The term acute renal failure (ARF) has now been replaced with the term acute kidney injury (AKI), and is now used to encompass mild renal dysfunction to complete anuric kidney failure. In neonates, ARF/AKI is defined as a serum creatinine >1.5 mg/dL (132.6 μmol/L), regardless of age or urine output, with normal maternal renal function. ARF/AKI can be anuric (absence of urinary output by 24–48 hours of age), oliguric (urine output of <1.0 mL/kg), or nonoliguric (>1.0 mL/kg). ARF/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. See Table 68–1.
In some studies, as many as 24% of neonatal intensive care unit (NICU)-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. Renal incidence is 6–8% and postrenal 3–5%.
The normal newborn kidney has poor concentrating ability (maximum specific gravity 1.025). Renal injury leads to problems with volume overload, hyperkalemia, acidosis, hyperphosphatemia, and hypocalcemia. Postnatally ARF/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 ARF/AKI. Common causes include hemorrhage, dehydration, septic shock, congestive heart failure, patent ductus arteriosus (PDA), and necrotizing enterocolitis (NEC). Other causes include respiratory distress syndrome (RDS), hypoxia, congenital heart disease, hypoalbuminemia, perinatal asphyxia, extracorporeal membrane oxygenation/ extracorporeal life support (ECMO/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 (COX)-2 inhibitors can also decrease renal blood flow.
Intrinsic renal failure refers to structural damage to the kidneys, which causes renal tubular dysfunction. It includes acute tubular necrosis, congenital anomalies, vascular lesions, and infections/toxins. Acute tubular necrosis (ATN) is the most common cause, and it can be caused by prolonged poor renal perfusion, ischemia or hypoxia, sepsis, cardiac surgery (blood product transfusions), or nephrotoxins (aminoglycosides, NSAIDs, amphotericin B, contrast agents, or acyclovir). Other causes include congenital anomalies (eg, bilateral renal agenesis, polycystic kidney disease, congenital nephrotic syndrome of the Finnish type, renal hypoplasia/dysplasia), vascular lesions (bilateral renal vein/artery thrombosis, cortical necrosis, disseminated intravascular coagulation [DIC]), infections (congenital: syphilis, toxoplasmosis; candidiasis, pyelonephritis), exogenous toxins (uric acid nephropathy, myoglobinuria, hemoglobinuria).
Postrenal/obstructive. All of the causes involve obstruction of urinary outflow after the urine has been produced by the kidneys. The most common cause in males is posterior urethral valves. Other causes include urethral strictures, meatal stenosis, bilateral uteropelvic/vesical junction obstruction, neurogenic bladder, large ureteroceles, blocked urinary drainage catheters, megaureter, and prune belly syndrome. Rare causes in neonates include extrinsic tumor compression of the bladder ...