Acute

Kidney Injury in Children • If there seems to be a discrepancy

Dr. Cabansag between the eCCL and the Urine Output,
consider the more severe criteria
OLIGURIA •
• passage of insufficient volume to maintain CLASSIFICATION of AKI
homeostasis A Pre – renal • Contributes to 55 –
• <500 ml/ 24 hrs or <1.0 ml/kg/hr in K • (-) 65 % of AKI
infants or <0.5 ml/kg/hr in children I parenc • Pre renal Azotemia
ANURIA hymal • Transient diminished
• complete cessation of urine damage ECV -> inadequate
POLYURIA • Na+ renal perfusion ->
• normal or excessive urinary output >2 conser decrease in delivery
ml/kg in the presence of acutely rising ving of O2 & energy
BUN or creatinine mode sources -> decreased
GFR
ACUTE KIDNEY INJURY • If underlying cause is
• formerly called Acute Renal Failure reversed promptly,
• defined as sudden loss of renal function renal function
due to inadequate renal perfusion returns to normal
o decrease in ECV • If hypoperfusion is
o arterial or venous obstruction sustained, intrinsic
o renal cell injury renal parenchymal
o obstruction to urine flow damage can develop
o abrupt increase in blood • COMMON CAUSE:
concentration of creatinine and Decrease in Effective
nitrogenous substances Intravascular Volume
o inability of the kidney to - GI losses
appropriately regulate fluid and (vomiting,
electrolytes diarrhea,
o CARDINAL FEATURE: reduction nasogastric
in GFR drainage)
CRITERIA ESTIMATED CCL URINE - Renal losses (salt-
OUTPUT wasting
RISK eCCL decrease by <0.5 nephropathy,
25% ml/kg/hr diabetes
for 8 hrs insipidus)
INJURY eCCL decrease by <0.5 - Drug-induced or
50% ml/kg/hr osmotic diuresis
for 16 hrs - Hemorrhage
FAILURE eCCL decrease by <0.3 (surgery, trauma,
75% or eCCL <35 ml/kg/hr GIB)
ml/min/1.73m2 for 24 hrs - Insensible losses
or ANURIC (burns,
for 12 hrs hyperthermia)
LOSS Persistent failure - Redistribution
>4 weeks (sepsis, heart
END- End-stage Renal failure, third
STAGE Disease space losses,
(Persistent failure hypoalbuminemia
>3 mos) )
 Intrinsic Renal Injury
Pre- Renal Injury • Transport capacity of tubule is
• Pre-glomerular vascular constriction impared
• Reduced renal cortical blood flow • Disruption of epithelial cytoskeleton
• Decreased glomerular filtration • Obstruction of tubular lumen
• Decreased glomerular capillary pressure • Back leak of filtrate contents
• Increase NaCl & H2O reabsorption • Further renal injury

A Intrinsic • Contributes to 35-40% of
K Renal ARF
I (+) • Includes a variety of
parenchy disorders characterized by
mal renal parenchymal damage
damage including sustained
hypoperfusion/ischemia

• GLOMERULAR
- GN
1. Post-infectious,
Lupus
2. HSP
3. Membranoprolifera Phases of AKI
tive 1. Pre-renal: no damage to tubular cells
4. Anti-GBM 2. Initiation: exfoliation and tubular
• VASCULAR destruction
- HUS 3. Extension: CMJ hypoxia
- Malignant HPN 4. Maintenance: slow recovery
- Renal artery/ Vein 5. Repair: repolarization
thrombosis A Post- • Contributes to 5 % of
• INTERSTITIAL K Renal ARF
- Acute Interstitial I • Includes a variety of
Nephritis (Infectious, disorders characterized
Allergic, Drug-induced) by obstruction of urinary
• TUBULAR tract distal to the kidney
- ACUTE TUBULAR • Causes:
NECROSIS - Posterior urethral
1. Ischemic-hypoxic valves
insults - Ureteropelvic
2. Nephrotoxins junction obstruction
3. Drugs e.g - Ureterovesical
Aminoglycosides) junction obstruction
- INTRATUBULAR - Ureterocoele
OBSTRUCTION - Urolithiasis
1. Pigment - Hemorrhagic cystitis
Nephropathy, e.g - Neurogenic cystitis
Hemoglubinuria/
Myoglobulinuria Clinical Manifestation of AKI
2. Tumor Lysis • Oliguria
Syndrome) • Edema
 • Hypertension (meq/L) 0 0 (acut
• Dyspnea e)
• Pallor >40
• Vomiting (few
• Lethargy days
• Anorexia )
Urine >4 <3 <350 >400 <350
Investigations Osmolity 00 50
• CBC with platelet (mOsm/kg)

o Anemia (dilutional or hemolytic) Fractional <1 >1 Varies <1 <1

o Leukopenia/ Leukocytosis (d/t exretion of (acut
Na+ e)
SLE or sepsis)
o Thrombocytopenia (SLE, renal >1
vein thrombosis, sepsis or HUS) (few
o High eosinophil count (d/t Acute days
interstitial nephritis)
• Urinalysis • Electrolytes & Acid-Base
o Hematuria, proteinuria (GN) o Hyponatremia
o Urinary eosinophils (drug-induced § Dilutional
tubule-interstitial nephritis) § More commonly due to
o Hemoglobinuria (hemolysis) overload
o Myoglobinuria (rhabdomyolysis) o Hypocalcemia
§ Inadequate GI calcium
absorption due to
Hyp Acu Acute GN Obstr inadequate vitamin D
ovo te Interstiti uction production by the kidney
lem Tub al o Hyperphosphatemia
ia ular Nephriti
Nec s
§ Decrease in GFR ->
rosi decrease in excretion
s o Hyperkalemia
Sediment Bla Br WBCs, RBCs, Bloo § Decrease in GFR ->
nd oa eosino blood d or decrease in excretion
d, phils, cell bloo § Metabolic acidosis
br cellular casts dy o Metabolic Acidosis
ow casts § Decrease in GFR ->
nis decrease in excretion of
h, acids
gra • ANA & anti-dsDNA
nul o SLE
ar • C3 & C4 complements
cas o Low C3
ts § PSGN
Protein No No Minim INC low o Low C3 & C4
ne ne al but § SLE
or or may be • ANCA & anti – GBM
Lo lo increas o RPGN/ crescentic GN
w w ed w/ • UTZ
NSAID o To exclude obstruction
S o Assess siz of kidneys
Urine Na+ <2 >3 >30 <20 <20
 o With Doppler: to evaluate renal o Creatinine: 0.5 mg/dl
perfusion o k for a 4 yr old child: 0.55
• Renal biopsy k 𝑥 𝐿
Estimated GFR (ml/min/1.73m2 =
o In patients with evidence of PCr
rapidly progressive GN Estimated GFR (ml/min/1.73m2
o Unexplained ARF 0.55 𝑥 100
=
0.5
Glomerular Filtration Rate (GFR) 110 𝑚𝑙/𝑚𝑖𝑛
• used clinically to follow the course of • Other biomarkers of AKI
renal disease o Neutrophil gelatinase- associated
o reduction in GFR implies lipocalin (NGAL)
progression o Cystatin C
o increase in GFR indicates o Interleukin – 18 (Il-18)
improvement o Kidney Injury molecule – 1 (KIM-
o unchanged GFR implies stable 1)
disease • Urinary – sediment & indices – most
• Estimated GFR (ml/min/1.73m2 = !"#
!!! important in determining cause of ARF
Pre- Intrinsin
k: proportionality constant
Renal
L: height (cm)
Urine Sp. Gr >1.020 <1.020
PCr: plasma Creatinine (mg/dl)
Urine Osm >500 <500
• Proportionality Constant for Calculating
GFR Urine Na <20 >40
k values FeNa <1% >2%
Low BW during 0.33 BUN/Creatinine >20 <20
1st yr of life (<2.5
𝑈𝑁𝑎 𝑥 𝑃𝐶𝑅
kg) 𝐹𝑒𝑁𝑎 % = 𝑥 100
Term AGA during 0.45 𝑃𝑁𝑎 𝑥 𝑈𝐶𝑅

1st yr of life
>2%: Intrinsic RF
Children & 0.55
<1%: Pre-renal failure
adolescent girls

Adolescent boys 0.70
• Normal Values of GFR APPROACH TO MANAGEMENT OF ARF
AGE Range ARF (Oliguria/

(ml/min/1.73m2)
anuria)

Assess volume status by history

Neonates <34 wks:
(volume losses) & PE (wt, BP, HR,
skin turgor, cap. rekill

• 2 – 8 days 11 - 15
Challenge w/
isotonic saline @
10 -20 ml/kg for
• 4-28 days 15 - 28 1 - 2 doses
(+) urine
• 30-90 days 40 - 65 output (-) Urine
output or (+)
signs of RF
Neonates >34 wks:
Hydrate
•  Crystalloid
•  BT for blood loss

• 2 – 8 days 17 – 60 •  inotropes for cardiac support

optimal nutrition

• 4 -28 days 28 - 68 dialysis

kluid restricton

• 30-90 days 30 - 86 low salt intake

correct e & acid base imb.
-

1 – 6 mos 39 – 114
6 – 12 mos 49 – 157 • Medical/ Non-dialytic Treatment
12 – 19 mos 62 – 191 o Hyponatremia
2 yrs – Adult 89 - 165 § If Na >120mEq/L: Fluid
• Computation of GFR restriction
o 4 year old Girl § If Na < 120 mEq/L (child is
o Height 100 cm at higher risk for seizures)
 § Correct to 125 mEq/L with remaining to be
hypertonic (3%) saline incorporated in the
using IV to run for 24 hrs
Na = (125 – PNa) x wt in kg x 0.6 v CAUTION: Ensure
o Hyperkalemia first that Serum
§ Leads to cardiac arrhythmia Calcium Normal
§ Tx indicated if cardiac since tx of acidosis
conduction abnormalities will decrease levels
are noted or if serum K are of ionized Ca and
>6-7 meqs that can cause tetany
§ Pharmacologic Treatment o Dopamine Renal Dose 3 -5
for Hyperkalemia: ug/kg/min
v Calcium Gluconate – o Diuretic therapy: IV furosemide or
for reversal of effect mannitol
to the heart o Anti-hypertensives: IV sodium
v Salbutamol – push K nitroprusside, nicardipine,
to the cell labetalol, diazoxide, hydralazine,
v SPS/dioxylate – enalapril
potassium binded & o Seizure control: Diazepam @0.1 –
sodium exchanger 0.3 mg/k/dose
v Dialysis – last choice
if all else fails RENAL DOSE ADJUSTMENT
o Hyperphosphatemia • Based on level of Renal Function
§ Dietary phosphate o GFR >50; 20-50; <20
restriction • Methods
§ Phosphate binders to 1. Dose adjustment – reducing the
prevent GI absorption individual dose leaving the normal
§ Avoid reaching Ca & P interval between the doses unchanged
product of 55 in the serum OR
o Hypocalcemia 2. Interval adjustment – increasing the
§ Treat with oral calcium interval between doses without
caronate or other calcium changing the dose
salts • Avoid nephrotoxic drugs
§ For severe or symptomatic RENAL REPLACEMENT THERAPY
hypocalcemia: Treat with • Dialysis
10% Calcium Gluconate o Choice depends on:
(100mg/kg up to max 1 g) § Local standard of care
for 30 – 60 mins w/ § Experience
continuous ECG monitoring § Access
o Metabolic Acidosis § Hemodynamic instability of
§ Treat with Oral/Parental patient
Sodium Bicarbonate or Oral § Goal of dialysis
Sodium Citrate § Indications:
§ Sodium Bicarbonate IV is 1. Anuria/oliguria
computed as: 2. Volume overload w/
v NAHCO3 (meq) evidence of
required = wt in kg x hypertension &/or
(desired – actual) x pulmonary edema
0.3 3. Persistent hyperkalemia
v Half- given by drip
for 1 hr, the
 4. Calcium/phosphorus CHRONIC KIDNEY DISEASE
imbalance
5. Uremia Criteria for Definition of CKD (NKF KDOQI
(Encephalopathy, Guidelines)
pericarditis, • Patient has CKD if either of the following
neuropathy) criteria are present:
6. BUN > 100-150 mg/dl 1. Kidney Damage >3 mos
(or lower if rapidly functional, structural
rising) abnormalities, with or without
7. Calcium/phosphorus decreased GFR, manifested by
imbalance with one of more of the ff features:
hypocalcemic tetany a. Abnormalitiesin
that cant be controlled composition of blood or
by other measures urine
Types of Dialysis: b. Abnormalities in
1. Intermittent Hemodialysis - for imaging tests
px with relatively stable c. Abnormalities on kidney
hemodynamic status biopsy
2. Peritoneal dialysis – most o GFR <60 ml/min/1.73 for <3 mos
commonly employed in or w/o other signs of kidney
neonates & infants with ARF damage as described above
3. Continuous Renal Replacement Causes of CKD
Therapy – for px with unstable • May be a result of congenital, acquired,
hemodynamic status, inherited or metabolic disease
concomitant sepsis or • Underlying cause correlatd closely with
multiorgan failure in the age
intensive care setting <5 y/o >5y/o
Prognosis of Intrinsic Causes of RF CONGENITAL ABN ACQUIRED
-depends on the underlying • Dysplasia (glomerulonephriti
cause • Obstructive s) or INHERITED
Recovery Guarded uropathy (familial juvenile
ATN ✔ • Renal nephronophthisis,
Interstitial hypoplasia Alport Syndrome)
Nephritis Metabolic & inherited disorders present
HUS ✔ throughout childhood years
RPGN
Cortical ✔ Standard Terms for Stages of CKD
necrosis STAGE DESCRIPTION GFR
1 Kidney >90
PREVENTION OF ARF damage with
• Appropriate use of diuretics Normal or
• Normalize blood pressure Increased
• Hydrate & maintain intravascular volume GFR
to maintain adequate renal perfusion 2 Kidney 60-89
• Avoid potentially nephrotoxic substances damage with
with impaired kidney function (NSAIDS, Mild
aminoglycosides, radiographic contrast decreasein
agents, general anesthetics, ACEI, amp B, GFR
chemo drugs) 3 Moderate 30-59
decrease in
 GFR o Decreased Erythrocyte survival
4 Severe 15-29 o Aluminum toxicity
decrease in o Inhibition of EPO
GFR • Short stature/Growth failure
5 Kidney failure <15 on o Contributory factors:
dialysis § Inadequate caloric intake
§ Metabolic acidosis
PATHOGENESIS § Renal osteodystrophy
• Hyperfiltration Injury 2 types:
o FINAL common pathway for 1. High Bone turnover
glomerular destruction disease – most common;
o Vicious cycle secondary
o Causes: hyperparathyroidism
§ Systemic or intrarenal (prime factor due to (1)
hypertension phosphate retention, (2)
§ Persistent proteinuria impaired synthesis of
§ High protein diet calcitriol, (3) skeletal
resistance of calcemic
Intraglomerul action of PTH, (4) PTG
ar
hypertension dysfxn), osteitis fibrosa
cystica
increase
leakage of
proteins
2. Low Bone turnover
disease – due to
acquisition of
inklammatory
oversuppression of PTH,
osteomalacia, adynamic
cells

release of
bone disease
IF GFR <50%: ê1-a-
vasoactive
substances

hydroxylase -> impaired

kibroblast
proliferation
interstitial
inklammatory
reactions
synthesis of Vit D3 - >
êintestinal CA
Renal Scarring
reabsorption -> êCa -
>éPTH w/c
compensates by
• Progression of Renal Injury increasing bone
o Other factors: resorption
§ Proteinuria IF GFR <20-25%:
§ Uncontrolled hypertension cannot excrete P -> éP -
§ Hyperphosphatemia >êCa & éPTH
resulting to calcium- § Anemia
phosporus deposition § Insulin resistance
§ Hyperlipidemia (oxidant- § GH resistance
mediated injury) LABORATORY
CLINICAL MANIFESTATIONS • Hyperkalemia
• PALLOR (anemia) • Hyponatremia (if commune
• Edema , hypertension, volume overload overloaded)
(GN) • Hypernatremia (loss of free water)
• FTT, polyuria, dehydration, UTI • Metabolic acidosis
• Multifactorial • Hypocalcemia
o EPO deficiency • Hyperphosphatemia
o Iron/ Folate/ Vit B12 deficiency • Increased uric acid
 •Proteinuria - Wastes are removed from
•Hypoalbuminemia peritoneal capillaries into dialysate
•Normochromic, normocytic o Hemodialysis
anemia - accomplishes both fluid & electrolyte
• Increased BUN & creatinine removal in 3 – 4 hrs using a pump
ACUTE TREATMENT OF CKD drive extracorporeal circuit & large
• Replace absent or diminished renal central venous catheter
functions • Renal Transplantation
• Slow the progression of renal dysfunction o Ultimate goal for children with
• Nutrition ESRD
o Dietary phosphorus, potassium,
sodium restriction
o Recommended dietary allowance
of caloric intake for age
§ Protein intake
recommendations:
1. 100 – 400 % of DRI for
ideal weight for children
with Stage 3 CKD
2. 100 – 120 % in Stages 4
– 5 CKD
3. 100 % with allowance
for dialysis loss in CKD
stage 5
o Water-soluble vitamin
supplementation
• Renal Osteodystrophy
o Vit D therapy
o Calcium
o Phosphate binders
• Growth
o Recombinant human growth
hormone
• Anemia
o Recombinant human EPO
o Darbepoietin – longer acting
• Hypertension
o Loop diuretic (Furosemide)
o ACEI (Capropril, Enalapril,
Lisinopril)
o ARBS (Losartan)
o CCB (Amlodipine, Nifedipine)
o B-blockers (Propanolol, Atenolol)
• Immunizations
• Adjustment in drug dose
• Renal Replacement Therapy
o Peritoneal Dialysis
- Employs patient’s peritoneal
membrane as dialyzer