3. Definition
Acute kidney injury (AKI) - a sudden
impairment in kidney function, that
results in the retention of nitrogenous
waste products and alters the
regulation of extracellular fluid volume,
electrolytes, and acid-base
homeostasis.
“ recognize the injury , don’t wait for
the failure” ( Mehta 2007)
4. Creatinine based definition
Creatinine ≥1.5 mg/dL independent of
day of life and regardless of the rate of
urine output.
Problems of this approach
1. Will not change till 25 – 50 % func loss
2. Overestimates renal function
3. Varies by muscle mass, age , sex, hydr
4. Different methods of est ( Jaffe/
enzymatic)
5. Easily dialysed
Avery diseases of the neonate – 9 th edition
5. P- RIFLE
Creatinine 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 24hr
or anuric for 12 hours
Loss Persistent failure >4 wk
End
stage
Persistent failure > 3 months
Proposed by bellomo et al ; modified by ackan - arikan
6. AKIN criteria ( Mehta et al ,
2007)
Abrupt (within 48 h) reduction in
kidney function currently defined as an
absolute increase in serum creatinine
of 0.3 mg/dL or more or
A percentage increase in serum
creatinine of 50% or more (1.5-fold
from baseline) or
A reduction in urine output
(documented oliguria of < 0.5 mL/kg/h
for >6 h)
7. KDIGO staging for AKI severity
( Mehta et al 2007)
Creatinine Urine output
Stage 1 1.5-1.9 times
baseline
or
≥0.3 mg/dL
increase
<0.5 mL/kg/hr for 6 hr
Stage 2 2- 2.9 times
baseline
<0.5 mL/kg/hr for 12 hr
Stage 3 3 times baseline
or
Increase in serum
creatinine to ≥4
mg/dL
or
< 0.3 mL/kg/h for 24 h
or
Anuria for ≥12 h
8. Problems
Delineation between the 1st week of life
and changes in SCr level after the 1st
week - needed in a neonatal AKI
classification system.
Despite these working classification
systems, the diagnosis of AKI is
problematic, because current diagnosis
relies on two functional abnormalities:
functional changes in SCr (marker of
GFR) and oliguria.
Avery diseases of the neonate – 9 th edition
9. Acute Renal Failure in the Neonate
Steven Alan Ringer Neoreviews
2010;11;e243
11. Prerenal failure – pathophysio
Alteration in
plasma flow
Catecholami
ne surge
Prostagland
in & RAAS
activation
Dilation of
afferent
arteriole /
constric of
efferent
Acute Renal Failure in the Neonate
Steven Alan Ringer Neoreviews 2010;11;e243
12. Intrinsic renal failure Increased
transcapillary
hydraulic pressure
Failure of
autoreg +-
renal
immaturity
Tubular damage
systemic
inflammatory
response
Acute Renal Failure in the Neonate
Steven Alan Ringer Neoreviews 2010;11;e243
14. Evaluation
Identify prerenal causes
Is there a volume contraction ?
- Inadeq feeding
- Dehydration
- Large fetomaternal h’hage
- Subgaleal bleeds
- Warm shocks
Congestive cardiac failure
Acute Renal Failure in the Neonate
Steven Alan Ringer Neoreviews 2010;11;e243
15. Investigations
Serum sodium, potassium, chloride,
bicarbonate, calcium, phosphorus,
magnesium, urea, creatinine, uric
acid, glucose, blood gases,
hemoglobin, and platelets
S.Cr often does not rise for days after
an injury, thus monitoring these values
for several days after the inciting event
is necessary to determine if AKI
occurred.
17. Management
Supportive –
keep the kid
and kidney
alive
Acute Renal Failure in the Neonate
Steven Alan Ringer Neoreviews
2010;11;e243
18. Dopamine
Dopamine can increase renal
perfusion in the sick pre- term and
term infant with prerenal azotemia
caused by hypoxemia, acidosis, or
indomethacin administration (Seri,
1995; Seri et al, 1998, 2002).
Compared with placebo, low-dose
dopamine does not improve survival,
shorten hospital stay, or limit dialysisAcute Renal Failure in the Neonate
Steven Alan Ringer Neoreviews 2010;11;e243
19. Fenoldopam is a selective dopamine-1
receptor agonist whose effects include
vasodilation of renal and splanchnic
vasculature, increased renal blood
flow, and increased GFR.
Fenoldopam is approved to treat
severe hypertension in adults, but is
not clinically approved for the
treatment of AKI.
Avery ‘s diseases of newborn – 9th edition
20. Diuretic
No studies in neonates, children, or
adults have shown that diuretics are
effective in preventing AKI or
improving outcomes once AKI occurs
(Bellomo et al, 2000).
If loop diuretics are to be used in
neonates, continuous doses of
furosemide may be superior to larger
intermittent doses
21. Volume & electrolyte / acidbase
imbalance
Hyponatremia:
Na Required (mEq) =(Na Desired − Na +
Actual) × Body weight (kg) × 0.7
Hypocalcemia -100 to 200 mg/kg of
calcium gluconate should be infused
over 10 to 20 minutes and repeated
every 4 to 8 hours as necessary.
Hyperphosphatemia - Breastmilk and
Simi- lac 60/40 both contain low
phosphorous and low potassium
compared with other neonatal infant
formulas .
22. Treatment of hyperkalemia
Vemgal and Olhson (2007) -no firm clinical practice recommendations on
which treatment modality was best to treat preterm infants with
hyperkalemia are available, except that insulin plus glucose may be better
in premature infants.
23. Nutrition & drugs
Nutritional goals in infants with AKI are
similar to those of infants without AKI.
Feeds or parenteral nutrition will need
to be concentrated to avoid excessive
fluid
a neonate is receiving continuous
peritoneal dialysis or hemodialysis, an
additional 1 g/kg/day of protein is
needed to supplement the protein
losses that occur with these forms of
dialysis (Zappitelli et al, 2008, 2009).
24. Indications For Renal Support
Severe electrolyte abnormalities that are
not correctable with medicalinterventions
Life-threatening intoxication by
medications that can be cleared with
dialysis
inborn errors of metabolism
fluid overload
Acidosis – refractory to medical
management
Coma
Neonatal Peritoneal Dialysis
Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin Neoreviews 2005;6;e
DOI: 10.1542/neo.6-8-e384
25. Renal replacement therapy
The timing of dialysis initiation in
infants with AKI is controversial.
Several observational studies show a
clear advantage in adults receiving
dialysis early versus late (Liu et al,
2006; Ronco et al, 1986).
Neonatal Peritoneal Dialysis
Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin
Neoreviews 2005;6;e384
DOI: 10.1542/neo.6-8-e384
26. Basic Physiology of Dialysis And
Ultrafiltration
Molecular movement across
semipermeable membrane
Basic mechanisms of water and
particle removal include
Diffusion
Convection
Ultrafiltration
27. Diffusion
Movement of dissolved particles
across semi- permeable membrane
from area of high concentration to
area of low concentration
Favors movement of smaller particles
Stops when concentration gradient
achieves equilibrium
28.
29. Convection
Dissolved particles pass across semi
permeable membrane due to effects
of pressure gradient
Ultrafiltration
Describes movement of water across
semipermeable due to pressure
32. PERITONEAL DIALYSIS
Physiology
Peritoneum can be used as a dialysing
membrane
Instillation of a dialysate into the peritoneal
space permits diffusion of particles out of the
blood across the peritoneum
Through the use of a hypertonic solution , water
also passes across the membrane generating
an ultrafiltrate
Water movement tends to drag particles across
the peritoneum by convection
After the dwell is complete , the spent dialysate
is drained from the abdomen and fresh
dialysate may be introducedNeonatal Peritoneal Dialysis
Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin
Neoreviews 2005;6;e384
DOI: 10.1542/neo.6-8-e384
33. Indications
Remove excess fluid and provide
volume control in the patient with
oligoanuria
Much slower than intermittent
hemodialysis
Preferable in the critically ill patient
Provides metabolic control
Neonatal Peritoneal Dialysis
Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin
Neoreviews 2005;6;e384
DOI: 10.1542/neo.6-8-e384
34.
35. Technique
Instill sterile dialysate into peritoneal cavity
Allow it to dwell
End of dwell time the dialysate is removed
Dialysate contains base in the form of
lactate
Ultrafiltration accomplished by osmotic
pressure thro dextrose
Should be warmed to body temp
Start with 10 – ml/kg ( 500 ml/m2)
Dwell period of 30 - 60 min
Neonatal Peritoneal Dialysis
Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin
Neoreviews 2005;6;e384
DOI: 10.1542/neo.6-8-e384
37. Complications
Peritonitis
Leakage around the catheter exit site
Tunnel infection
Catheter malfunction, and obstruction by
omentum (Coulthard and Vernon, 1995).
Fluid leakage into other compartments
(including the chest in patients without
an intact diaphragm) can occur and if
suspected, the fluid composition will
reveal high glucose levels if a leak is
presentNeonatal Peritoneal Dialysis
Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin
Neoreviews 2005;6;e384
DOI: 10.1542/neo.6-8-e384
38. Issues
Loss of protein – supplement it
Hyperglycemia
GER – stomach comp
Critically ill – inc intra abd pressure
leading to dec Venous return and dec
diaphragm excursion
Neonatal Peritoneal Dialysis
Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin
Neoreviews 2005;6;e384
DOI: 10.1542/neo.6-8-e384
39. Poor candidates for PD
worsening respiratory status or
ventilatory
Diaphragmatic hernias
Abdominal wall defects
Neonatal Peritoneal Dialysis
Marsha M. Lee, Annabelle N. Chua and Peter D. Yorgin
Neoreviews 2005;6;e384
DOI: 10.1542/neo.6-8-e384
40.
41. AKI to CKD
Adult studies – 3- 5 % go on to have
CKD
Stapleton – retrospective study – 40 –
88 % CKD prevalence
Preterms did worse than term babies
