/liter (g/L), in which case the values are 10 times those reported as g/dL (13.5 g/dL = 135
g/L).
Adapted from: Hollowell JG, van Assendelft OW, Gunter EW, et al. Hematological and iron-related analytes-reference data for persons aged 1
year and over: United States, 1988-94. Vital Health Stat 2005; 11:1.


Risk stratification and management for children with conditions predisposing to

accelerated atherosclerosis and early cardiovascular disease


FH: familial hypercholesterolemia; NAFLD: nonalcoholic fatty liver disease; PCOS: polycystic ovary syndrome; HCM: hypertrophic
cardiomyopathy; TGA: transposition of the great arteries; CVD: cardiovascular disease; BMI: body mass index; BP: blood
pressure; FG: fasting glucose; HgbA1c: hemoglobin A1c; LDL-C: low-density lipoprotein cholesterol.
* Family history of premature CVD is generally defined as heart attack, treated angina, interventions for coronary artery disease,
sudden cardiac death, or stroke in a first-degree relative (parent or sibling) before age 55 (males) or 65 (females).
¶ For details of management of hypertension, dyslipidemia, and other specific conditions listed in this algorithm, refer to separate
UpToDate content on these conditions in children.
Modified from:
1. Daniels SR, Benuck I, Christakis DA, et al. Expert panel on integrated guidelines for cardiovascular health and risk
reduction in children and adolescents: Full report, 2011. National Heart Lung and Blood Institute. Available at:
www.nhlbi.nih.gov/guidelines/cvd_ped/peds_guidelines_full.pdf.
2. Goldstein BI, Carnethon MR, Matthews KA, et al. Major depressive disorder and bipolar disorder predispose youth to
accelerated atherosclerosis and early cardiovascular disease: A scientific statement from the American Heart Association.
Circulation 2015; 132:965.
3. De Ferranti SD, Steinberger J, Ameduri R, et al. Cardiovascular risk reduction in high-risk pediatric patients: A scientific
statement from the American Heart Association. Circulation 2019; 139:e603.

Dietary treatment recommendations for children with dyslipidemia and CKD stage 5 and
kidney transplant
Serum LDL-C
Macronutrient Serum TG >150 mg/dL
>100 mg/dL
Energy If associated with excess weight, energy balance + activity recommendations

for weight loss
Dietary fat <30 percent of calories Low
Dietary cholesterol <200 mg/d
Trans fatty acids Avoid
Saturated fatty acids <7 percent of calories
Carbohydrate Low simple carbohydrate
CKD: chronic kidney disease; LDL-C: low-density lipoprotein cholesterol; TG: triglycerides.
Reproduced with permission from: National Kidney Foundation. KDOQI Clinical Practice Guideline for Nutrition in Children with CKD: 2008
update. Executive summary. Am J Kidney Dis 2009; 53:S11. Illustration used with the permission of Elsevier Inc. All rights reserved.

Dietary recommendations for children to reduce the risk of cardiovascular disease
Age Dietary recommendations
Birth to Infants should be exclusively breastfed (no supplemental formula or other foods) until age 6 months*
6
months
6 to 12 Continue breastfeeding* until at least age 12 months while gradually adding solids; transition to iron-fortified formula until 12
months months if reducing breastfeeding
Fat intake in infants less than 12 months of age should not be restricted without medical indication
Limit 100% fruit juice <4 oz/d; no sweetened beverages; encourage water
12 to Transition to reduced-fat ¶ (2% to fat-free) unflavored cow's milk Δ (see Supportive actions bullet 1)
24
Limit/avoid sugar-sweetened beverage intake; encourage water
months
Transition to table food with:
Total fat 30% of daily kcal intake based on energy requirements
Saturated fat 8 to 10% of daily intake based on energy requirements
Avoid trans fat as much as possible
Monounsaturated and polyunsaturated fat up to 20% of daily intake based on energy requirements
Cholesterol <300 mg/d
Supportive actions:
The fat content of cow's milk to introduce at age 12 to 24 months should be decided together by parents and health care
providers based on the child's growth, appetite, intake of other nutrient dense foods, intake of other sources of fat, and
potential risk for obesity and CVD
100% fruit juice (from a cup) no more than 4 oz/d
Limit sodium intake
Consider DASH-type diet rich in fruits, vegetables, whole grains, low-fat/fat-free milk and milk products; lower in sugar
2 to 10 Primary beverage: Fat-free unflavored milk

years
Limit/avoid sugar sweetened beverages; encourage water
Fat content:
Total fat 25 to 30% of daily kcal intake based on energy requirement
Limit saturated fat 8 to 10% of daily kcal intake based on energy requirements
Avoid trans fats as much as possible
Monounsaturated and polyunsaturated fat up to 20% of daily kcal intake based on energy requirements
Encourage high dietary fiber intake from foods ◊
Supportive actions:
Teach portions based on energy requirements determined by activity level, age, and gender
Encourage moderately increased energy intake during periods of rapid growth and/or regular moderate to vigorous
physical activity
Encourage dietary fiber from foods: Age plus 5 g/d ◊
Limit naturally sweetened juice (no added sugar) to 4 oz/d
Limit sodium intake
Support DASH-style eating plan
11 to Primary beverage: Fat-free unflavored milk

21
Limit/avoid sugar sweetened beverages; encourage water
years
Fat content:
Total fat 25 to 30% of daily kcal intake based on energy requirements
Saturated fat 8 to 10% of daily caloric intake based on energy requirements for activity level/age/gender
Avoid trans fat as much as possible
Monounsaturated and polyunsaturated fat up to 20% Grade D of daily caloric intake based on energy requirements for
activity level/age/gender
Encourage high dietary fiber intake from foods ◊
Supportive actions:
Teach portions based on energy requirements determined by activity level, age, and gender

Encourage moderately increased energy intake during periods of rapid growth and/or regular moderate to vigorous
physical activity
Advocate dietary fiber: Goal of 14 g/1000 kcal ◊
Limit naturally sweetened juice (no added sugar) to 4 to 6 oz/d
Limit sodium intake
Encourage healthy eating habits: Breakfast every day, eating meals as a family, limiting fast food meals
Support DASH-style eating plan
* Infants that cannot be fed directly at the breast should be fed expressed milk. Infants for whom expressed milk is not available should be
fed iron-fortified infant formula.
¶ Toddlers 12 to 24 months of age with a family history of obesity, heart disease, or high cholesterol should discuss transition to reduced-fat
milk with pediatric care provider after 12 months of age.
Δ Continued breastfeeding is still appropriate and nutritionally superior to cow's milk. Milk reduced in fat should be used only in the context of
an overall diet that supplies 30% of calories from fat.
◊ Naturally fiber-rich foods are recommended (fruits, vegetables, and whole grains); fiber supplements are not advised. Limit refined
carbohydrates (sugars, white rice, and white bread).
Modified from: Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents: Summary
Report. Available at: https://www.nhlbi.nih.gov/node/80139 (Accessed January 3, 2012).

Equations to estimate energy requirements for children with chronic kidney disease at healthy
weights
Estimated energy requirement (EER) (kcal/day) = total energy expenditure + energy

Age
deposition
0 to 3 months EER = [89 x weight (kg) - 100] + 175
4 to 6 months EER = [89 x weight (kg) - 100] + 56
7 to 12 EER = [89 x weight (kg) - 100] + 22

months
13 to 35 EER = [89 x weight (kg) - 100] + 20

months
3 to 8 years Boys: EER = 88.5 - 61.9 x age (years) + PA x [26.7 x weight (kg) + 903 x height (m)] + 20
Girls: EER = 135.3 - 30.8 x age (years) + PA x [10 x weight (kg) + 934 x height (m)] + 20
9 to 18 years Boys: EER = 88.5 - 61.9 x age (years) + PA x [26.7 x weight (kg) + 903 x height (m)] + 25
Girls: EER = 135.3 - 30.8 x age (years) + PA x [10 x weight (kg) + 934 x height (m)] + 25
CKD: chronic kidney disease; PA: physical activity coefficient.

Recommended dietary protein intake in children with chronic kidney disease*
Dietary reference intake (DRI)
Recommended for Recommended for

Age CKD stage 3 CKD stages 4 or 5
Recommended for Recommended for
DRI (g/kg/day) (g/kg/day) (100 (g/kg/day) (100
HD (g/kg/day) ¶ PD (g/kg/day) Δ
to 140 percent to 120 percent
DRI) DRI)
0 to 6 months 1.5 1.5 to 2.1 1.5 to 1.8 1.6 1.8
7 to 12 months 1.2 1.2 to 1.7 1.2 to 1.5 1.3 1.5
1 to 3 years 1.05 1.05 to 1.5 1.05 to 1.25 1.15 1.3
4 to 13 years 0.95 0.95 to 1.35 0.95 to 1.15 1.05 1.1
14 to 18 years 0.85 0.85 to 1.2 0.85 to 1.05 0.95 1
CKD: chronic kidney disease; HD: hemodialysis; PD: peritoneal dialysis.

* Children with chronic kidney disease stages 3 to 5.
¶ DRI + 0.1 g/kg/day to compensate for dialytic losses.
Δ DRI + 0.15 to 0.3 g/kg/day depending on patient age to compensate for peritoneal losses.

Dietary reference intake (DRI) for water-soluble vitamins
Pantothenic
Life Thiamine Riboflavin Niacin Vitamin B6 Biotin Vitamin C
acid
stage (mg/day) (mg/day) (mg/day)* (mg/day) (mcg/day) (mg/day)
(mg/day)
group
RDA/AI UL RDA/AI UL RDA/AI UL RDA/AI UL RDA/AI UL RDA/AI UL RDA/AI UL
Infants
0 to 6 0.2 ¶ ND 0.3 ¶ ND 2¶ ND 1.7 ¶ ND 0.1 ¶ ND 5¶ ND 40 ¶ ND

months
7 to 12 0.3 ¶ ND 0.4 ¶ ND 4¶ ND 1.8 ¶ ND 0.3 ¶ ND 6¶ ND 50 ¶ ND

months
Children
1 to 3 0.5 ND 0.5 ND 6 10 2¶ ND 0.5 30 8¶ ND 15 400

years
4 to 8 0.6 ND 0.6 ND 8 15 3¶ ND 0.6 40 12 ¶ ND 25 650

years
Males
9 to 13 0.9 ND 0.9 ND 12 20 4¶ ND 1 60 20 ¶ ND 45 1200

years
14 to 1.2 ND 1.3 ND 16 30 5¶ ND 1.3 80 25 ¶ ND 75 1800

18
years
19 to 1.2 ND 1.3 ND 16 35 5¶ ND 1.3 100 30 ¶ ND 90 2000

30
years
31 to 1.2 ND 1.3 ND 16 35 5¶ ND 1.3 100 30 ¶ ND 90 2000

50
years
51 to 1.2 ND RDA ND 16 35 5¶ ND 1.7 100 30 ¶ ND 90 2000

70
years
>70 1.2 ND 1.3 ND 16 35 5¶ ND 1.7 100 30 ¶ ND 90 2000

years
Females
9 to 13 0.9 ND 0.9 ND 12 20 4¶ ND 1 60 20 ¶ ND 45 1200

years
14 to 1 ND 1 ND 14 30 5¶ ND 1.2 80 25 ¶ ND 65 1800
18
years
19 to 1.1 ND 1.1 ND 14 35 5¶ ND 1.3 100 30 ¶ ND 75 2000

30
years
31 to 1.1 ND 1.1 ND 14 35 5¶ ND 1.3 100 30 ¶ ND 75 2000

50
years
51 to 1.1 ND 1.1 ND 14 35 5¶ ND 1.5 100 30 ¶ ND 75 2000

70
years
>70 1.1 ND 1.1 ND 14 35 5¶ ND 1.5 100 30 ¶ ND 75 2000

years
Pregnancy
14 to 1.4 ND 1.4 ND 18 30 6¶ ND 1.9 80 30 ¶ ND 80 1800

18
years
19 to 1.4 ND 1.4 ND 18 35 6¶ ND 1.9 100 30 ¶ ND 85 2000

30
years
31 to 1.4 ND 1.4 ND 18 35 6¶ ND 1.9 100 30 ¶ ND 85 2000

50
years
Lactation
14 to 1.4 ND 1.6 ND 17 30 7¶ ND 2 80 35 ¶ ND 115 1800

18
years
19 to 1.4 ND 1.6 ND 17 35 7¶ ND 2 100 35 ¶ ND 120 2000

30
years
31 to 1.4 ND 1.6 ND 17 35 7¶ ND 2 100 35 ¶ ND 120 2000

50
years
Dietary reference intakes (DRIs) include the following measures describing optimal nutrient intake:
Recommended dietary allowance (RDA) – The level of dietary intake that is sufficient to meet the daily nutrient requirements
of 97% of the individuals in a specific life stage group.
Adequate intake (AI) – An approximation of the average nutrient intake that sustains a defined nutritional state, based on
observed or experimentally determined values in a defined population.
Upper tolerable level (UL) – The maximum level of daily nutrient intake that is likely to pose no risk of adverse health effects in
almost all individuals in the specified life stage or gender group.
RDAs and AIs may both be used as goals for individual intake. The AI is used when there are insufficient data to determine the RDA
for a given nutrient.
* Niacin is dosed as niacin equivalents (NE), where 1 mg niacin = 60 mg of tryptophan. Infants 0 to 6 months: only preformed niacin (not
NE).
¶ As AI.
Dietary Reference Intakes: The Essential Guide to Nutrient Requirements. Otten JJ, Hellwig JP, Meyers LD (Eds), The National Academies
Press, Washington, DC 2006. pp.530-541. Reprinted with permission from the National Academies Press, Copyright © 2006, National
Academy of Sciences.
Sources: Dietary reference intakes for Thiamin, Riboflavin, Niacin, Vitamin B 6 , Folate, Vitamin B 12 , Panthothenic acid, Biotin, and Choline
(1998); Dietary reference Intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids (2000). These reports may be accessed via
www.nap.edu.

Dietary reference intakes for fat-soluble vitamins
Adverse effects of
Nutrient Age group RDA*/AI ¶ UL Δ
excess
Vitamin A
1 mcg retinol activity Micrograms daily Micrograms daily Ataxia, alopecia,

equivalent = 3.3 unit hyperlipidemia,
Infants
vitamin A hepatotoxicity, bone and
0 to 6 months 400 ¶ 600
muscle pain; teratogenic
7 to 12 months 500 ¶ 600
Children
1 to 3 years 300 600
4 to 8 years 400 900
Males
9 to 13 years 600 1700
14 to 18 years 900 2800
≥19 years 900 3000
Females
9 to 13 years 600 1700
14 to 18 years 700 2800
≥19 years 700 3000
Pregnancy
<18 years 750 2800
≥19 years 770 3000
Lactation
<18 years 1200 2800
≥19 years 1300 3000
Vitamin D
(calciferol) Micrograms daily Micrograms daily Hypercalcemia,

1 mcg calciferol = 40 hypercalciuria,
Infants
int. unit polydipsia, polyuria,
0 to 12 months 10 (400 int. unit) ¶ 0 to 6 months: 25 (1000
confusion, anorexia,
int. unit)
vomiting, bone
6 to 12 months: 37.5 (1500 demineralization
int. unit)
Children and adolescents

1 to 18 years 15 (600 int. unit) 1 to 3 years: 62.5 (2500
int. unit)
4 to 8 years: 75 (3000 int.
unit)
9 to 18 years: 100 (4000
int. unit)
Males and females (including pregnancy and lactation)

19 to 50 years 15 (600 int. unit) 100 (4000 int. unit)
50 to 70 years 15 100
>70 years 20 (800 int. unit) 100
Vitamin E
(alpha-tocopherol) Milligrams daily Milligrams daily Increased risk of

1 mg = 1.47 int. unit bleeding; possibly
Infants
"natural source" increased risk of
0 to 6 months 4¶ ND
vitamin E or 2.2 int. necrotizing enterocolitis
7 to 12 months 5¶ ND in infants
unit synthetic vitamin
E Children
1 to 3 years 6 200
4 to 8 years 7 300
Males and females (including pregnancy)

9 to 13 years 11 600

14 to 18 years 15 800
>18 years 15 1000
Lactation
≤18 years 19 800
>19 years 19 1000
Vitamin K
Micrograms daily Micrograms daily No adverse effects

associated with vitamin
Infants
K consumption from
0 to 6 months 2¶ ND
food or supplements
7 to 12 months 2.5 ¶ ND have been reported;
Children however, data are
limited
1 to 3 years 30 ¶ ND
Males
>19 years 120 ¶ ND
Females (including pregnancy and lactation)

>19 years 90 ¶ ND
Vitamin A doses given as RAE. 1 RAE = 1 mcg retinol, 12 mcg beta-carotene, 14 mcg alpha-carotene, or 24 mcg beta-cryptoxanthin.
RDA: recommended dietary allowance; AI: adequate intake; UL: upper tolerable level; int. unit: international units; ND: not determined;
RAE: retinol activity equivalents.
* Values in this column represent the RDA unless otherwise indicated. The RDA is the level of dietary intake that is sufficient to meet the daily
nutrient requirements of 97% of the individuals in a specific life stage group.
¶ These values represent an AI. The AI represents an approximation of the average nutrient intake that sustains a defined nutritional state,
based on observed or experimentally determined values in a defined population.
Δ The UL is the maximum level of daily nutrient intake that is likely to pose no risk of adverse health effects in almost all individuals in the
specified life stage or gender group.
Dietary Reference Intakes: The Essential Guide to Nutrient Requirements. Otten JJ, Hellwig JP, Meyers LD (Eds), The National Academies
Press, Washington, DC 2006. pp.530-541. Modified with permission from the National Academies Press, Copyright © 2006, National Academy
of Sciences.
Sources: Dietary reference intakes for Thiamin, Riboflavin, Niacin, Vitamin B 6 , Folate, Vitamin B 12 , Panthothenic acid, Biotin, and Choline
(1998); Dietary reference intakes for Vitamin C, Vitamin E, Selenium, and Carotenoids (2000); Dietary Reference Intake reports of the Food
and Nutrition Board, Institute of Medicine (2010). These reports may be accessed via www.nap.edu.

Contributor Disclosures
Tarak Srivastava, MD Grant / Cercetare / Asistență clinică: Retrofină [FSGS (RE-021)]; Bristol-Myers Squibb [abatacept].
Consiliere / Consiliere consultativă: Alnylam (ARNA interference therapeutics). Bradley A Warady, MD Grant / Cercetare /
Asistență clinică: Baxter [Dializă peritoneală (soluție și echipament de dializă peritoneală)]. Consiliere / Consiliere consultativă:
Amgen [Anemie, oase / minerale (ASE, Cinacalcet)]; Roche [Anemia (Mircera)]; Relypsa [Hipercalemie (Patiromer)]; Akebia
[Anemia (Vadadustat) și metabolismul fierului (citrat feric)]; Bayer [Boala renală cronică (finerenonă)]. Tej K Mattoo, MD,
DCH, FRCP Consultant / Advisory Board: Kite Medical Limited [reflux vesicoureteral (Bioimpedance)]. Melanie S Kim, MD
Nimic de dezvăluit
Dezvăluirile colaboratorilor sunt analizate pentru conflictele de interese de către grupul editorial. Când sunt găsite, acestea
sunt abordate prin verificare printr-un proces de revizuire pe mai multe niveluri și prin cerințe pentru referințele care trebuie
furnizate pentru a susține conținutul. Este necesar un conținut corespunzător referit de toți autorii și trebuie să se conformeze
standardelor de dovezi UpToDate.
Politica de conflict de interese

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2020 Overview of the management of chronic kidney disease in children - UpToDate

Reimprimare oficială de la UpToDate ®

Prezentare generală a managementului bolilor renale cronice la

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anomalii patologice detectate de histologie sau deduse prin imagistică.

● G1 - Normal GFR (≥90 ml / min per 1,73 m 2 )

● Tratează disfuncția renală reversibilă

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REVERSIBLE KIDNEY DYSFUNCTION

● Administration of nephrotoxic drugs – Common nephrotoxic drugs include nonsteroidal anti-inflammatory

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SLOWING CHRONIC KIDNEY DISEASE PROGRESSION

CHRONIC KIDNEY DISEASE COMPLICATIONS

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Sodium and intravascular volume

Management to prevent hyperkalemia in children with CKD consists of the following:

● Low potassium diet.

● Administration of a loop diuretic (eg, furosemide) to increase urinary potassium loss.

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● There was no difference in adverse events between the two groups.

We use the following target BP goals for office measurements:

● In adolescents, we use a target BP of ≤120/80 mmHg.

● To evaluate for the presence of masked hypertension

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Therapeutic interventions — Therapy includes both nonpharmacologic and pharmacologic interventions:

● Red blood cell indices

● Levels below 10 and 11 g/dL:

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● Levels above 12 g/dL:

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● Infection or inflammation (see "Inflammation in renal insufficiency")

● Chronic blood loss (see "Approach to the child with anemia")

● Aluminum toxicity (see "Aluminum toxicity in chronic kidney disease")

● Hemolysis (see "Overview of hemolytic anemias in children")

● Carnitine deficiency (rare)

● Copper deficiency (rare)

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• CKD stages G2 to G5: From 0.5 to 3 months

• Patients receiving dialysis: From 0.5 to 2 months

● >3 years of age:

• CKD stage G2: From 6 to 12 months

• CKD stage G3: Every 6 months

• CKD stage G4 and G5: From 3 to 4 months

The following parameters are measured:

● Dietary intake (three-day diet record or three 24-hour dietary recalls)

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● Correction of anemia; an improved Hb (hematocrit) is believed to facilitate increased interaction between

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END-STAGE KIDNEY DISEASE

● Poor total calorie intake resulting in failure to thrive

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SOCIETY GUIDELINE LINKS

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INFORMATION FOR PATIENTS

SUMMARY AND RECOMMENDATIONS

Reversing kidney dysfunction and slowing CKD progression

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