Acute Kidney Injury

Definition

 Serum creatinine >1.5 mg/dL (132.6 μmol/L),

regardless of age or urine output, with normal
maternal renal function

 AKI could be:

 anuric (absence of urinary output by 24–48 hours of
age)
 oliguric (urine output of <1.0 mL/kg)
 nonoliguric (>1.0 mL/kg)
 AKI can present with normal urinary output (seen
in asphyxiated neonates).

 Normal urine output is ~1–3 mL/kg/h with almost

all infants voiding within 24 hours of birth
 Incidence

 24% of neonatal intensive care unit (NICU)-

admitted neonates

 Prerenal (85% of cases)  most common

 Renal incidence is 6–8%

 Postrenal 3–5%
 Pathophysiology

 Renal injury leads to problems with volume

overload, hyperkalemia, acidosis,
hyperphosphatemia, and hypocalcemia

: decreased renal blood

flow/perfusion   renal function in a normal
kidney
Causes:
 hemorrhage, dehydration, septic shock, congestive
heart failure, patent ductus arteriosus (PDA), and
necrotizing enterocolitis (NEC)  common
 structural damage
to the kidneys, which causes renal tubular
dysfunction
 acute tubular necrosis
 congenital anomalies
 vascular lesions
 Infections
 Exogenous toxins
 obstruction of
urinary outflow after the urine has been produced
by the kidneys
 cause in males is posterior urethral valves, urethral
strictures, meatal stenosis, bilateral
uteropelvic/vesical junction obstruction, neurogenic
bladder, large ureteroceles, blocked urinary
drainage catheters, megaureter, and prune belly
syndrome
 extrinsic tumor compression of the bladder or
ureters (sacrococcygeal teratoma)
 intrinsic obstruction (nephrolithiasis, bilateral
fungal bezoar).
 Diagnostic fluid challenge

Administer normal saline or colloid solution, 5–10

mL/kg as an intravenous bolus, and repeat once as
needed  no response  give furosemide, 1 mg/kg
IV  no increase in urine output  USG to rule out
obstruction above the level of the bladder  intrinsic
renal failure (if USG normal)
 Management

1. Prerenal failure: providing volume to increase

and restore renal perfusion and to treat the
underlying causes

2. Postrenal failure: bypassing the obstruction with a

bladder catheter or by percutaneous nephrostomy
drainage

3. Intrinsic renal disease Stop or adjust doses of any

nephrotoxic medications, Diuretics (furosemide, 1–2
mg/kg/dose)
4. Renal replacement therapy (peritoneal dialysis,
hemodialysis, hemofiltra- tion with or without
dialysis).
 DAFTAR PUSTAKA
 Gomella TL, Cunningham MD, et al. Neonatology. Mc
Graw Hill Education. Edisi 7. 2013. P 830-40
 Momtaz HE, Sabzehei MK, Rasuli B, Torabian S. The
main etiologies of acute kidney injury in the newborns
hospitalized in the neonatal intensive care unit.
Journal of clinical neonatology. 2014 Apr;3(2):99.
 Suhas M, Nafday, et al, In Renal Disease – Avery’s
Neonatology pathophysiology and management of
newborn, 6th e, editors M G MacDonald; Lippincott
Williams and Wilkins. 981- 1065.
 Gouyon J B, Guignard J P. Management of acute renal
failure in newborns. Pediatr Nephrol 2000;14:1037-1044.
Thank You