RENAL DISORDERS IN THE NEWBORN INFANT
Saturday, August 16, 2008
Renal function depends on postconceptional age. The glomerular filtration rate (GFR) is 20 mL/ min/1.73 m2 in term neonates and 10–13 mL/min/ 1.73 m2 in infants born at 28–30 weeks’ gestation. The velocity of maturation after birth is also dependent on postconceptional age. Creatinine can be used as a clinical marker of GFR. Values in the first month of life are shown in Table 1–27. Creatinine at birth reflects the maternal level and should decrease slowly over the first 3–4 weeks. An increasing serum creatinine is never normal. The ability to concentrate urine and retain sodium is also dependent on gestational age. Infants born at less than 28–30 weeks’ gestation are compromised in this respect and if not observed carefully can become dehydrated and hyponatremic. Preterm infants also have an increased bicarbonate excretion and a low tubular maximum for glucose (approximately 120 mg/dL).
RENAL FAILURE
Renal failure is most commonly seen in the setting of birth asphyxia, hypovolemia, or shock from any cause. The normal rate of urine flow is 1–3 mL/kg/h. After a hypoxic or ischemic insult, acute tubular necrosis may ensue. Typically, there are 2–3 days of anuria or oliguria associated with hematuria, proteinuria, and a rise in serum creatinine. The period of anuria or oliguria is followed by a period of polyuria and then gradual recovery. During the polyuric phase, excessive urine sodium and bicarbonate losses may be seen.
The initial step in management is restoration of the infant’s volume status as needed. Thereafter, restriction of fluids to insensible water loss (40–60 mL/ kg/d) without added electrolytes, plus milliliter-for-milliliter urine replacement, should be instituted. Serum and urine electrolytes and body weights should be followed frequently. These measures should be continued through the polyuric phase. After urine output has been reestablished, urine replacement should be decreased to between 0.5 and 0.75 mL for each milliliter of urine output to see if the infant has regained normal function. If that is the case, the infant can be returned to maintenance fluids.
Finally, many of these infants experience fluid overload and should be allowed to lose enough water through urination to return to birth weight. Hyperkalemia, which may become life-threatening, may occur in this situation despite the lack of added intravenous potassium. If the serum potassium reaches 7–7.5 mEq/L, therapy should be started with glucose and insulin infusion, giving 1 unit of insulin for every 3 g of glucose administered, plus binding resins. Calcium gluconate (100 mg/kg bolus) can also be helpful for arrhythmia resulting from hyperkalemia.
Peritoneal dialysis is occasionally needed for the management of neonatal acute renal failure.
URINARY TRACT ANOMALIES
Abdominal masses in the newborn are most frequently caused by renal enlargement. Most common is a multicystic or dysplastic kidney; congenital hydronephrosis is second in frequency. Chromosomal abnormalities and syndromes with multiple anomalies frequently include renal abnormalities. An ultrasound examination is the first step in diagnosis. In pregnancies associated with oligohydramnios, renal agenesis or obstruction secondary to posterior urethral valves should be considered. Only bilateral disease or disease in a solitary kidney is associated with oligohydramnios, significant morbidity, and death. Such infants will generally also have pulmonary hypoplasia and die from pulmonary rather than renal insufficiency.
Prenatal ultrasonography identifies infants with renal anomalies (most often hydronephrosis) prior to birth. Postnatal evaluation of these infants should include renal ultrasound and a voiding cystourethrogram at about 1 week of age. Until genitourinary reflux is ruled out, these infants should receive antibiotic prophylaxis with low-dose penicillin or ampicillin.
RENAL VEIN THROMBOSIS
Renal vein thrombosis occurs most often in IDMs and in the context of dehydration and polycythemia. Of particular concern is the IDM who is also polycythemic. If fetal distress is superimposed on these problems, prompt reduction in blood viscosity is indicated. Thrombosis usually begins in intrarenal venules and can extend into larger veins. Clinically, there may be an enlarged kidney, with blood and protein in the urine. With bilateral renal vein thrombosis, anuria ensues. Diagnosis can be confirmed with an ultrasound examination that includes Doppler flow studies of the kidneys. Treatment involves correcting the predisposing condition and systemic heparinization for the thrombosis. Use of thrombolytics for this condition is controversial. Prognosis for a full recovery is uncertain. Some infants will go on to develop significant atrophy of the affected kidney and systemic hypertension.
RENAL FAILURE
Renal failure is most commonly seen in the setting of birth asphyxia, hypovolemia, or shock from any cause. The normal rate of urine flow is 1–3 mL/kg/h. After a hypoxic or ischemic insult, acute tubular necrosis may ensue. Typically, there are 2–3 days of anuria or oliguria associated with hematuria, proteinuria, and a rise in serum creatinine. The period of anuria or oliguria is followed by a period of polyuria and then gradual recovery. During the polyuric phase, excessive urine sodium and bicarbonate losses may be seen.
The initial step in management is restoration of the infant’s volume status as needed. Thereafter, restriction of fluids to insensible water loss (40–60 mL/ kg/d) without added electrolytes, plus milliliter-for-milliliter urine replacement, should be instituted. Serum and urine electrolytes and body weights should be followed frequently. These measures should be continued through the polyuric phase. After urine output has been reestablished, urine replacement should be decreased to between 0.5 and 0.75 mL for each milliliter of urine output to see if the infant has regained normal function. If that is the case, the infant can be returned to maintenance fluids.
Finally, many of these infants experience fluid overload and should be allowed to lose enough water through urination to return to birth weight. Hyperkalemia, which may become life-threatening, may occur in this situation despite the lack of added intravenous potassium. If the serum potassium reaches 7–7.5 mEq/L, therapy should be started with glucose and insulin infusion, giving 1 unit of insulin for every 3 g of glucose administered, plus binding resins. Calcium gluconate (100 mg/kg bolus) can also be helpful for arrhythmia resulting from hyperkalemia.
Peritoneal dialysis is occasionally needed for the management of neonatal acute renal failure.
URINARY TRACT ANOMALIES
Abdominal masses in the newborn are most frequently caused by renal enlargement. Most common is a multicystic or dysplastic kidney; congenital hydronephrosis is second in frequency. Chromosomal abnormalities and syndromes with multiple anomalies frequently include renal abnormalities. An ultrasound examination is the first step in diagnosis. In pregnancies associated with oligohydramnios, renal agenesis or obstruction secondary to posterior urethral valves should be considered. Only bilateral disease or disease in a solitary kidney is associated with oligohydramnios, significant morbidity, and death. Such infants will generally also have pulmonary hypoplasia and die from pulmonary rather than renal insufficiency.
Prenatal ultrasonography identifies infants with renal anomalies (most often hydronephrosis) prior to birth. Postnatal evaluation of these infants should include renal ultrasound and a voiding cystourethrogram at about 1 week of age. Until genitourinary reflux is ruled out, these infants should receive antibiotic prophylaxis with low-dose penicillin or ampicillin.
RENAL VEIN THROMBOSIS
Renal vein thrombosis occurs most often in IDMs and in the context of dehydration and polycythemia. Of particular concern is the IDM who is also polycythemic. If fetal distress is superimposed on these problems, prompt reduction in blood viscosity is indicated. Thrombosis usually begins in intrarenal venules and can extend into larger veins. Clinically, there may be an enlarged kidney, with blood and protein in the urine. With bilateral renal vein thrombosis, anuria ensues. Diagnosis can be confirmed with an ultrasound examination that includes Doppler flow studies of the kidneys. Treatment involves correcting the predisposing condition and systemic heparinization for the thrombosis. Use of thrombolytics for this condition is controversial. Prognosis for a full recovery is uncertain. Some infants will go on to develop significant atrophy of the affected kidney and systemic hypertension.
1 comments:
Good post!
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