Is the clinical syndrome in which sudden decreasing in 
renal function result in inability of kidney to maintain
fluid and electrolyte homeostasis, 2-3% in children, 8%
in neonatal ICU.
CRITERIA
ESTIMATED CCl
URINE OUTPUT
Risk
eCCl decrease by 25%
<0.5 mL/kg/hr for 8 hr
Injury
eCCl decrease by 50%
<0.5 mL/kg/hr for 16 hr
Failure
eCCl decrease by 75% or eCCl
<35 ml/min/1.73 m2
<0.3 mL/kg/hr for 24 hr
or anuric for 12 hr
Loss
Persistent failure >4 wk
End-stage
End-stage renal disease
(persistent failure >3 mo)
eCCl, estimated creatinine clearance;
pRIFLE, pediatric risk, injury, failure, loss
and end-stage renal
Causes
A-prerenal causes1- 
dehydration
2- 
hemorrhage
3- 
hypoalbunimia
4- heart 
failure
B- intrinsic causes , 
glomeruler diseases
1- post infectious GN

2- lupus GN, HSP,

3- HUS

4- acute tubuler necrosis 
5- RVT
C- post renal 1- posterior 
urethral valve
2- uretro-
pelvic junction obstruction
- vomiting, diarrhea 3 days
prerenal
- 6 years child with recent pharangitis+edema+HT=PSGN
- critical ill child with protracted HT and HX of exposure
to nephrotoxin
ATN
- neonate with hydronephrosis in prenatal U/S
congenital P UJ obstruction.
Physical examination
- volume status, tachycardia, dry mouth, poor peripheral
circulation,
prerenal cause
- peripheral edema, basal creptation, gallop rythem,
suggest GN, ATN
- rash +nephritis=SLE, HSP
anemia due to 1- hemolytic(SLE, 
RVT, HUS)
2- delutional
- leucopenia(SLE)
- thrombocytopenia((SLE, RVT, HUS)
- hyponatremia(delutional)
-metabolic acidosis
-BUN, S.Cre
increase
-uric acid , K+, Ph++, increase
- CA++ low
- C3 level low in(SLE, PSGN, radiation 
GN, membarenoprolefrative)
- Abs in PSGN
-GUA 1- RBC, protienurea, granuler 
cast,
internsic cause
2- WBC, WBC cast, low grade 
protienurea, RBC, tubulointerstesial
disease
Indices
Pre renal
Sp.gravity
>1.020
Ur.osmolality
>500
Ur.NA+(Mag/L)
<20
FENA+
<1
BUN/S.cre
>20
FENA+=Una X Pcre/P na X Ucre
- CXR cardiomegaly, pulmonary edema.
- Renal U/S
hydronephrosis, hydroureter, obstruction
- Renal biopsy may needed.
Intrinsic
<1.010
<350
>40
>2
<20
1- infant and children with obstruction or non ambulatory child 
bladder catheter, to collect UOP
2- fluid therapy according to volume status 
A- in case of Hypovolemia, N/S 20 CC/kg within 30 min may be 
repeted 2 or 3 times and watch the UOP in 2 hour , if no possible
of internsic or post renal.
Diuretics indicated provided that good volume status 
Frusamide 2-4 mg/kg+MANITOL 0.5g/kg , if no UOP within 30 min
, consider diuretic infution , if no UOP, consider
Dopamin
2-3Mig/kg/min with diuretic , if no UOP, stop diuretic and fluid
should be restricted.
B-in case of normal volemia consider(insensible water loss) 400 
cc/m2 /day + the fluid equal to the UOP.
C- in case of Hypervolemia insensible water loss and UOP 
should be omitted.
Type of the fluid is glucose-containing solution 10-30% as 
maintaince .
Input, output, UOP, chemistry sh be checked daily. 
3- Hyperkalemia >6mg/dl may lead to cardiac arrythemia 
(ECG=tent T wave , widing QRS, ST depression, and arrest).
Indication of withholding of K+(fluid, diet)+Resin 1g/kg orally or 
rectally by enema every 2-4 hour.
If >7mg/dl give the flowing
1- Ca.gluconate 10% 1cc/kg within 3-5min
2- NACO3 1-2cc/kg over 5-10min
3- Reguler insulin 0.1U/kg with glucose 50% 1cc/kg over 1hour.
If inspite of all these measure , still persistent hyperkalemia 
consider dialysis.
4- Acidosis if mild rarely need treatment , if sever PH <7.15 
NAHCO3 <8 with hyperkalemia need NAHCO3 infusion (desire PH
7.2, NAHCO3 12).
5- Hypocalcemia primarily treated by lowering S.PH++ , and Ca++ 
sh be not given I-V unless with tetany to ovoid Ca . deposition in
tissue, use Ca. carbonate 1-3 tab with meal.
6- Hyponatremia delutional need fluid restriction , if 
<120 or symptomatic(seizure, lethargy )need 3%NACL .
NACL in m.ag required=0.6XBwt X (125- s.NA)
7- Bleeding due to platelet dysfunction, stress, 
heparin(dialysis), need oral or I.V H2 blocker ranitidine
8- HT in GN, HUS, need salt and water restriction, 
Nefidipine 0,25-0,5mg/kg every 2-6hour(max 10mg),
B.blocker,long acting Ca.cannel blocker., if sever crisis
need NA nitropruside or Labetalol infusion.
9- Anemia mild, delutional , packed RBC, 10 cc/kg within 
4-6hour if Hb <7g/dl(better fresh)
10- nutrition NA, PH, K, should be restricted in most cases, 
protein should be moderately decrease, increase calorie
intake.
a-volume over load +evidence of HT, and /or pulmonary
edema refractory to treatment
b- persistent hyperkalemia
c- sever acidosis unresponsive to treatment
d- neurological symptoms(alter mental state , seizure)
e- BUN >100-150mg/dl or lower if rapidly rising.
f- Ca/Ph imbalance with hypocalcemia tetany .
g- inability to provide adequate nutritional intake because of
need for sever fluid restriction.
is defined as either renal injury (proteinuria) and/or a
glomerular filtration rate <60 mL/min/1.73 m2 for <3 mo
GFR (ml/min/1.73m²)= K x height(cm)/S.Cre(mg/dl)
K =0.33 for LBW infant<1year
K =0.45 for infant <1year
K =0.55 for child and adolescent female
K =0.7 for adolescent male
ml/min/1.73m²
-STAGE DESCRIPTION GFR (mL/min/1.73 m2)
Stage 1 Kidney damage with normal or increased GFR >90
Stage 2 Kidney damage with mild decrease in GFR 60–89
Stage 3 Moderate decrease in GFR 30–59
Stage 4 Severe decrease in GFR 5–29
Stage 5 Kidney failure <15 or on dialysis
End-stage renal disease (ESRD) is an administrative term in
the USA, defining all patients treated with dialysis or
kidney transplantation. Patients with ESRD are a subset of
the patients with Stage 5 CKD
1- congenital most common in <5 year of age (renal
dysplesia, obstreuctive uropathy)
2- acquired various glomeruler disease
3- inherited Alpert syndrome , both are more common
>than 5year of age
4- metabolic
cystenosis
Many factors play role
1- hyperfilteration theory
2- persistent proteiurea
3- systemic arterial renal hypertention
4- renal calcium-phosphrous deposition
5- hyperlipidemia
-acidosis
- ↑ nitrogeniuos products
- NA+ retention
- NA+ wasting
- Hyperkalemia
- Renal osteodystrophy
1- impair HCO3 absorption
2- ↓net acid excretion
↓↓ GFR
1- ↑ rennin 
2- oliqurea
1- solute diuresis
2- tubuler damage
1- ↓ GFR 
2- acidosis
3- ↑ K intake
1- impair renal production of active D3
2- hyper ph++
3- secondary hyperparathyroidism
4- inadequate caloric intake --
- Growth retardation
- Anemia
- Bleeding tendency
- Infection
- Neurological symptoms
- HT
- Pericarditis
1- renal ostiodystrophy
2- metabolic acidosis
3- anemia, 
4- growth H resistence
1- ↓ erythropioten production
2- iron, folate, B12 ↓↓
3- ↓↓ RBC survival 
1- platelet dysfunction
1- granulocyte dysfunction
2- cellular immunity dysfunction
1- uremic toxin
2- aluminum toxicity
3- HT
1- volume overload
2- excess rennin
1- HT
2- fluid over load
Hyper K+, hypoNA+, acidosis, hypoCA++,
hyperph++, hyperurecimia.
GUA protienurea
CBC, normochromic normocytic anemia
1- fluid therapy and electrolyte management
Most patient have normal NA+ and water balance 
Renal dysplesia significant NA+ loss, so we give 
benefit of higher volume , low caloric density feedung
with NA+ supplementation.
In HT, NA+ resterction, +diuretic therapy 
Hyperkalemia, treated by Resin, alkanizing agent, and 
no K+ in diet
2- Acidosis 
either Bicitra((1 mq NA+ citrate or NA+ 
Bicorbonate9680 mq equal 8mq base to maintain S.HCO3
22mq/l
3- Nutrition 
PH++, K+, NA+, should be restricted according to patient 
lab finding and fluid balance, Similac formula can be
used(low PH++)
Calorie according to age recommendation
Protein, should be 2.5g/kg/day , with high biological 
value(to soluble aminoacid rather than nitrogenious
substance)(egg, milk, meat, and fish)
Water soluble vitamin (Nephrocap), zinc and iron are 
needed, while fat soluble vitamin is not.
4- Growth
Recombinant human GH, 0,05mg/kg/day s.c to achieve 
normal height velocity for age with periodic assessment
give until
A- reach 50th centile of midparental HT
B- final adult HT
C- undergo renal transplant
5- Renal ostiodystrophy
Indicate spectrum of bone disorder seen in patient with CRF, ,
high bone turnover with secondary hyperparathyroidism and
skeletal pathological finding is a Ostitis Fibrosa Cystica , occur
when GFR <50% of normal,
↓↓ active D3 →→↓↓ in intestinal CA++
absorption→hypoCA++→↑↑parath H→↑ bone resorption →↑CA++
level
When GFR < TO 20-25% of normal , PH++ excretion decrease
→hyperph++ and lead to hypoCA++ and ↑parath H
C/F
Muscle weakness, bone pain, fracture with minor trauma
Ricketic chnges
Lab finding, ↓S.Ca,↑S.ph, ↑ AKP, normal or ↑parath H
X.rays
widing of metaphyseal space , subperiostial 
resorption.
Treatment 1- low ph diet(similac formula)
2-Ca.carbonate or acetate (ph. Binder agent), site 
effect is hypercalcemia, now we use non-ph. Binder agent
3- most important is Vit D indicated in 
A- renal ostiodystrophy with PTH >than 3 times its 
level
B- persistent hypoCa , inspite of ↓↓S.ph
Dose is 0.01-0.05Mg/kg/day
Calciterol (one α.cap or drop)
Many nephrologists recommends to maintain Ca/Ph, Ca x Po4 
less than 55 to decrease the possibility of Ca.Ph salt deposition.
6- Anemia
Desired Hb level is 11-12 g/dl
Use of Erythropoietin 50-150mg/kg/dose s.c one to 3 times
/week when Hb <10g/dl
With use of Erythropoietin , give iron oral or i.v
7- HT
Volume over load
diuretics
Excessive rennin
ACE inhibitors , Angio II blocker (Lasartan)
, effective in lowering of HT
8-Immunization
MMR, Varecella , should be given before transplantation
Influenza vaccine should be given annually.
Flow up
Hb, S.electrolyte, BUN, S.Cre, Ca, Ph, AKP, , PTH, X.rays of bo