There is no unified definition of acute kidney injury (AKI), previously termed acute renal failure, in neonates. Historically, neonatal AKI is defined as absolute serum creatinine ≥1.5 mg/dL, regardless of age or urine output, with normal maternal renal function. In 2013, a panel of experts at a National Institutes of Health-sponsored workshop proposed the adaptation of the categorical modified Kidney Disease: Improving Global Outcomes (KDIGO) definition to predict neonatal clinical outcomes (Table 86–1). According to neonatal KDIGO definition, AKI is defined as an absolute rise of ≥0.3 mg/dL or a ≥50% rise from lowest baseline serum creatinine. AKI can be anuric (absence of urinary output by 24–48 hours of age), oliguric (urine output of <1.0 mL/kg/h over 24 hours), or nonoliguric (>1.0 mL/kg/h). AKI can present with normal urinary output (seen in asphyxiated neonates). Normal urine output is approximately 1 to 3 mL/kg/h with almost all infants voiding within 24 hours of birth. See Table 73–1.
In some studies, as many as 30% of neonatal intensive care unit–admitted neonates have some degree of renal failure. Prerenal is the most common type in the neonate, which may be identified in up to 85% of cases. Intrinsic renal disease incidence is 11%, and postrenal incidence is 3% to 5%.
The normal newborn kidney has poor concentrating ability (maximum urine concentration is approximately 700 mOsm/L in the first few days after birth as compared to 1200 mOsm/L at 1 year of age). Renal injury leads to problems with volume overload, hyperkalemia, acidosis, hyperphosphatemia, and hypocalcemia. Neonatal AKI is traditionally divided into 3 categories:
Prerenal failure is due to decreased renal blood flow/perfusion, which leads to a decreased renal function in a normal kidney. Any condition that causes inadequate renal perfusion can cause prerenal AKI. Common causes include: hemorrhage, dehydration, septic shock, congestive heart failure, patent ductus arteriosus, and necrotizing enterocolitis. Other causes include respiratory distress syndrome, hypoxia, congenital heart disease, hypoalbuminemia, perinatal asphyxia, ECLS, and hypotension. Medications in neonates that can decrease renal blood flow include indomethacin, ibuprofen, angiotensin-converting enzyme (ACE) inhibitors, and phenylephrine eye drops. Maternal use of nonsteroidal anti-inflammatory drugs (NSAIDs), ACE inhibitors, or cyclooxygenase-2 inhibitors can also decrease renal blood flow.
Intrinsic renal failure refers to direct damage to the glomeruli, renal tubules, vessels, or interstitium of the kidneys. Prolonged prerenal and postrenal AKI often results in some degree of intrinsic renal dysfunction. Etiologies of intrinsic renal failure include: acute tubular necrosis (ATN), congenital anomalies, vascular lesions, and infections/exogenous toxins. ATN is the most common cause, and it can be due to prolonged poor renal perfusion, ischemia or hypoxia, sepsis, cardiac surgery (blood product transfusions), or nephrotoxins (aminoglycosides, NSAIDs, amphotericin B, contrast agents, or acyclovir). Congenital anomalies (eg, bilateral renal agenesis, polycystic kidney disease, congenital nephrotic syndrome of the Finnish type, renal hypoplasia/dysplasia), vascular lesions (eg, bilateral renal vein/artery thrombosis, cortical necrosis, ...