Renal injury in sick newborn infants: a prospective evaluation using urinary beta 2-microglobulin concentrations.

Urinary concentrations of beta 2-microglobulin and creatinine were measured serially in 140 sick infants, of whom 109 were asphyxiated, and in 35 healthy preterm and term infants. First voided urines and samples from days 3 and 7 postpartum were studied. Urinary beta 2-microglobulin concentrations in healthy infants averaged 1.34 +/- 1.34 mg/L (mean +/- SD) in first voided specimens and 1.32 +/- 0.98 mg/L in day 3 samples; the calculated upper limit of normal (95% confidence limit) was 4.00 mg/L. Elevated values (those exceeding the 95% confidence limit) occurred most often in the sick asphyxiated patients (56%); the first voided sample value in these patients was 10.0 +/- 10.4 mg/L. The equivalent value in the sick nonasphyxiated infants was 8.32 +/- 7.27 mg/L. Values were significantly and persistently elevated in the sick infants on days 3 and 7. Factoring beta 2-microglobulin levels by urinary creatinine concentration did not affect the significance of the findings. The increased urinary beta 2-microglobulin levels were not (1) related to gestational age; low beta 2-microglobulin values occurred at all gestational ages for both healthy and sick infants; (2) a consequence of urine flow rate; urinary beta 2-microglobulin did not correlate with urinary creatinine concentration or with urine to plasma creatinine ratio; and (3) a consequence of increased production of beta 2-microglobulin; urinary and serum beta 2-microglobulin values did not correlate (r = .03). Thus, we propose that the elevated levels of urinary beta 2-microglobulin in the sick infants were the consequence of tubular injury. This was associated with hematuria but not with a high incidence of azotemia or oliguria.(ABSTRACT TRUNCATED AT 250 WORDS)

Renal injury in the asphyxiated newborn infant: relationship to neurologic outcome.

The relationship of renal and central nervous system injury was prospectively evaluated in 120 asphyxiated infants. Renal evaluation findings were considered abnormal if there was oliguria (urine output less than 1 ml/kg/hr), which was designated transient if present in the first 24 hours only and persistent if present for at least 36 hours, or if the urinary beta 2-microglobulin concentration from first-void urine was elevated: (1) Thirteen infants had persistent oliguria; the urinary beta 2-microglobulin level was elevated in all. The six term infants had clinical signs consistent with hypoxic-ischemic encephalopathy (HIE); all six had ultrasonographic abnormalities. The outcome was poor (i.e., death or long-term neurologic deficits) in five of six infants. The seven preterm infants with persistent oliguria had clinical evidence of HIE, and three infants had intraventricular hemorrhage; all seven infants died. (2) Fifteen infants had transient oliguria (beta 2-microglobulin level was elevated in eight infants). Two of the eight term infants had evidence for HIE; the cranial ultrasound scan was normal in all. At follow-up, seven term infants are normal and one is abnormal. Six of the seven preterm infants with transient oliguria had clinical evidence of HIE; three infants had intraventricular hemorrhage. Three infants died, and the four survivors are normal at follow-up. (3) Ninety-two infants had normal urine output. Of the 22 term infants, two developed signs of HIE, and the ultrasound scan was abnormal in three infants. Of the 70 preterm infants, eight (11%) had clinical signs consistent with HIE, the ultrasound scan was abnormal in 20 of 64 (31%) infants scanned, and 14 (20%) infants died. Most of the followed infants are normal. Thus oliguria was significantly associated with clinical signs of HIE, including seizures, death (specifically in the premature infant), and long-term neurologic deficits. These data suggest that oliguria in the perinatal period is a sensitive indicator of infants at risk for long-term neurologic deficits.

Renal failure in sick hypertensive premature infants receiving captopril therapy.

A retrospective study of nine sick premature infants with chronic lung disease who received captopril for control of systemic hypertension (systolic blood pressure (BP) greater than 113 mm Hg) was carried out to determine efficacy of therapy and associated complications. All nine infants had markedly elevated peripheral renin values, 134.3 +/- 128.1 ng/mL/hr (mean +/- SD). Five infants had abnormal renal sonographic and perfusion scans with evidence of renal artery thrombosis, parenchymal disease, or both. Captopril therapy (0.3 mg/kg) was instituted at a postnatal age of 123 +/- 108 days. After the initial dose, the systolic BP decreased significantly in all infants, the decrease ranging from 21% to 58% of the pretreatment value. Dosage was subsequently halved in all infants. Seventeen episodes of unpredictable decreases in BP more than 40% from baseline occurred during the reduced maintenance therapy. Four infants had a total of seven episodes during which the BP decreased by 57 +/- 10% from baseline; this decrease persisted for 17 +/- 6 hours and was unresponsive to volume reexpansion and inotropic therapy. All seven episodes were accompanied by oliguria (urine output less than 1 mL/kg/hr) that persisted for 18 +/- 12 hours. These episodes were accompanied by neurologic signs (subtle seizures, lethargy, and/or apnea) within 18 +/- 6 hours after the onset of oliguria. The remaining five infants had a total of 13 episodes of decreased BP of 50 +/- 8% of baseline, which were of significantly shorter duration and responded to volume reexpanders, inotropic therapy, or both and were unaccompanied by oliguria. These data suggest the need for close observation of BP in infants receiving maintenance captopril therapy.

Sonography of focal foveolar hyperplasia causing gastric obstruction in an infant.

A young infant is presented with a mass partially obstructing the distal stomach. Sonography demonstrated the superficial origin of the lobulated lesion which proved to be focal foveolar hyperplasia, the most common cause of a gastric polypoid mass in adults but rare in children.

Pyloric stenosis in the sick premature infant. Clinical and radiological findings.

The clinical and radiographic features of five sick premature infants with idiopathic hypertrophic pyloric stenosis are presented. Clinical features were nonspecific, the common findings being recurrent nonbilious emesis, persistent abdominal distention, and the inability to place a nasojejunal feeding tube through the pylorus. Plain abdominal radiographs demonstrated persistent gastric dilatation in four of the infants. Idiopathic hypertrophic pyloric stenosis should be considered in the differential diagnosis of premature infants with upper gastrointestinal tract symptoms.

Acute systemic organ injury in term infants after asphyxia.

The systemic manifestations of "asphyxia" were evaluated prospectively in 35 consecutively intubated term newborn infants. The following systemic organ injuries were identified most often: (1) renal, ie, oliguria less than 1 mL/kg per hour for at lest 24 hours (40%), an elevated urinary beta-2-microglobulin concentration (57%), azotemia (11%), and an elevated serum creatinine level (17%); (2) central nervous system, ie, hypoxic-ischemic encephalopathy (including seizures) (31%) or an abnormal cranial ultrasound scan, ie, diffuse parenchymal echogenicity, slitlike ventricles, and poor visualization of the sulci, and/or intracranial hemorrhage (26%); (3) cardiovascular, ie, an abnormal echocardiogram (25%) or abnormal electrocardiogram (11%); (4) pulmonary complications, including persistent pulmonary hypertension (23%); and (5) gastrointestinal complications, which were rare. Traditional markers of fetal distress were not related to the frequency and/or distribution of systemic organ injury. An important implication of this study relates to the recognition of the extent and distribution of organ injury in the "asphyxiated" infant.

Sonographically detectable cysts in polycystic kidney disease in newborn and young infants.

Autosomal dominant (adult type) and autosomal recessive (infantile type) polycystic kidney disease are 2 distinct forms of hereditary cystic renal disease with differing pathologic and clinical features. Glomerulocystic kidney disease is probably a separate entity, whose pathologic features may closely resemble those of autosomal dominant polycystic kidney disease, especially in small infants. An example of each of these conditions in a small infant is presented, all of which had sonographically detectable cysts. Pathologic correlation was available in each case. While there are typical sonographic features of autosomal dominant and autosomal recessive polycystic kidney disease in newborn and young infants, there is no specific appearance of either condition, and glomerulocystic kidney disease can apparently resemble either one. Other investigations, particularly family studies and pathologic verification, are important in order to establish the correct diagnosis.