|Year : 1997 | Volume
| Issue : 3 | Page : 260-268
|Acute Renal Failure in the Neonate
Robert L Chevalier
Department of Pediatrics, University of Virginia, School of Medicine, Charlottesville, Virginia, USA
Click here for correspondence address and email
|How to cite this article:|
Chevalier RL. Acute Renal Failure in the Neonate. Saudi J Kidney Dis Transpl 1997;8:260-8
| Introduction|| |
The clinical spectrum of acute renal failure (ARF) in the neonate differs markedly from that in older children and adults. This results from the fact that the nature of renal injury is dependent on the level of renal maturation; many cases of neonatal ARF are the consequence of intra-uterine or perinatal events.
In view of the patient's short life at the time of diagnosis, the distinction between acute and chronic renal failure is essentially a moot point, and for the purposes of this review, the term ARF will be used to denote conditions from which an infant may either recover or which may progress to chronic renal insufficiency and renal failure in later life.
| Diagnosis|| |
Neonatal ARF can be defined as a rise in serum creatinine concentration greater than 88 µmol/L in the face of normal maternal renal function  . While a rise in creatinine may occur in non-oliguric ARF, oliguria in the neonate is defined as urine flow less than 1 ml/kg/hr after the first day of life  . It should be noted that this is a physiologic definition. The neonate is unable to concentrate urine above 500 rnOsm/kg, and the usual osmotic intake through breast milk or formula feeds lies between 7 and 15 mOsm/ kg/day  . The minimal volume of water necessary to maintain solute balance in the neonate therefore calculates to approximately 1 ml/kg/hr. In a study of the time of first urine voiding by neonates, Clark found that each of 500 normal neonates voided within the first 24 hours of life regardless of gestational age  . Based on this data, any infant failing to void beyond the first day of life should be suspected of having renal insufficiency. Since the neonatal bladder is an abdominal rather than a pelvic organ, examination of the abdomen may reveal a distended bladder resulting from bladder outlet obstruction.
Estimation of glomerular filtration rate (GFR) is difficult in neonates: obtaining accurately timed urine samples is problematic, particularly in females; there is a lack of a steady state resulting from the transition from intra-uterine to extra-uterine life; and plasma creatinine measurements are less reliable in the low concentrations present in small infants. The plasma creatinine concentration remains the most generally available index of GFR in the neonate, and should be less than 130 µmol/L throughout the first two months in the pre-term infant, and less than 90 µmoI/L in the term infant. A progressive rise in the plasma creatinine concentration suggests a falling GFR regardless of the urine output.
With the exception of urine flow rate, signs suggestive of ARF in the neonate are relatively non-specific, and include lethargy, pallor, vomiting, poor feeding, and convulsions. A number of these signs may also be present in infants with septicemia, or congenital heart disease. Edema may be present as a result of Rh isoimmunization or fetal supraventricular tachycardia. Renal causes of edema include bilateral obstructive nephropathy and congenital nephrotic syndrome.
Hypertensive infants who do not have evidence for volume overload may have renin-dependent hypertension as a result of embolization from an indwelling umbilical artery catheter  . Aortic coarctation, intracranial hemorrhage, autosomal recessive poly cystic kidney disease, and congenital adrenal hyperplasia are other causes of hypertension in the newborn. Systolic blood pressure in term infants should be less than 90 mm Hg in the first week of life, and less than 110 mm Hg in the second month. In pre-term infants, systolic pressure should be less than 70 mm Hg in the first week and less than 90 mm Hg in the second month.
| Etiology|| |
The etiology of neonatal ARF may be divided into three broad categories [Table - 1]. The majority (Group I) present with asphyxia or circulatory disorders which may be further subdivided into pre-renal (dehydration, congestive heart failure, or congenital nephrotic syndrome), and parenchymal (asphyxia, septicemia, disseminated intravascular coagulation, and renal thrombosis/ necrosis). Studies in experimental animals suggest that the immature kidney is actually more resistant to anoxia than that of the adult  . It is of prime importance to distinguish cases of pre-renal from parenchymal ARF, as treatment differs markedly.
Fractional Excretion of Sodium (FE Na )
Infants with pre-renal ARF can be most easily identified by calculation of the fractional excretion of sodium (FE Na ) on a random urine specimen obtained prior to the administration of diuretics. The urine sample can be obtained by an in-and-out catheter, obtained concurrent with a blood sample for sodium and creatinine concentration. The FE Na is calculated according to the following formula:
FE Na = (U Na X P Cr )/(P Na X Ucr).
Since infants greater than 30 weeks gestational age with pre-renal ARF are expected to retain sodium, the FE Na should be less than 3% in the face of oliguria  . If the FEN a is low and there is no evidence of edema or congestive heart failure, urine output may be increased by infusion of normal saline, 20 ml/kg. Very low birth weight pre-term infants (less than 30 weeks gestational age), may not be able to reduce the FE Na below 3% even in the face of volume contraction  . Moreover, very low-birth weight infants are at higher risk for intraventricular hemorrhage as a result of rapid volume expansion. Oliguric infants with FENa greater than 3% should have fluid restricted to replace insensible losses and any urinary or extrarenal fluid losses.
Renal Vein Thrombosis
Renal vascular resistance is normally increased in the neonate compared to the older child. This may contribute to the risk of renal vascular thrombosis. Renal venous thrombosis typically presents in an infant with oliguria, gross hematuria, enlarged kidney, and an acute decrease in the hematocrit and platelet count. Factors predisposing to the development of renal venous thrombosis include asphyxia, cyanotic congenital heart disease, and radiographic contrast nephropathy. Renal ultrasonography reveals kidney enlargement, increase in echo texture, and reduced blood flow by Doppler measurement. Supportive treatment generally suffices if involvement is unilateral, but if bilateral, heparin can be infused until the platelet count and clotting studies have normalized  .
Renal necrosis may result from severe renal ischemia, usually in desperately ill infants with septicemia and disseminated intravascular coagulation. The areas of necrosis can be patchy, leaving areas of intrarenal calcification that may become apparent later in life. Severe hypertension may be treated with nifedipine or clonidine. As discussed below, the use of angiotensin-converting enzyme inhibitors (e.g., captopril, enalapril) may further decrease GFR.
| Congenital Malformations and Cystic Kidney Disease|| |
The second major category of neonatal ARF comprises congenital malformations and cystic renal disease (Group II) [Table - 1]. There are scattered reports of neonates presenting with ARF who have no obvious renal anomalies, but may have a delay or an arrest in renal maturation which impairs GFR , . These are likely to be the result of intra-uterine insults which have not been identified , . Hypoplasia, dysplasia, obstructive nephropathy, and cystic kidney disease may all result in decreased GFR inthe neonatal period. Renal ultrasonography should be performed promptly in any neonate with a palpable abdominal mass or a suspected renal anomaly. The ultrasound can reveal renal size, position, echotexture, location of cysts, and presence of hydronephrosis. Normograms showing the expected kidney size for infants of varying gestational age have been published  . Cysts smaller than 5 mm in diameter may not be picked up by sonography, but increased echotexture is consistent with numerous small cysts. The relative distribution of kidney function between the two sides can be determined by renal scintigraphy using 99m Tc-mercaptoacetyltriglycine (MAG-3) (followed by furosemide injection if there is any evidence of obstruction). Infants with prompt uptake of nuclide during the initial period of renal insufficiency are likely to recover, whereas those without detectable uptake are more likely to have irreversible renal damage  . An infant maintained on peritoneal dialysis for longer than six to eight weeks should undergo open renal biopsy if the diagnosis or prognosis remains unclear.
In some cases, it may be beneficial to search for renal anomalies if abnormalities are present in other organs. Conditions resulting in severe prolonged intra-uterine oliguria can result in the "Potter facies", which includes large, flat ears, infraorbital skin folds sweeping laterally from the inner canthus, and a flat nasal profile  . This appearance may be seen as a result of bilateral renal agenesis, or any severe bilateral renal malformation causing oliguria (such as hypoplasia, dysplasia, or bilateral cystic disease). While pulmonary hypoplasia is also a feature of Potter Syndrome, pneumothorax may result from less severe renal maldevelopment. In view of the close association between malformations of the pinna and renal anomalies, infants with significant malformations of the ears should undergo screening renal ultrasonography  .
A palpable abdominal mass in the newborn is most likely due to renal enlargement. Possibilities include obstructive nephropathy, cystic kidney disease, renal thrombosis, or tumor. The finding of hypoplastic abdominal musculature ("prune belly", triad syndrome,or Eagle Barrett Syndrome) is associated with abnormal renal development. It should be noted that cryptorchidism is associated with underlying renal anomalies even in the absence of abdominal wall defects  .
The constellation of vertebral defects, imperforate anus, tracheo-esophageal fistula, and radial dysplasia makes the VATER association. Because renal anomalies are also present in a large fraction of reported cases, such patients should all undergo renal ultrasonography and voiding cystourethrography. Myelomeningocele is also associated with neurogenic bladder of variable severity, which can lead to reflux nephropathy and progressive renal insufficiency. Additional anomalies associated with renal maldevelopment include supernumerary nipples, scoliosis. and single umbilical artery. Although the relationship between these abnormalities and renal maldevelopment is less tight than the aforementioned entities, a screening renal ultrasound should be performed in all such infants. It should be noted also that a number of dysmorphic findings may also be consistent with a chromosomal defect. Down's syndrome is associated with hydronephrosis, while Turner's Syndrome is associated with horseshoe kidney or duplicated collecting system  . For these reasons, all affected infants should undergo screening renal ultrasonography.
Obstructive nephropathy should be suspected in any infant found to have hydronephrosis by prenatal or post-natal ultrasonography. To rule out the presence of vesicoureteral reflux or posterior urethral valves, these infants must undergo voiding cystourethrography. Furosemide scintigraphy should also be performed to determine the presence and location of functional obstruction.
Cystic Kidney Disease
Cystic kidney disease is also generally identified by ultrasonography. It is important to distinguish multicystic dysplastic kidney from autosomal recessive or autosomal dominant polycystic kidney disease. The former is often unilateral, in which case sonography and voiding cystourethrography are important in ruling out an abnormality of the opposite kidney. Ureteropelvic junction obstruction or vesicoureteral reflux are frequently seen in the opposite kidney. Autosomal recessive polycystic kidney disease is often associated with severe hypertension and hepatic dysfunction. Although autosomal dominant polycystic kidney generally does not become apparent until the second and third decades of life, it may present in the pre-term neonate  .
| Toxic Nephropathy|| |
The third broad group of causes of ARF in the neonate includes drugs which interfere with the structural development or physiologic function of the fetal or neonatal kidney (Group III) [Table - 1]. There are two categories of compounds which have been shown recently to interfere both with renal development and with neonatal renal function: angiotensin converting enzyme inhibitors (ACEI), and non-steroidal antiinflammatory drugs (NSAID).
Angiotensin Converting Enzyme Inhibitors
The potential hazards of human fetal exposure to ACEI were first identified in the early 1980's with reports of oligohydramnios and post-natal oliguric acute renal failure in infants exposed to these agents during late pregnancy  . However, recognition of ACEI fetopathy did not evolve until the last several years  . At this time over 50 cases have been reported showing the characteristics of fetal anuria and oligohydramnios, intra-uterine growth retardation, and hypocalvaria. Postnatally, these infants have severe hypotension and oliguria, and mortality may be as high as 25%  . Renal histologic changes include immature glomeruli and tubular dilatation. Prolonged treatment of neonatal rats (in which glomerular development is analogous to that of mid-trimester humans) with an angiotensin receptor inhibitor resulted in abnormalities of the renal vasculature and tubules which are very similar to those in the human  .-In fact, the addition of enalapril (an ACEI) to water containing tadpoles causes similar abnormalities in the kidneys of these amphibians when they have metamorphosed to frogs  . These results highlight the importance of angiotensin II as a growth factor in the developing kidney, and indicate that ACEI should never be used during pregnancy. Moreover,, the administration of ACEI to neonates can result in profound hypotension, anuria, and may even precipitate ARF. The reason for this as shown in [Figure - 1] is that GFR in the neonate is dependent upon maintenance of glomerular capillary pressure by a preponderance of efferent arteriolar constriction maintained by angiotensin II. Efferent arteriolar dilatation resulting from ACEI lowers the pressure necessary for filtration and therefore results in oliguria. Doses of captopril or enalapril used in the neonate must therefore be reduced by tenfold compared to those used in older children or adults.
Nonsteroidal Anti-inflammatory Drugs
The first reports of fetal renal abnormalities resulting from exposure to NSAID were also made in the early 1980's  . Within the last several years, over 13 cases had been reported, with fetal oliguria and anuria, gastric or ileal perforation, and severe renal insufficiency in the neonatal period. In one series of fetuses exposed to indomethacin during pregnancy, it was estimated that over 20% of the infants developed at least transient renal insufficiency post-natally  . Histologically, these infants have tubular and glomerular dilatation and interstitial fibrosis  . As with the effect of ACEI, a cellular mechanism for the toxicity of NSAIDs has emerged from experimental studies. Disruption of the prostaglandin synthase II gene in mice results in abnormal kidney development, including glomerulosclerosis, tubular atrophy, and interstitial fibrosis  . It is therefore important to minimize the dose of NSAID in pregnancy, and to monitor closely the volume of amniotic fluid. As indomethacin is commonly used in the post-natal period to close a patent ductus arteriosus, the vasoconstrictor effects of this compound must also be appreciated  . As shown in [Figure - 1], interference with endogenous renal prostaglandin production will increase angiotensin II-dependent vasoconstriction, leading to reduced GFR and renal insufficiency. It is therefore important to monitor closely renal function in pre-term infants receiving indomethacin.
Antibiotics and Furosemide
Blood levels of aminoglycosides and amphotericin should be monitored carefully in neonates to avoid nephrotoxicity. Long-term use of furosemide, especially when combined with administration of prednisone for treatment of bronchopulmonary dysplasia, may contribute to nephrocalcinosis and nephrolithiasis  . This in turn, may lead to renal insufficiency in later life , .
| Treatment|| |
The treatment of ARF in the neonate is generally supportive, including first the treatment of suspected infection with broad spectrum antibiotics, the maintenance of tissue perfusion with appropriate volume expansion or colloids, provision of adequate oxygenation by intensive cardiopulmonary support, and attention to acid-base and electrolyte balance. Successful management of the infant with ARF results from careful attention to detail.
One of the most useful parameters to follow is the body weight. This should be measured accurately at least every 12 hours, as trends in body weight should be correlated with calculated intake and output data. Fluid replacement for insensible losses is approximately 0.5 to 1 ml/kg/hr for term infants, but must be reassessed every day  . The rate of insensible loss for pre-term infants is greater (at least 1.5 ml/kg/hr for a 1,000 gram infant)  . Insensible losses should be replaced with 10-15% dextrose and water, and the volume required to flush vascular catheters must be included in the daily balance. As with older patients, fluid losses as urine, gastrointestinal, and surgical drainage, must be replaced with fluids of similar composition.
The arterial pH should be maintained above 7.2 by appropriate ventilation and infusion of sodium bicarbonate. In the face of inadequate GFR, severe metabolic acidosis may result in hypernatremia, hypertension, and possible intracranial hemorrhage. Inability to correct severe metabolic acidosis is one of the most frequent indications for beginning peritoneal dialysis or continuous veno-venous hemofiltration in the critically ill neonate with ARF.
If the patient has established ARF, hyponatremia generally reflects overhydration. However, adrenal insufficiency should be suspected if severe hyperkalemia accompanies hyponatremia in the face of a modest increase in serum creatinine concentration. If the patient is clearly volume contracted, and there is no evidence of cardiac insufficiency, 20 ml/kg volume expansion should result in improvement. If the infant is manifesting seizure activity in the face of hyponatremia, 3% sodium chloride solution can be infused to raise the serum sodium above 125 mmol/L. A dose of sodium (mmol) equivalent to three times the infant's weight (kg), is expected to raise the serum sodium by 5 mmol/L.
Hyperkalemia is better tolerated in the neonate compared to the older child or adult. If there is electrocardiographic evidence of hyperkalemia (peaked t waves), 10% calcium gluconate solution, 1 ml/kg, should be infused over several minutes with continuous electrocardiographic monitoring. Sodium bicarbonate solution, 2 mmol/kg, should also be infused, followed by 25% glucose solution at 2 ml/kg/hr. Salbutamol has been used to acutely reduce plasma potassium concentration in infants and children  . A cation exchange resin, Kayexalate (1 g/kg in 4 ml/kg 10% sorbitol) can be administered as a retention enema. Caution should be exercised in the use of Kayexalate in the neonate, as the resin may cause bowel obstruction and perforation  . Exchange transfusion with low potassium washed red blood cells reconstituted with fresh frozen plasma may also be an effective means to remove potassium and possibly eliminate the need for dialysis or hemofiltration.
As with older patients. ARF may result in hypocalcemia- Infants should receive a formula with a high calcium to phosphorus ratio and low potassium content. Calcium carbonate may be administered orally to maintain plasma phosphorus in the normal range. Both calcium and phosphorus must be monitored closely, however, as infants are prone to develop hypercalcemia even without vitamin D supplementation. Aluminum-containing phosphate binding compounds should never be used in the neonate due to the enhanced toxic effects of aluminum on the developing central nervous system and skeleton. Infants with prolonged renal failure generally require aggressive nutritional supplementation with tube feeding or parenteral nutrition.
The treatment of severe hypertension in the neonate with ARF should be aggressive, because these patients are particularly prone to ventricular hemorrhage. If hypertension is due to volume overload, hemofiltration is generally the most rapid and effective means to remove the excess fluid. Renal ischemic injury may result in renindependent hypertension, in which case an ACEI may be most effective. As indicated above, however, the dose of captopril should be no more than 0.1 mg/kg/day with very careful monitoring of the patient's creatinine and urine output. Prolonged hypertension can be managed in the neonate with a clonidine patch. Although the lowest dose commercially available is 0.1 nig (100 /.tg) per day, the area of exposure to the skin may be partially covered to reduce the daily dose to 5-25 //g/kg/day.
If renal failure is prolonged, or if volume overload or acidosis become intractable, the decision must be made to initiate dialysis.
Peritoneal dialysis is generally highly effective in the neonate , , but because temporary peritoneal catheters are subject to leakage and bacterial and fungal invasion, a neonatal single cuff Tenckhoff silastic catheter should be surgically placed even if it is to be used for only several days. Due to the higher permeability of the neonatal peritoneal membrane, dwell times should never exceed 1 hour. In addition, critically ill infants unable to metabolize acetate or lactate in commercial dialysate, may need to be dialyzed with a specially prepared solution using sodium bicarbonate as the source of alkali. Continuous veno-venous hemofiltration is particularly useful in infants with ARF, and may eventually supplant peritoneal dialysis as a preferred treatment for these patients  .
| Long-Term Outlook|| |
Mortality from neonatal oliguric ARF exceeds 50%, and is higher for infants with congenital heart disease or major renal anomalies  . Death results generally from non-renal causes, and is related to the extent of multiple organ failure. Prognosis is better for non-oliguric ARF, although GFR may be persistently reduced , . Renal uptake of nuclide by scintigraphy is also associated with better prognosis  . In survivors of oliguric ARF, GFR is decreased in up to 40% of cases in Groups I and III, but in nearly 90% in those with Group II  . Multiple tubular defects may persist after recovery, leading to acidosis, rickets, and somatic growth retardation  . Cortical atrophy or papillary necrosis can impair long-term renal growth, which may be confused with congenital hypoplasia/dysplasia if the antecedent history of ARF is not recognized  .
| Conclusion|| |
The etiology of neonatal ARF is changing due to pre-natal diagnosis of congenital abnormalities, the survival of less mature pre-term infants, and the development of new drugs affecting the fetus or neonate  . The prognosis for survivors of neonatal ARF depends on the stage of renal maturation as well as the nature of the insult. The diagnostic approach to the neonate with suspected ARF should include careful physical examination, and laboratory and radiologic investigations to define the most likely etiology. Successful clinical management requires strict attention to detail, and appropriate use of peritoneal dialysis or hemofiltration when necessary. Long-term follow up should include monitoring of blood pressure, GFR, and renal and somatic growth. Prospective multicenter studies of infants with ARF will be required to improve management in the future.
| Acknowledgments|| |
The author's research was supported in part by National Institutes of Health Research Center of Excellence in Pediatric Nephrology and Urology, DK44756; NIH O'Brien Center of Excellence in Nephrology and Urology, DK45179; and NIH Child Health Research Center, HD 28810.
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Robert L Chevalier
Department of Pediatrics, University of Virginia, School of Medicine, Charlottesville, Virginia
[Figure - 1]
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