1. Acute Renal
Failure in Neonates
Prepared by
MAGED ZAKARIA
NICU RESIDENT

2. Acute
Renal Failure
Rapid elevation in the
concentration of
BUN, creatinine, and
other cellular waste
products in the blood
resulting from
diminished GFR in the
kidney.

3. Causes of ARF in Neonates
1. Pre-renal Failure
• A decrease of systemic circulation to the kidney.
• Renal Hypoperfusion (hypovolemia)
Hemorrhage - Dehydration - operative fluid loss - Sepsis -
NEC - Hypoalbuminemia
• Increased Renal Vascular Resistance
Polycythemia - Indomethacin
• Renal Hypoperfusion with normovolemia
Asphyxia - Septic shock - Heart failure (PDA - Aortic
Coarctation).

4. Causes of ARF in Neonates
2. Intrinsic Renal Failure
• A damage or necrosis of the parenchyma of the kidney.
• Sustained renal hypoperfusion leading to ATN.
• Congenital Disorders:
 Agenesis - Hypoplasia - Dysplasia - PKD (AD – AR).
• Bilateral Renal Vein or Artery Thrombosis.
• Nephrotoxins:
 Aminoglycosides - Radiographic contrast media.
 Maternal use of captopril or indomethacin.
• Congenital Infection (Toxoplasmosis or Syphilis).

5. Causes of ARF in Neonates
3. Post-renal Failure
• A distal obstruction to urine flow.
• Bladder retention:
 Urethral valves
 Massive VUR
 Meningomyelocele (Neurogenic bladder).
• Bilateral ureteral obstruction:
 UPJ or UVJ obstruction - Lithiasis - Fungus ball.
• Extrinsic compression:
 Uroascites (i.e., ruptured urinary tract).
 Bladder perforation (UAC or direct bladder trauma).

6. Renal Failure with Hypoxic Ischemic Injury
• In the early stages, hypoperfusion results from pump failure
and diminished cardiac output due to bradycardia and
cardiac depression.
• If the problem is not corrected, the injury may progress as
vasoconstriction and reduced capillary perfusion result in
acute tubular necrosis (ATN) and diminished function.
• Renal damage can occur directly from tissue hypoxia and
ischemia.

7. Renal Failure with Hypoxic Ischemic Injury
• Measurement of certain urinary indices (urine
osmolality, sodium, and the fractional excretion of sodium)
may be helpful in differentiating ATN from prerenal disease.
• Table 2 shows Urine Indices in Prerenal and Intrinsic RF:
Fractional
Osmolality Urine Sodium
Excretion
(mOsm/L) (mEq/L)
of Sodium (%)
Prerenal Failure > 350 < 20-30 < 2.5
ATN < 350 >30-40 > 2.0

8. Fractional Excretion of Sodium (%)

9. Assessment of a Neonate with ARF
• Maternal History (medications, and unusual exposures
during the pregnancy, oligohydramnios in the absence of
AF leakage or ROM or polyhydramnios)
• Prenatal Ultrasonography
• Delivery history. Perinatal asphyxia or shock due to volume
loss.
• Family History including any prior fetal or neonatal deaths.
There is a clear genetic basis for PKD and congenital
nephrotic syndrome.

10. Assessment of a Neonate with ARF
 Anomalies that alert to the possibility of underlying renal
defects including
 Abnormal external auricles or Aniridia (congenital
absence of the iris).
 Microcephaly or Meningomyelocele
 Pectus excavatum
 Hemihypertrophy (one side of the body or a part of one
side is larger than the other).

11. Assessment of a Neonate with ARF
 Anomalies that alert to the possibility of underlying renal
defects including
 A persistent urachus or Exstrophy of the bladder
 Cloaca or abnormal external genitalia
 Cryptorchidism or Imperforate anus
 Limb deformities.
 Single umbilical artery

12. Assessment of a Neonate with ARF
• Evaluate blood pressure and hydration state.
• Hypertension: PKD, ARF, renovascular or aortic thrombosis or
obstructive uropathy.
• Hypotension: volume depletion, hemorrhage, or sepsis (may
lead to ARF).
• Edema: ARF, hydrops fetalis, or congenital nephrotic
syndrome.

13. Assessment of a Neonate with ARF
• Abdominal mass: two thirds of neonatal abdominal
masses are genitourinary in origin (e.g. hydronephrosis,
multicystic dysplastic kidney, PKD, RVT, ectopic or fused
kidneys, and a renal tumor).
• Absence of or laxity in the abdominal muscles: Eagle-
Barrett (“prune-belly”) syndrome.
• Distention of the bladder: lower urinary tract obstruction or
an occult spinal cord lesion.

14. Prune belly syndrome
Eagle-Barrett syndrome
Marked wrinkling of the skin
and flaccid abdominal wall
which bulges laterally as a
result of lack of the underlying
abdominal muscles.
The triad of findings include
absence of the abdominal
muscles, urinary tract
abnormalities, and
cryptorchidism. The abdomen
has a doughy consistency on
palpation, and the abdominal
viscera can be felt with unusual
ease.

15. Assessment of a Neonate with ARF
Micturition
• 17% of newborns void in the delivery room
• About 90% void by 24 hours and 99% void by 48 hours.
• Normal urine output is 1 - 3 mL/kg/hour.
• The most common cause of delayed or decreased urine
production is inadequate perfusion of the kidneys;
however, delay in micturition may be due to intrinsic
renal abnormalities or obstruction of the urinary tract.

16. Assessment of a Neonate with ARF
Potter Sequence
• Seen in infants with severe bilateral congenital
renal disease
• Severe oligohydramnios causes fetal deformation
by compression of the uterine wall.

17. Potter Sequence
• Characteristic facial
features:
1. Epicanthal folds
2. Hypertelorism
3. A crease below lower
lip
4. A depressed nasal
Associated anomalies bridge
include a small compressed 5. A beaked nose
chest wall with resulting 6. A receding chin
7. A posteriorly rotated,
pulmonary hypoplasia and
low-set ears.
arthrogryposis.

18. Assessment of a Neonate with ARF
URINALYSIS
• A specimen collected by cleaning the perineum and
applying a sterile adhesive plastic bag is useful in screening
but it may give a false positive urine culture because of fecal
contamination.
• Bladder catheterization is more reliable but may be
technically difficult in preterm infants.
• Suprapubic bladder aspiration is the collecting method of
choice in infants without intra-abdominal pathology or
bleeding disorders.

19. Assessment of a Neonate with ARF
URINALYSIS
• The urine should be obtained initially, i.e., before
any diuretic or fluid challenge.
• USG > 1.025 in pre-renal failure while USG < 1.014 in
intrinsic RF.

20. Assessment of a Neonate with ARF
RENAL FUNCTION TESTS
• Serum creatinine value measured immediately after birth
reflects the maternal rather than infant’s renal function.
• Table 1 shows normal creatinine values at birth
Gestational Age (wk) Creatinine (mg/dL)
23 to 26 0.77 to 1.05
27 to 29 0.76 to 1.02
30 to 32 0.70 to 0.80
33 to 45 0.77 to 0.90

21. Assessment of a Neonate with ARF
• The standard indicators of renal function are serum levels of
BUN and creatinine; their ratio is normally about 10:1.
• This ratio may increase when renal perfusion or urine flow is
decreased, as in urinary tract obstruction or dehydration.
• Because BUN levels are more affected by many factors (eg,
nitrogen intake, catabolism, use of corticosteroids) than are
creatinine levels, the most reliable single indicator of
glomerular function is the serum level of creatinine.

22. Assessment of a Neonate with ARF
• In term babies, the serum creatinine normally rises in the 1st
24-36 hrs after birth, subsequently decreasing and stabilizing
at ~ 0.4 mg/dL by 5 days of age.
• In preterm infants, the peak value occurs between 2-3 days
after birth, and stabilization is delayed until 6 days of age.
• It is difficult to use a single value (rather than serial follow up)
to diagnose renal failure, except a clearly elevated value
beyond the normal range.

23. Assessment of a Neonate with ARF
Ultrasonography
 Indicated in infants with an abdominal mass, renal
failure, hypertension, hematuria, oliguria, congenital
malformations, or specific findings that suggest
anomalies of the urinary tract.
 A Doppler flow study of the renal arteries and aorta may
be helpful in the evaluation of thrombosis in infants with
suspected renovascular hypertension or ARF.

24. Assessment of a Neonate with ARF
Ultrasonography
• Because of relative hypovolemia during the 1st
few days of life, repeat US after the 1st week of
life if previous findings were normal in a child with
previously diagnosed antenatal hydronephrosis
before making a final determination that the
hydronephrosis has resolved.

25. Assessment of a Neonate with ARF
Voiding Cystourethrography
• It involves the instillation of a radiopaque contrast agent
into the bladder by urinary catheterization. Films of the
urethra during voiding and of the bladder and ureters
toward the end of voiding are essential.
• Essential in infants with hydronephrosis, renal dysplasia or
anomaly or documented UTI.
• Used to evaluate the urethra and bladder and ascertain
the presence or absence of vesicoureteral reflux.

26. Assessment of a Neonate with ARF
Radioisotopic Renal Scanning
• Of value in locating anomalous kidneys, determining
kidney size, identifying obstruction or renal scarring. RBF to
each kidney and the contribution of each kidney to overall
renal function.
• It should not be done in the neonatal period because renal
immaturity doesn’t allow for accurate estimation of renal
function.

27. Assessment of a Neonate with ARF
Abdominal Computed Tomography
• Useful in the diagnosis of
1. Renal tumors
2. Renal abscesses
3. Nephrolithiasis.

28. Clinical Signs of RF
1. Oliguria (urine output < 0.5 ml/kg/h)*.
2. Systemic hypertension.
3. Cardiac arrhythmia.
4. Evidence of fluid overload or dehydration.
5. Decreased activity, seizure and vomiting.
*ARF associated with asphyxia is predominantly non-oliguric.
Thus, unless Pcr is monitored daily in the severely asphyxiated
neonate, renal failure will be easily missed.

29. Laboratory Evidence of RF
1. Elevated serum creatinine and BUN
2. Hyperkalemia
3. Metabolic acidosis
4. Hypocalcemia and hyperphosphatemia

30. Management of ARF
Zappitelli and Goldstein, 2008
1. Treatment of underlying disease
2. Avoid/manage fluid depletion/overload
3. Correct electrolyte and acid base abnormalities
4. Avoid further renal injury
5. Drug dosing for renal function
6. Provision of adequate nutrition
7. Renal replacement therapy.

31. Fluid Management
• Patients with pre-renal failure will often respond to fluid
resuscitation, whereas patients with ATN should be treated
with volume restriction.
• Generally, a safe starting point is to provide insensible
losses plus replacement of ongoing losses (urinary, GI, chest
tubes) however this may not be appropriate in the setting
of acute volume depletion.
• Insert a urinary catheter and obtain weights and serum
electrolyte levels at least daily.

32. Fluid Management
• Neonates with intravascular volume depletion require
vigorous fluid resuscitation. A fluid challenge (20 mL/kg of
crystalloid solution, e.g., isotonic saline over 30 min);
repeated twice if necessary, after careful monitoring to
avoid possible fluid overload.
• If anuria persists after 3 fluid boluses (confirmed by bladder
catheterization), central venous monitoring may be
required to guide further management.
• Source: http://emedicine.medscape.com/article/980830-treatment

33. Fluid Management
• Diuretics may convert an oliguric to a nonoliguric ARF,
which is more easily managed (no need for fluid restriction,
allows for maximal nutritional support).
• The current recommendation is that a trial of high dose (2-5
mg/kg) furosemide IV should be attempted with oliguria of
< 48 h duration if not responded to adequate hydration.
• When renal hypoperfusion or toxic injury is anticipated,
administration of fluids and low-dose dopamine have been
used to prevent or reverse renal injury.

34. Fluid Management
• Patients who fail to respond to furosemide may
respond to Edemex® (bumetanide 5 mg/kg/dose
IV), a more potent loop diuretic (not evaluated in
acute neonatal oligoanuria).
• A diuretic challenge test should be done first in
patients thought to be hypervolemic or in heart
failure, whereas a fluid challenge should be
done first in those thought to be hypovolemic.

35. Electrolytes Management
• Patients with oligo-aneuric RF or ATN should not
receive K+ or phosphorus unless they exhibit
hypokalemia or hypophosphatemia.
• Na+ intake should be restricted to 2–3
mEq/kg/day, together with fluid restriction, to
prevent Na+ and fluid retention with resultant
hypertension.

36. Acid Base Management
• Metabolic Acidosis
 Severe acidosis (a plasma bicarbonate concentration
of 12 mEq/L or less or plasma pH below 7.20) should be
corrected by the administration of IV or oral NaHCO3.
 Adequate ventilation is necessary in order to exhale the
CO2 produced.
 NaHCO3 may precipitate hypernatremia or
hypocalcemia (decreases ionized Ca).

37. Electrolytes Management
1. Serum Potassium
Normal level in a non-hemolyzed blood specimen at
normal pH is 3.5-5.5 mEq/L
Management of Hyperkalemia:
1. Eliminate all sources of K+ from the diet or IVF .
2. Administer a cation exchange resin such as
Kayexalate® (sodium polystyrene sulfonate) or
Sorbisterit® (calcium polystyrene sulfonate).

38. Electrolytes Management
Management of Hyperkalemia:
3. Administer IV NaHCO3 1 mEq/kg IV over 10 to 30 min
(causes a rapid shift of K+ into cells) (used with caution;
can precipitate hypocalcemia and Na+ overload).
4. Infusion of glucose and insulin (Glucose 0.5 g/kg; insulin
0.1 U/kg IV over 30 min)
5. Beta-agonists (Salbutamol 0.4 mg (0.08 mL)/kg/dose
Q2h via nebulizer; can cause tachycardia).

39. Electrolytes Management
Management of Hyperkalemia:
6. Exchange transfusion with washed packed cells.
7. Calcium gluconate 0.5 to 1.0 mL/kg IV over 5 to 10 min
should be administrated in presence of ECG changes
(with continuous ECG monitoring for bradycardia and
arrhythmias) to counteract the effects of hyperkalemia
on the myocardium.
8. The definitive therapy for significant hyperkalemia in
oliguric ATN is dialysis

40. ECG Manifestations of Hyperkalemia

41. Electrolytes Management
2. Serum Sodium
Normal level is 134–146 mEq/L
Hyponatremia in Renal Failure
• Treated by free water restriction.
• Serum sodium of < 120 mEq/L requires hypertonic (3%)
NaCl infusion (1-3 mL/kg initial dose), especially if CNS
dysfunction is present (obtundation or seizure activity).

42. Electrolytes Management
3. Hyperphosphatemia
• Dietary restriction
• Oral phosphate binders (calcium carbonate).
4. Hypocalcemia
• Oral calcium salts
• 10% calcium gluconate infusion

43. Adjustment of Medications
• Avoid nephrotoxic agents e.g. contrast
media, aminoglycosides, and NSAIDs.
• The interval of administration of medications with renal
elimination (e.g., antibiotics, paralyzing
agents, theophylline, antiepileptic drugs, and digoxin) should
be adjusted to actual renal function (spontaneous or renal
replacement therapy) to avoid toxic levels.
• Monitoring drug levels will allow additional adjustments.
• When possible, medications with minimal or no renal toxicity
should be chosen.

44. Adjustment of Medications
DOSE IN SEPSIS:
20 mg/kg/dose IVI Q12h
Dose in Renal Impairment
Cr Cl 26-50 mL/min/1.73m2  use normal dose Q12h
Cr Cl 10-25 mL/min/1.73m2  use half normal dose Q12h
Cr Cl <10 mL/min/1.73m2  use half normal dose Q24h
An empirically derived formula to estimate CrCl:
In Preterm neonates =
In Term neonates =

45. Provision of Adequate Nutrition
• If the infant is tolerating oral feedings, maternal human
milk or a renal formula that has a low renal solute load
and low phosphorus should be used.
• Infants who have oliguria frequently cannot receive
adequate calories with maternal human milk or formula
alone because of the need for fluid restriction.
Therefore, high-caloric additives that have low osmolality
may be required.

46. Provision of Adequate Nutrition
• If oral feedings are not tolerated, nutrition should
be administered IV to provide:
1. A minimum of 50 kcal/kg/day
2. 1-2 g/kg/day of proteins (tailored via
measurements of BUN).

47. Renal Replacement Therapy (Dialysis)
• Common Indications For Dialysis:
1. Fluid overload that is unresponsive to diuretics
or hinders adequate nutritional support
2. Hyperkalemia with oliguria
3. Symptomatic acid-base imbalances
4. Refractory hypertension
5. Symptomatic uremia (pleuritis, pericarditis,
CNS symptoms)

48. Renal Replacement Therapy (Dialysis)
• Before renal replacement therapy is initiated,
consideration should be given to the possibility
that the patient may have either a dysmorphic
syndrome with a very poor prognosis regarding
the future quality of life, or severe irreversible
multiorgan failure.

49. Renal Replacement Therapy (Dialysis)
• Removes toxins and to maintain
fluid, electrolyte, and acid-base balance until
renal function returns.
• In general, peritoneal dialysis is the preferred
method in infants and younger children.

54. Complications of Renal Failure
• Infections (30-70%): Defenses are impaired due
to uremia, excessive use of antibiotics and
invasive maneuvers.
• Cardiovascular complications
(hypertension, CHF and pulmonary edema)
result from fluid and Na+ retention.
• Hyperkalemia (ECG abnormalities and cardiac
arrhythmias).

55. Complications of Renal Failure
• Other Complications Include The Following:
1. GI (eg, anorexia, nausea, vomiting, ileus, bleeding)
2. Hematologic (eg, Anemia, Bleeding tendency from
abnormal platelet function and, in some patients
(e.g., those with RVT), from thrombocytopenia)
3. Neurologic (eg, somnolence, seizures)
4. Electrolyte disturbances (eg, hyponatremia,
hyperkalemia, hypocalcemia, hyperphosphatemia)
5. Metabolic acidosis

56. Mortality from RF in Neonates
• Mortality from renal failure in the newborn has been
reported to be as high as 25-50%.
• The risk is highest in:
1. Intrinsic renal disease.
2. Infants in need for dialysis or mechanical ventilation.
3. Prolonged anuria
4. Absent uptake on renal radionuclide scans.
• There is no correlation between peak creatinine values and
mortality risk.