Definition. In neonates, acute renal failure is defined as the absence of urinary output (anuria) or as urine output of <0.5 mL/kg/24 h (oliguria) with an associated increase in serum creatinine. One hundred percent of infants void by 24 h (for average times from birth to first voiding, see Table 61–1).
Incidence. In some studies, as many as 23% of neonates have some form of renal failure; prerenal factors are identified as the cause in 73%. In a recent study causes included cardiac (27%), prematurity (27%), septic (10%), hepatic (9%), renal (9%), and other (18%) causes. Twelve infants needed transient dialysis treatment.
Pathophysiology. Normal urine output is ~1–3 mL/kg/h in newborns. The normal newborn kidney has poor concentrating ability. Renal failure leads to problems with volume overload, hyperkalemia, acidosis, hyperphosphatemia, and hypocalcemia. Acute renal failure is traditionally divided into three categories:
Prerenal failure. Prerenal failure is due to decreased renal perfusion. Causes include dehydration (poor feeding or increased insensible losses referable to radiant warmers), perinatal asphyxia, and hypotension (septic shock, hemorrhagic shock, or cardiogenic shock resulting from congestive heart failure).
Intrinsic renal failure. If poor renal perfusion persists, acute tubular necrosis with intrinsic renal failure may result. Other causes are nephrotoxins such as aminoglycosides, nonsteroidal anti-inflammatory medications and methoxyflurane anesthesia, congenital anomalies (eg, renal agenesis or polycystic kidney disease), disseminated intravascular coagulation (DIC), renal vein or renal artery thrombosis, and isolated cortical necrosis.
Postrenal failure. All of the causes involve obstruction of urinary outflow. These include bilateral ureteropelvic obstruction, bilateral ureterovesical obstruction, posterior urethral valves, urethral diverticulum or stenosis, large ureterocele, neurogenic bladder, blocked urinary drainage tubes, and extrinsic tumor compression.
Risk factors. Dehydration, sepsis, asphyxia, and administration of nephrotoxic drugs to the neonate are risk factors for acute renal failure. Maternal diabetes may increase the risk for renal vein thrombosis and subsequent renal insufficiency.
Decreased or absent urine output. Low or absent urine output is usually the presenting problem. Virtually all infants void by 24 h (see Table 61–1).
Family history. A history of urinary tract disease in other family members should be sought as well as a history of oligohydramnios, which frequently accompanies urinary outflow obstruction or severe renal dysplasia or agenesis.
Physical examination. The following abnormalities on physical examination are significant:
Abdominal mass, suggesting a distended bladder, polycystic kidneys, or hydronephrosis.
Potter facies, associated with renal agenesis.
Meningomyelocele, associated with neurogenic bladder.
Pulmonary hypoplasia, resulting from severe oligohydramnios in utero secondary to inadequate urinary output.
Urinary ascites, which may be seen with posterior urethral valves.
Prune belly (hypoplasia of the abdominal wall musculature and cryptorchidism), associated with urinary abnormalities.
Bladder catheterization. Perform bladder catheterization, using a 5F or 8F feeding tube to confirm inadequate urine output (see Chapter 25). Immediate passage of large volumes of urine suggests obstruction (eg, posterior urethral valves) or a hypotonic (neurogenic) bladder.
Blood urea nitrogen and creatinine levels
A blood urea nitrogen level 15–20 mg/dL suggests dehydration or renal insufficiency.
Creatinine level. Normal serum creatinine values are 0.8–1.0 mg/dL at 1 day, 0.7–0.8 mg/dL at 3 days, and <0.6 mg/dL by 7 days of life. Higher values suggest renal disease except in low birthweight infants, in whom a creatinine level of <1.6 mg/dL is considered normal. (Rule of thumb: If the creatinine doubles, then 50% of the renal function has been lost.)
Urinary indices of acute renal failure are listed in Table 113–1. ...
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