Pediatric Annals

CME 

Acute Renal Failure in the Neonate

Owais A. Khan, MD, MPH; Joseph R. Hageman, MD; Christopher Clardy, MD

Abstract

Acute renal failure (ARF) in a neonate is a serious condition that impacts 8% to 24% of hospitalized neonates. There is a need for prompt evaluation and treatment to avoid additional complications. In this review, a neonate was found to have renal failure associated with renal vein thrombosis. There are varying etiologies of ARF. Causes of ARF are typically divided into three subsets: pre-renal, renal or intrinsic, and post-renal. Treatment of ARF varies based on the cause. Renal vein thrombosis is an interesting cause of renal or intrinsic ARF and can be serious, often leading to a need for dialysis. [Pediatr Ann. 2015;44(10):e251–e253.]

Abstract

Acute renal failure (ARF) in a neonate is a serious condition that impacts 8% to 24% of hospitalized neonates. There is a need for prompt evaluation and treatment to avoid additional complications. In this review, a neonate was found to have renal failure associated with renal vein thrombosis. There are varying etiologies of ARF. Causes of ARF are typically divided into three subsets: pre-renal, renal or intrinsic, and post-renal. Treatment of ARF varies based on the cause. Renal vein thrombosis is an interesting cause of renal or intrinsic ARF and can be serious, often leading to a need for dialysis. [Pediatr Ann. 2015;44(10):e251–e253.]

An infant was born at approximately 33 weeks gestation to a 28-year-old mother via emergency Cesarean delivery. Maternal history was significant for gestational hypertension, which was controlled with labetalol. On the day of delivery, the patient’s mother was involved in a vehicular accident, with concern of direct trauma to the abdomen. The mother presented to labor and delivery with abdominal pain, and was found to have severe range elevated blood pressures and fetal heart tracing was significant for a prolonged deceleration in triage. Maternal serologies were: O positive, hepatitis B negative, rapid plasma reagin negative, rubella immune, HIV negative, and Group B streptococcus unknown.

The mother was taken for a Cesarean delivery and evidence of abruption was present at delivery. At birth, the infant was limp and apneic and required positive pressure ventilation. The infant’s heart rate subsequently decreased when intubation was attempted and required chest compressions as further attempts were made. The newborn was successfully intubated within 20 minutes of the delivery. APGAR (Activity, Pulse, Grimace, Appearance, Respiration) scores were assigned as 1 at 1 minute, 1 at 5 minutes, and 1 at 10 minutes. Cord blood gases were unavailable. The infant’s initial capillary blood gas values were 7.06 pCO2, 50 mm Hg, and base excess of −16. The infant was given an intravenous (IV) normal saline (NS) bolus prior to transfer, and the capillary blood gas values improved to 7.31 pCO2, 30 mm Hg, and base excess of −10 prior to transport.

Neonatal Intensive Care Course and Diagnosis

An umbilical venous catheter was inserted at admission. The infant had poor perfusion and mean arterial blood pressures ranging from 16 to 41 mm Hg. The infant received IV NS boluses and packed red blood cells (PRBCs), and was started on dopamine and hydrocortisone due to the fluctuations in blood pressure readings. The patient had an initial urine output (UOP) of 2.4 mL/kg/h in the first 12 to 24 hours after birth. The UOP subsequently decreased from 0.6 to 0.1 mL/kg/h to 0 mL/kg/h by day 3. Over the same time period, the infant’s creatinine rose from 1.9 to 3.8 mg/dL. The patient was fluid restricted to 60 mL/kg/d. The patient continued to require blood products including PRBCs, fresh frozen plasma, and cryoprecipitate. The fibrinogen was as low as 73 mg/dL. Prothrombin time was 33 seconds, partial thromboplastin time was 84 seconds, and the international normalized ratio was 3.4. Electrolytes and creatinine were closely monitored (Table 1).

Electrolyte Abnormalities

Table 1.

Electrolyte Abnormalities

Renal ultrasound obtained on day 2 was concerning for a clot in the bladder, echogenic, edematous kidneys, and bilateral grade 1 hydronephrosis. These findings were concerning for bilateral renal vein thrombosis. A furosemide drip and chlorthiazide were started per recommendations from the pediatric nephrology department. The patient was also placed on a dopamine IV drip. As the patient’s creatinine continued to rise, a peritoneal catheter was placed by pediatric surgery on day 4. On day 5, the patient’s creatinine was 5.1 mg/dL. The patient subsequently began voiding again on day 5 with UOP levels at 0.3 mL/kg/d and increasing to 2.2 mL/kg/d 4 days later. Therefore, the patient did not require peritoneal dialysis as UOP continued to improve. Dopamine was discontinued and hydrocortisone and chlorthiazide were also weaned. Creatinine peaked at 7.3 mg/dL on day 17. The peritoneal catheter was removed by day 42. At that time, creatinine was 2.6 mg/dL and potassium was 4.4 mEq/L.

Discussion

Acute renal failure (ARF) in a neonate is a serious condition with a rapid onset, decline in glomerular filtration rate, elevation in creatinine, and potential anuria.1 ARF affects approximately 8% to 24% of hospitalized neonates.2 Prompt evaluation and treatment may be needed to avoid additional complications. There are varying etiologies of ARF, which are typically divided into three subsets: pre-renal, renal or intrinsic, and post-renal. In pre-renal pathology, there is renal hypoperfusion with preserved parenchymal integrity. Pre-renal ARF accounts for 55% to 60% of cases. Pre-renal causes include dehydration, decreased cardiac output, hypoalbuminemia leading to decreased intravascular volume, and vasomotor nephropathy.1 Pre-renal ARF is associated with oliguria, low urinary Na (sodium), and highly concentrated urine. Post-renal ARF is less common in neonates and accounts for <5% of the overall cases. Post-renal etiologies are primarily urinary tract obstructive pathologies, which include posterior urethral valves, prune belly syndrome, and bilateral ureteropelvic junction obstruction.1

Renal or intrinsic ARF accounts for 35% to 45% of cases. Renal or intrinsic causes include pyelonephritis, acute tubular necrosis, acute interstitial nephritis, toxic nephropathy, renal artery thrombosis, and renal vein thrombosis. Renal or intrinsic ARF is associated with high urinary Na, normal concentration of urine, and poor response to fluids.1

Our illustrative case of renal vein thrombosis involved an intrinsic cause of ARF. Renal vein thrombosis in the neonate results from a prothrombotic state, which could be caused by perinatal asphyxia, hypovolemia, septicemia, dehydration, polycythemia, congenital heart disease, and central venous catheters.3 Neonates are more susceptible to renal vein thrombosis due to immaturity of the hemostatic system, small vessel diameter, and underlying disease. About 90% of renal vein thrombosis in the neonate is caused by the placement of central venous catheters. Clinical signs of a renal vein thrombosis in the neonate include flank mass, hematuria, thrombocytopenia, and hypertension.3 The gold standard for diagnoses is contrast angiography, but the less invasive, Doppler ultrasonography is more commonly used due to its ease of availability.3

Treatment of ARF varies based on the cause. The goal of pre-renal ARF is to establish renal perfusion usually by increasing intravascular volume. Post-renal ARF is usually resolved by relieving the obstruction. Intrinsic or renal ARF is most often treated medically with diuretics, electrolyte correction, and fluid restriction.2 ARF may also necessitate dialysis in a neonate until the underlying etiology is corrected. Reasons to initiate dialysis include recalcitrant electrolyte abnormalities, worsening uremia, fluid overload, persistent acid-base abnormalities, and need to increase fluid intake to achieve appropriate nutritional goals in an infant with anuria.4 Peritoneal dialysis (PD) is considered the optimal dialysis modality in neonates.4 PD allows for slow removal of fluid and solutes while avoiding hemodynamic instability. Complications of PD dialysis include slower correction of metabolic parameters and risk of peritonitis.4

Conclusion

Our illustrative case involved a neonate with ARF secondary to renal vein thrombosis. ARF may impact up to 24% of hospitalized neonates with most causes being pre-renal. Renal vein thrombosis is an interesting cause of renal or intrinsic ARF and can be serious, often leading to a need for dialysis.

References

  1. Ringer SA. Acute renal failure in the neonate. NeoReviews. 2012;11(5):e243–e251. doi:10.1542/neo.11-5-e243 [CrossRef]
  2. Chua AN, Sarwal MM. Acute renal failure management in the neonate. NeoReviews. 2005;6(8):e369–e376. doi:10.1542/neo.6-8-e369 [CrossRef]
  3. Ramasethu J. Management of vascular thrombosis and spasm in the newborn. NeoReviews. 2005;6(6):e298–e311. doi:10.1542/neo.6-6-e298 [CrossRef]
  4. Lee MM, Chua AN, Yorgin PD. Neonatal peritoneal dialysis. NeoReviews. 2005;6(8):e384–e391. doi:10.1542/neo.6-8-e384 [CrossRef]

Electrolyte Abnormalities

Laboratory Values Day 1 Day 2 Day 3 Day 4 Day 5 Day 6 Day 7 Day 17 Day 42
Sodium (mEq/L) 130 123 122 124 132 137 141 126 144
Potassium (mEq/L) 5.6 6.3 5.2 4.6 3.4 2.8 2.8 3.9 4.4
Chloride (mEq/L) 96 87 81 80 79 81 84 79 105
HCO3 (mEq/L) 18 16 20 21 20 22 22 22 21
Blood urea nitrogen (mg/dL) 9 20 22 32 84 96 101 72 63
Creatinine (mg/dL) 1.9 2.8 3.2 3.8 5.1 5.3 5.7 7.3 2.6
Albumin (g/dL) 2.2 2.4 2.6 3.2 3.3
Aspartate aminotransferase (IU/L) 1,931 1,782 457 56
Alanine aminotransaminase (IU/L) 335 281 122 81
Authors

Owais A. Khan, MD, MPH, is a Fellow in Neonatology. Joseph R. Hageman, MD, is an Emeritus Attending Pediatrician, the Director of Pediatric Resident Research, and a Senior Clinician Educator. Christopher Clardy, MD, is the Section Chief in Pediatric Nephrology and an Associate Professor of Pediatrics. All authors are affiliated with the Pritzker School of Medicine, University of Chicago.

Address correspondence to Owais A. Khan, MD, MPH, Pritzker School of Medicine, University of Chicago, Comer Children’s Hospital, 5841 S. Maryland Avenue, MC 6060, Chicago, IL 60637; email: owais.khan@uchospitals.edu.

The authors have no relevant financial relationships to disclose.

10.3928/00904481-20151012-10

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