Seminar presentation on AKI and CKD in pediatrics

Presentation out line(AKI &CKD)
Definition
Epidemiology
Aetiology
Pathogenesis
Pathophysiology
Clinical features
Differential diagnosis
Diagnostic modalities
Medical and/or surgical management
Evidence based nursing interventionsseptember 22/2016 2

Seminar objective
At the end of this session,we will be ….
Define and Identify the cause of AKI and CKD
Explain the clinical feature of AKI and CKD
Identify the diagnostic modality of renal failure
Describe the treatment option for renal failure
and ESRD
Apply evidence based nursing intervention
september 22/2016 3

Acute Kidney Injury
september 22/2016 8

Definition
 It is a Rapid deteriotion of renal function resulting in
retention of nitrogenous wastes and inability of kidney to
regulate fluid and electrolyte homeostasis. Nelson 20 ed
september 22/2016 9

pRIFLE, AKIN, and KDIGO
• AKI incidences across the cohort according to pRIFLE,
AKIN, and KDIGO were 51.1%, 37.3%, and
40.3%.Mortality was higher among patients with AKI
across all definitions (pRIFLE, 2.3%; AKIN, 2.7%;
KDIGO, 2.5%;P,0.001 versus no AKI [0.8%–
1.0%](Scott M. Sutherland et.al,2015).
• Despite the above definition criteria Research has
identified improved biomarkers of acute kidney injury
(AKI). Cystatin C (CysC) is a better glomerular
filtration rate marker than serum creatinine (SCr) and
may improve AKI definition (Zappitelli et al,2015)
september 22/2016 10

Epidemiology of AKI in world
A systematic review (2004–2012) of large cohort
studies was conducted to estimate the world
incidence of AKI and its stages.“Among the 154
studies (n=3,585,911) that adopted a KDIGO-
equivalent AKI definition, the pooled incidence rates
of AKI were 21.6% in adults (95% confidence
interval [95% CI], 19.3 to 24.1) and 33.7% in
children (95% CI, 26.9 to 41.3). The pooled AKI-
associated mortality rates were 23.9% in adults (95%
CI, 22.1 to 25.7) and 13.8% in children (95% CI, 8.8
to 21.0)”. (Paweena S.et.al,2013).

World Incidence of AKI: A Meta-Analysis
Paweena Susantitaphong,*†‡ Dinna N. Cruz,§ Jorge Cerda,‖ Maher Abulfaraj,* Fahad Alqahtani,* Ioannis
Koulouridis,*† and Bertrand L. Jaber
Background and objectives
The burden of AKI around the globe has not been systematically examined.
Design, setting, participants, & measurements
A systematic review (2004–2012) of large cohort studies was conducted to estimate the world incidence
of AKI and its stages of severity and associated mortality, and to describe geographic variations
according to countries, regions, and their economies. AKI definitions were reclassified according to the
Kidney Disease Improving Global Outcomes (KDIGO) staging system. Random-effects model meta-
analyses and meta-regressions were used to generate summary estimates and explore sources of
heterogeneity.
Results
There were 312 studies identified (n=49,147,878) , primarily in hospital settings. Most studies originated
from North America, Northern Europe, and Eastern Asia, from high-income countries, and from nations
that spent ≥5% of the gross domestic product on total health expenditure. Among the 154 studies
(n=3,585,911) that adopted a KDIGO-equivalent AKI definition, the pooled incidence rates of AKI were
21.6% in adults (95% confidence interval [95% CI], 19.3 to 24.1) and 33.7% in children (95% CI, 26.9 to
41.3). The pooled AKI-associated mortality rates were 23.9% in adults (95% CI, 22.1 to 25.7) and 13.8%
in children (95% CI, 8.8 to 21.0). The AKI-associated mortality rate declined over time, and was inversely
related to income of countries and percentage of gross domestic product spent on total health
expenditure.
Conclusions
Using the KDIGO definition, 1 in 5 adults and 1 in 3 children worldwide experience AKI during a hospital
episode of care. This analysis provides a platform to raise awareness of AKI with the public, government

Epidemiology in developing country
• According to J. Prakash et al.,2013.“We studied 2405
(1375 male and 1030 female) cases of AKI in the age
range 1–95 (mean: 40.32) years. The incidence of
CAAKI 4.14 per1000
• In Ethiopia, Case records of 30 pediatric patients
with the diagnosis of acute renal failure (ARF)
admitted to Tikur Anbessa Hospital. October
2001were analyzed There were 15 females and 15
males. Three patients had GN, one child had
obstructive uropathy. Twenty-three patients had post-
diarrheal hemolytic uremic syndrome. The age ranges
b/n 0.6 years and 7 years with a median age of 2.2
years. (Shimelis D,Tadesse Y, 2004)

1.Pre renal
ETHIOLOGY
2. Intrinsic Renal
3. Post-renal

Pre-renal
vomiting, diarrhea, poor fluid intake,
fever, use of diuretics
hemorrhage
cardiac failure
liver dysfunction, or
septic shock

Intrinsic renal
I. Renal Major vessel obstruction
-renal vein thrombosis , renal arterial obstruction, hemolytic uremic
syndrome , HSP , polyarteritis and other vasculitis.
II. Glomerular
- Acute glomerulonephritis ( post streptococcal , other infections ).
III. Acute tubulointerstitial nephritis
IV. Acute tubular necrosis
- Prolongation of pre-renal insult , intravascular hemolysis , sepsis ,
nephrotoxic agents , multiorgan failure , snakebite etc.
Cited by Up to date 21.2september 22/2016 18

Post renal
 Posterior urethral valves
Ureteropelvic junction obstruction
Ureterovesicular junction obstruction
Ureterocele
 Tumor
 Urolithiasis
Hemorrhagic cystitis
Neurogenic bladder
Cited by Up to date 21.2

Pathogenesis
Prerenal AKI, also called prerenal azotemia, is
characterized by
• diminished effective circulating arterial volume, which
leads to inadequate renal perfusion and a decreased
GFR. Evidence of kidney damage is absent.
• If the underlying cause of the renal hypoperfusion is
reversed promptly, renal function returns to normal. If
hypo-perfusion is sustained, intrinsic renal parenchymal
damage can develop

Cont…d
• Among pre renal cause of AKI Sepsis has long
been recognized as a foremost precipitant of AKI.
Sepsis-associated AKI (SA-AKI) portends a high
burden of morbidity and mortality in both children
and adults with critical illness .
• Sepsis associated-AKI poses significant clinical
challenges for clinicians( Alobaidi et al. 2015
January ).

Intrinsic renal AKI
It is characterized by:-renal parenchymal damage,
including sustained hypoperfusion and ischemia.
• Severe and prolonged ischemic/hypoxic injury and
nephrotoxic insult lead to acute tubular necrosis
(ATN), seen most often in critically ill infants and
children
• According to basile et.al,2014. The primary causes of
AKI include ischemia, hypoxia or nephrotoxicity. An
underlying feature is a rapid decline in GFR usually
associated with decreases in renal blood flow.

Cont….intrinsic AKI
 Tumor lysis syndrome is a specific form of AKI related
to spontaneous or chemotherapy-induced cell lysis in
patients with lymphoproliferative malignancies. This
disorder is primarily caused by obstruction of the tubules
by uric acid crystals.
 Acute interstitial nephritis is another common cause of
AKI and is usually a result of a hypersensitivity reaction
to a therapeutic agent or various infectious agents

pathophysiology

Postrenal AKI
 blockage in the urinary tract may cause urine to build up in one
or both kidneys. Over time, this fluid buildup can prevent the
normal flow of urine out of the kidney. Conditions that may lead
to postrenal acute kidney injury
 It includes a variety of disorders characterized by obstruction
of the urinary tract.
 In neonates and infants, congenital conditions, such as posterior
urethral valves and bilateral Ureteropelvic junction obstruction,
account for the majority of cases of AKI.

Clinical presentation
Pre renal
There may be history of volume loss from
vomiting, diarrhea, or blood loss and may
present with dehydration , hypotension ,
tachycardia , pallor , and decreased urine
output.

Renal
 Hematuria, edema, and hypertension indicates a
glomerular etiology for AKI.
Dysentery, petechiae and pallor- HUS
Presence of rash, arthritis might suggest SLE
History of prolong hypotension or with exposure
to nephrotoxic medication most likely have ATN.
Allergic interstitial nephritis should be suspected
with fevers, rash, arthralgia, and exposure to
certain medications.

Post renal
• History of interrupted urinary stream and
palpable bladder or kidney suggest obstructive
uropathy.
• Abdominal colic hematuria and dysuria suggest
urinary tract calculi.

Diagnosis
History and
Physical examination:-Obtaining a thorough physical
examination is extremely important when collecting evidence about the
etiology of AKI.
Skin :- Palpable purpura - Systemic vasculitis
Maculo papular rash - Allergic interstitial nephritis
Eye :- Evidence of uveitis may indicate interstitial nephritis
and necrotizing vasculitis.
Ear :- Hearing loss - Alport disease and amino glycoside toxicity
Mucosal or cartilaginous ulcerations – Wegener granulomatosis.
Pulmonary system :- Respiratory rate , pattern
On Auscultation of lungs crepitations

Cont..d
Cardiovascular examination may reveal the following:
 Murmurs - Endocarditis
 Pericardial friction rub - Uremic pericarditis
 Increased jugulovenous distention, S3 - Heart failure
Abdomen
 Abdominal or costovertebral angle tenderness - Nephrolithiasis,
papillary necrosis, renal artery thrombosis, renal vein
thrombosis
 distended bladder – Urinary obstruction

Laboratory investigation
Blood urea and S. creatinine level
Serum electrolyte and C3 level
Urinary indices may be useful in differentiating
prerenal AKI from intrinsic AKI.
Ultrasound - evaluates renal size, able to detect
masses, obstruction, stones
Renal biopsy - Patient in whom the etiology is
not identified
Clin J Am Soc Nephrol. 2014 Feb 7

• Clin J Am Soc Nephrol. 2014 Feb 7; 9(2): 382–394.
• Published online 2013 Nov 14. doi: 10.2215/CJN.04840513
• PMCID: PMC3913238
• Renal Relevant Radiology: Use of Ultrasonography in Patients with AKI
• Sarah Faubel,* Nayana U. Patel,† Mark E. Lockhart,‡ and Melissa A.
Cadnapaphornchai§
• Author information ► Copyright and License information ►
• This article has been cited by other articles in PMC.
• Go to:
• Summary
• As judged by the American College of Radiology Appropriateness Criteria, renal
Doppler ultrasonography is the most appropriate imaging test in the evaluation of
AKI and has the highest level of recommendation. Unfortunately, nephrologists are
rarely specifically trained in Ultrasonography technique and interpretation, and
important clinical information obtained from renal ultrasonography may not be
appreciated. In this review, the strengths and limitations of grayscale
ultrasonography in the evaluation of patients with AKI will be discussed with
attention to its use for (1) assessment of intrinsic causes of AKI, (2) distinguishing
acute from chronic kidney diseases, and (3) detection of obstruction. The use of
Doppler imaging and the resistive index in patients with AKI will be reviewed with
attention to its use for (1) predicting the development of AKI, (2) predicting the
prognosis of AKI, and (3) distinguishing prerenal azotemia from intrinsic AKI. Finally,
pediatric considerations in the use of ultrasonography in AKI will be reviewed.

DDX for AKI
Chronic Kidney Disease
Acute Tubular Necrosis
Azotemia
Hemolytic Uremic Syndrome in Emergency
Hyperkalemia
Hypertensive Emergencies
Lupus nephritis

Complication of AKI
Metabolic
• Hyponatremia
• Hyperkalemia
• Hypocalcemia, hyperphosphatemia
• Hyperuricamia
Pediatrics lecture note

Con..d
Metabolic acidosis
Cardiovascular
Pulmonary edema
CHF
Hypertension
Arrhythmias
Pericarditis
Neurologic :- Coma and Seizures
Hematologic :-Anemia and Coagulopathies & bleeding
diathesis E.T.C
Pediatrics lecture note

TREATMENT
Medical Management
• In infants and children with urinary tract obstruction,
such as in a newborn with suspected posterior ureteral
valves, a bladder catheter should be placed immediately
to ensure adequate drainage of the urinary tract.
• however, precautions to prevent iatrogenic infection
should be

Maintain fluid
• Determination of the volume status is of critical
importance when initially evaluating a patient
with AKI.
• If there is no evidence of volume overload or
cardiac failure, intravascular volume should be
expanded by intravenous administration of
isotonic saline, 20 mL/kg over 30 min.

Cont…d
• Determination of the central venous pressure may be helpful
if adequacy of the blood volume is difficult to determine.
• After volume resuscitation, hypovolemic patients generally
void within 2 hr; failure to do so suggests intrinsic or
postrenal AKI.
• Hypotension caused by sepsis requires vigorous fluid
resuscitation followed by a continuous infusion of nor -
epinephrine. Nelson 20 edseptember 22/2016 40

Cont…d
• According to KDIGO Aki Guideline 2012, several
diuretics(Furosemide and mannitol ) have
potentially Reno-protective effects that might prevent
development of AKI and hasten its recovery.
However, diuretics can also be harmful, by reducing
the circulating volume excessively and adding a
prerenal insult, worsening established AKI.
Therefore,
1. We recommend not using diuretics to prevent AKI.
2. We suggest not using diuretics to treat AKI, except in
the management of volume overload.

Prowle, J. R. et al. (2014)september 22/2016 42

Fenoldopam vs. low dose Dopamin
• A comparison between fenoldopam and low-dose dopamine in early renal dysfunction of critically ill patients*
• Brienza, Nicola MD, PhD; Malcangi, Vincenzo MD; Dalfino, Lidia MD; Trerotoli, Paolo MD; Guagliardi, Clementina MD;
Bortone, Dora MD; Faconda, Giuseppe MD; Ribezzi, Mario MD; Ancona, Giovanni MD; Bruno, Francesco MD; Fiore,
Tommaso MD
• Abstract
• Objective: Fenoldopam mesylate is a selective dopamine-1 agonist, with no effect on dopamine-2 and α1 receptors,
producing a selective renal vasodilation. This may favor the kidney oxygen supply/demand ratio and prevent acute renal
failure. The aim of the study was to investigate if fenoldopam can provide greater benefit than low-dose dopamine in early
renal dysfunction of critically ill patients.
• Design: Prospective, multiple-center, randomized, controlled trial.
• Setting: University and city hospital intensive care units.
• Patients: One hundred adult critically ill patients with early renal dysfunction (intensive care unit stay <1 wk, hemodynamic
stability, and urine output ≤0.5 mL/kg over a 6-hr period and/or serum creatinine concentration ≥1.5 mg/dL and ≤ 3.5
mg/dL).
• Interventions: Patients were randomized to receive 2 μg/kg/min dopamine (group D) or 0.1 μg/kg/min fenoldopam
mesylate (group F). Drugs were administered as continuous infusion over a 4-day period.
• Measurements and Main Results: Systemic hemodynamic and renal function variables were recorded daily. The two groups
were well matched at enrollment for illness severity and hemodynamic and renal dysfunction. No differences in heart rate
or systolic, diastolic, or mean arterial pressure were observed between groups. Fenoldopam produced a more significant
reduction in creatinine values compared with dopamine after 2, 3, and 4 days of infusion (change from baseline at time 2,
−0.32 vs. −0.03 mg/dL, p = .047; at time 3, −0.45 vs. −0.09 mg/dL, p = .047; and at time 4, −.041 vs. −0.09 mg/dL, p = .02, in
groups F and D, respectively). The maximum decrease in creatinine compared with baseline was significantly greater in
group F than group D (−0.53 ± 0.47 vs. −0.34 ± 0.38 mg/dL, p = .027). Moreover, 66% of patients in group F had a creatinine
decrease >10% of the baseline value at the end of infusion, compared with only 46% in dopamine group (chi-square = 4.06,
p = .04). Total urinary output during drug infusion was not significantly different between groups. After 1 day, urinary
output was lower in group F compared with group D (p < .05).
• Conclusions: In critically ill patients, a continuous infusion of fenoldopam at 0.1 μg/kg/min does not cause any clinically
significant hemodynamic impairment and improves renal function compared with renal dose dopamine. In the setting of
acute early renal dysfunction, before severe renal failure has occurred, the attempt to reverse renal hypoperfusion with
fenoldopam is more effective than with low-dose dopamine.

Treatment of hyperkalemia
 In AKI, rapid development of hyperkalemia (> 6 mEq/L)
can lead to cardiac arrhythmia, cardiac arrest, and death
 The earliest electrocardiographic change seen in patients
with developing hyperkalemia is the appearance of
peaked T waves.
 This may be followed by widening of the QRS intervals,
ST segment depression, ventricular arrhythmias, and
cardiac arrest. Cited by up to date 21.2

Treatment of hyperkalemia
When the serum potassium value rises to >6.0
mEq/L. Exogenous sources of potassium (dietary,
intravenous fluids, total parenteral nutrition) should
be eliminated.
Sodium polystyrene sulfonate resin (Kayexalate), 1
g/kg, should be given orally or by retention enema.
This resin exchanges sodium for potassium and can
take several hr to take effect.september 22/2016 45

Cont….d
A single dose of 1 g/kg can be expected to lower the
serum potassium level by about 1 mEq/L. Resin
therapy may be repeated every 2 hr.
More severe elevations in serum potassium (>7
mEq/L), especially if accompanied by
electrocardiographic changes, require emergency
measures in addition to Kayexalate.

Treatment of metabolic acidosis
Mild metabolic acidosis is common in AKI. but, it
rarely requires treatment.
• If acidosis is severe, The acidosis should be corrected
partially by the intravenous route, generally giving
enough bicarbonate to raise the arterial pH to 7.20.
The remainder of the correction may be
accomplished by oral administration of sodium
bicarbonate.

Treatment of hypocalcemia
• It is primarily treated by lowering the serum phosphorus
level. Calcium should not be given intravenously, except in
cases of tetany, to avoid deposition of calcium salts into tissues.
• Patients should be instructed to follow a low-phosphorus diet,
and phosphate binders should be orally administered to bind
any ingested phosphate and increase GI phosphate excretion.
• Low phosphate foods (white bread, crackers, cereals, rice and
pasta)
Up to date 21.2..

Treatment of hyponatremia
• It is most commonly a dilutional disturbance that
must be corrected by fluid restriction rather than
sodium chloride administration.
• Administration of hypertonic (3%) saline should be
limited to patients with symptomatic hyponatremia
or those with a serum sodium level <120 mEq/L.

Treatment hypertension
It can result from hyper reninemia associated with
the primary disease process and/or expansion of the
extracellular fluid volume and
It is most common in AKI patients with acute
glomerulonephritis or HUS.
Salt and water restriction is critical, and diuretic
administration may be useful

Cont..d
According to Wuhl E, trivelli A,et .al,2009 “Angiotensin
converting enzyme (ACE) inhibitors (enalapril) and
Angiotensin II blockers (losartan) are the antihypertensive
medications of choice in all children with proteinuria renal
disease because of their potential ability to slow the progression”.
• A short action Isradipine 0.05-0.15 mg/kg/dose, maximum dose 5
mg qid) may be administered.
• Long acting agents such as calcium channel blockers
(amlodipine, 0.1-0.6 mg/kg/24 hr QD or divided bid)

Treatment of anemia
 The anemia of AKI is generally mild (hemoglobin 9-10
g/dL) and primarily results from volume expansion
(hemodilution).
 Children with HUS, SLE, active bleeding, or prolonged
AKI can require transfusion of packed red blood cells if
their hemoglobin level falls below 7 g/dL.
 packed red blood cells (10 mL/kg) Slow (4-6 hr)
transfusion for diminishes the risk of hypervolemia
 Nelson 20 edseptember 22/2016 52

Dietary management of AKI
• Nutrition is of critical importance in children who
develop AKI. In most cases, sodium, potassium,
and phosphorus should be restricted.
• Protein intake should be moderately restricted
while maximizing caloric intake to minimize the
accumulation of nitrogenous wastes.

Nutrition
• The recommended energy provide target of 20–30
kcal/kg/day and a protein target of 1.5 g/kg/day, in the
absence of RRT. In case of RRT, an increase in protein
supply including glutamine and micronutrients are
suggested [Fiaccadori E, Parenti E,2008].
• According to KDIGO 2O12 guideline recommendations
have proposed the following protein intake depending
on the age of children presenting with AKI:
2–3 g/kg/day from 0 to 2 years,
 1.5–2 g/kg/day from 2 to 13 years,
 1.5 g/kg/day above 13 years.
september 22/2016 Thyophiline and renal dysfun

Indications for dialysis :
1. Anuria/ oliguria
2. Volume overload with evidence of hypertension and/or
pulmonary edema refractory to diuretic therapy
3. Persistent hyperkalemia
4. Severe metabolic acidosis unresponsive to medical
management
5. Uremia
6. Blood urea nitrogen >100-150 mg/dL
7. Calcium: phosphorus imbalance, with hypocalcemic tetany
that cannot be controlled by other measuresseptember 22/2016 55

Chronic Kidney Disease

Chronic kidney disease
Patient has CKD if either of the following criteria are
present:
1. Kidney damage for ≥3 mo, as defined by structural or
functional abnormalities of the kidney, with or without
decreased GFR, manifested by 1 or more of the
following features:
– Abnormalities in the composition of the blood or urine
– Abnormalities in imaging tests
– Abnormalities on kidney biopsy
2. GFR <60 mL/min/1.73 m2 for ≥3 mo, with or without the
other signs of kidney damage described above
National Kidney Foundation K/DOQI(2002)september 22/2016 57

STANDARDIZED TERMINOLOGY FOR STAGES OF
CHRONIC KIDNEY DISEASE (K/DOQI(2002)

Etiology
• Result of congenital, acquired, inherited, or
metabolic renal disease.
in children <5 yr old is
– most commonly a result of congenital abnormalities such as
renal hypoplasia, dysplasia, or obstructive uropathy
After 5 yr of age
acquired diseases (various forms of glomerulonephritis
including lupus nephritis) and inherited disorders (
Alport syndrome) predominate.

Epidemiology
• The incidence and prevalence of all stages of CKD
in children continues to increase worldwide. The
kidney replacement therapy incidence rate among
0–19 years of age rose 15 per million population in
children (Cynthia J.Wong,2012).
• According to coca et.al,2012 evaluating long-term
renal outcomes and non-renal outcomes in patients
with AKI. Patients with AKI had higher risks of
developing CKD (pooled adjusted hazard ratio 8.8,
95% CI 3.1-25.5), ESRD (pooled adjusted HR 3.1,
95% CI 1.9-5.0)september 22/2016 60

PATHOGENESIS
• In addition to progressive injury with ongoing
structural or metabolic genetic diseases, renal
injury can progress despite removal of the original
insult.
Hyper filtration injury
Proteinuria
hypertension
Hyperphosphatemia
Hyperlipidemia

Clinical Manifestations
• The clinical presentation of CKD is varied and
depends on the underlying renal disease
–Children and adolescents with CKD can
present with
–edema,
–hypertension,
–hematuria, and
–proteinuria

Cont….d
• Infants and children with congenital
disorders such as
–renal dysplasia and obstructive uropathy
can present in the neonatal period with
failure to thrive, polyuria, dehydration,
urinary tract infection, or overt renal
insufficiency

Diagnosis
On P/E:-Pallor and a sallow appearance.
– short stature and the bony abnormalities of renal
osteodystrophy (length/height-for age <3rd percentile).
– Children with CKD due to chronic glomerulonephritis
(edema, hypertension and fluid overload).
Laboratory Findings(Elevated BUN and serum
creatinine, hyperkalemia, hyponatremia, hypernatremia
Acidosis, hypocalcemia, hyperphosphatemia, and an
elevation in uric acid, hypoalbuminemia, hematuria and
proteinuria.

Differential diagnosis
Acute kidney injury Injury
Alport Syndrome
Glomerulonephritis
Diabetic Nephropathy
Good pasture Syndrome
Obstractive uropathy
Nephrolithiasis

Management
GENERAL PRINCIPLES
– Treat reversible kidney dysfunction
• Prevent or slow the progression of kidney
disease
– Treat the complications of CKD
– Identify and adequately prepare the
child/family in whom renal replacement
therapy will be required

REVERSIBLE KIDNEY
DYSFUNCTION
Prevent or treat Decreased kidney perfusion from
• Hypotension (eg, septic shock), Volume depletion from
vomiting, diarrhea, diuretic use, or bleeding, and
• the administration of drugs that lower the kidney perfusion
• Avoid Administration of nephrotoxic drugs

Blood pressure control
• volume overload glomerular disease salt-restricted
diet (2-3 g/24 hr) and can benefit from diuretic
therapy
• hydrochlorothiazide 2 mg/kg/24 hr divided bid for
CKD stages 1-3.furosemide 1-2 mg/kg/dose bid
stage 4 CKD (nelson textbook, 2015)
• According yan li et.al,2016, the combination of a CCB
and an ACEI should be a preferable antihypertensive
therapy in patients with CKD, considering their higher
effect in decreasing blood pressure

Meta-analysis
Abstract
Background: The renoprotective effect of inhibitors of renin-angiotensin system (RAS)
has been identified through placebo-controlled trials. However, the effect of calcium-
channel blockers (CCBs) on renal system is still controversial. Our current meta-
analysis includes available evidences to compare the effect of dihydropyridine CCBs
and ACEIs or ARBs on renal outcomes and mortality. We also further investigate
whether CCBs can be used in combination with inhibitors of RAS to improve the
prognosis of patients with chronic kidney disease (CKD).
Methods and results: Electronic databases were searched up to July 2012, for clinical
randomized controlled trials, assessing the effect of dihydropyridine CCBs on the
incidence of end-stage renal disease (ESRD) and all-cause mortality in contrast to
ACEIs or ARBs. Eight clinical trials were included containing 25,647 participants. ESRD
showed significantly higher frequency with CCBs therapy compared with ACEIs or
ARBs therapy, though blood pressure was decreased similarly in both groups in every
trial (OR, 1.25; 95% CI, 1.05–1.48; p = 0.01). In contrast, there was no significant
difference in the incidence of all-cause mortality between these two groups, though
ACEIs or ARBs exhibited better renoprotective effect compared to CCBs (OR, 0.96;
95% CI, 0.89–1.03; p = 0.24).
Conclusions: CCBs did not increase all-cause mortality incidence in patients with CKD
though they displayed weaker renoprotective, compared to ACEIs or ARBs therapy.
Our results suggest the combination of a CCB and an ACEI or ARB should be a
preferable antihypertensive therapy in patients with CKD, considering their higher
effect in decreasing blood pressure and fewer adverse metabolic problems caused.

Sodium and intravascular volume
dietary sodium restriction and diuretic therapy may correct the
increased water balance and prevent water retention from
recurring
adequate 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 / 2 to 3 g/day … in general/
Diuretic therapy includes either loop diuretics such as
furosemide
Some children with obstructive uropathy and/or dysplastic
kidneys have hypovolemia and hyponatremia. require ongoing
fluid and sodium replacement

cont…..treatment
hyperkalemia
Low potassium diet.
Administration of a loop diuretic
Resin therapy.
If failed do RRT
• Metabolic acidosis
–maintain the serum bicarbonate level at or
above 22 mEq/L(sodium bicarbonate )

Cont..d
• Bone deformity:-using both dietary and pharmacologic
interventions
– low-phosphorus diet
– so phosphate binders are used to enhance fecal phosphate excretion
-- Vitamin D therapy is the corner stone therapy
• According to alberz et.al 2012. “oral cholecalciferol
regimen was safe and sufficient to maintain serum
25(OH)D concentrations and prevent vitamin D
insufficiency in early CKD. Furthermore, serum PTH
improved after cholecalciferol treatment, particularly
in patients who had secondary hyperparathyroidism”.

Treatment of Anemia
Recombinant human
erythropoietin (rHuEPO)
• hemoglobin concentration
falls below 10 g/dL, at a dose
of 50-150 mg/kg/dose
subcutaneously 1-3 times
weekly.
• All patients receiving rHuEPO
therapy should be provided
with either oral or intravenous
iron supplementation(SusanM.
Koshy & Denis F. Geary 2008).

Nutrition
• Energy
– based upon the estimated energy requirement (EER) for
chronological age
• Protein
– Should be 2.5 g/kg/24 hr and should consist of proteins of
high biologic value that are metabolized primarily to usable
amino acids rather than to nitrogenous wastes.
– The proteins of highest biologic value are those of eggs and
milk, followed by meat, fish, and fowl
• Vitamins and minerals
– can become deficient in water-soluble vitamins either because
of inadequate dietary intake or dialysis lossesseptember 22/2016 76

Growth
Treatment with
rHuGH continues
until the patient
reaches the 50th
percentile for
midparental height or
achieves a final adult
height or undergoes
kidney transplantation

Immunization
• Children with CKD should receive all standard
immunizations according to the schedule used
for healthy children
• An exception must be made in withholding live
virus vaccines from children with CKD related to
glomerulonephritis, or any disease

End-Stage Renal Disease
– The state in which a patient's renal dysfunction has progressed to
the point at which homeostasis and survival can no longer be
sustained with native kidney function and maximal medical
management.
– At this point, renal replacement therapy (dialysis or
renal transplantation) becomes necessary
– It is recommended that plans for renal replacement therapy be
initiated when a child reaches stage 4 CKD

Rajit K. Basu 2011september 22/2016 80

Survival patterns of patients on
maintenance hemodialysis
Dialysis treatment
Forty-one (45.1%) deaths occurred during dialysis treatment and
21 (23.1%) of patients died within the first 90 days of starting dialysis.
Only 42.1% of them survived longer than a year.
The frequently registered causes of death were
septicemia (34.1%) and cardiovascular diseases
(29.3%). Use of catheter as vascular access was
associated with decreased short term and long term
survival (Tamiru .et al.2013 ).

Nursing Management
1. Assessing fluid status and identifying potential sources of
imbalance.
2. implementing a dietary program to ensure proper
nutritional intake
3. promoting positive feelings by encouraging increased self-
care and greater independence.
4. Provide explanations and information to the patient and
family concerning AKI, treatment options and potential
complications.
5. Provide emotional support to the patient and family
6. prepare the child/family in whom renal replacement
therapyseptember 22/2016 82

Reference
1. Scott M. Sutherland et.al. AKI in Hospitalized Children: Comparing the pRIFLE,
AKIN, and KDIG Definitions Department of Pediatrics, Stanford University and
Center for Acute Care Clin J Am Soc Nephrol 10: 554–561, April, 2015). 2015.
2. Zappitelli et al. Association of Definition of Acute Kidney Injury by Cystatin C Rise
With Biomarkers and Clinical Outcomes in Children Undergoing Cardiac Surgery JAMA
Pediatr. 2015 June 1; 169(6).
3. Paweena S.et.al, World Incidence of AKI: A Meta-Analysis Clin J Am Soc
Nephrol. 2013 Sep 6; 8(9): 1482–1493.
4. Jai Prakash1Changing epidemiology of community-acquired acute kidney injury
in developing countries: analysis of 2405 cases in 26 years from eastern IndiaClin
Kidney J (2013) 6: 150–155.
5. Shimelis D, Tadesse Y. Department of Pediatrics and Child Health, Tikur Anbessa
Hospital, Addis Ababa, Ethiopian medical journal 2004, 7-22.
6. Alobaidi et al. Sepsis-Associated Acute Kidney InjurySemin Nephrol 2015 January ;
35(1): 2.
7. Sarah Faubel et.al. Renal Relevant Radiology: Use of Ultrasonography in Patients
with AKI,Clin J Am Soc Nephrol. 2014 Feb 7; 9(2): 382–394.
8.ProwleJ et.al. Fluid management for the prevention and attenuation of acute kidney
injury Nat. Rev. Nephrol. 2014, 10, 37–47 .
9. Branza et.al.A comparison between fenoldopam and low-dose dopamine in early
renal dysfunction of critically ill patients. Crit Care Med.2006;34:707–14.
10..Wuhi E, Trivelli A,et.al.strict blood pressure control and progression of renal failure
in children .N Engl J M ed 2009;361:1639.september 22/2016 83

Cont…reference
11. Fiaccadori E, Parenti E, Maggiore U. Nutritional support in acute kidney injury. J Nephrol.
2008;21:645–56
12.KIDIGO 2012,Guideline
13. Cynthia J.Wong. CKiD (CKD in Children) Prospective Cohort Study: Am J Kidney Dis
2012;60;6.)
14.coca et.al. chronic kidney disease after acute kidney injury. epidemiological research
center,2012.
15 Hong-Jin Zhao. Effect of calcium channels blockers and inhibitors of the renin-angiotensin
system on renal outcomes and mortality in patients suffering from chronic kidney disease:
systematic review and meta-analysis,2016.
16. Alvarez et.al. High-dose cholecalciferol reduces parathyroid hormone in patients with early
chronic J Clin Nutr 2012;96:672–9.
17. Susan M. Koshy & Denis F. Geary .Anemia in children with chronic kidney disease, Pediatr
Nephrol 200823:209–219)
18 Esposito S et.al .administration in children with chronic kidney disease,2014,20:32.
19. Rajit K. Basu Acute Renal Replacement Therapy in Pediatrics, International Journal of
Nephrology ;2011,Volume 2011
20. Tamiru .et al. Survival patterns of patients on maintenance hemodialysis for end stage
renal disease in Ethiopia: BMC Nephrology 2013,14 :127
21. Nelson textbook of pediatrics 20 ed,2015
22. Up to date 21.2

Seminar presentation on AKI and CKD in pediatrics

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