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Issue 25, November 2008

Early Health and Neonatal Care

Acute renal failure in the newborn (II): Care and outcome


A. Rakow, MD

Alexander Rakow, MD
Consulting Neonatologist
Division of Neonatology
Astrid Lindgren Children's Hospital at Karolinska University Hospital
Stockholm, Sweden

Correspondence: Alexander Rakow, MD, Division of Neonatology, Astrid Lindgren Children's Hospital, Karolinska University Hospital, Stockholm, Sweden. (E-mail and other contact info can be obtained from CWWJ’s Editor-in-Chief).

Key Words: Renal failure, newborn, neonatal intensive care
Running title: Acute renal failure in the newborn (Part II)

Editor’s note: Information in the material Clinical Window publishes always and solely reflects the author's individual experience and opinions. Please note that Clinical Window's published information is intended only for healthcare professionals, not for the patients. Our purpose and intention is neither to make treatment recommendations, nor to influence patient-physician relationship in any way. Before reading any of our publications, our readers should adapt to our site rules accessible from the Clinical Window Web Journal home page: “About Clinical Window”, “Terms of Use”, and “Privacy Policy”. If you disagree, kindly don’t review our content.

Feedback and suggestions always appreciated, thanks I. Kalli, Editor

 

Clinical Window Web Journal #25: Acute renal failure in the newborn (Part II): Care and outcome (November 2008). ISSN 1795-6269.

 

Management of acute renal failure (ARF)

Pre-renal AFR may respond to fluid therapy

Most newborns admitted to neonatal intensive care units have pre-renal ARF and respond well to fluid therapy. Meticulous attention to fluid balance is essential in all types of ARF. Maintenance fluid is calculated as insensible water loss plus urine output and is adjusted according to clinical assessment of the patient. Remember that insensible water losses are significantly higher in very preterm infants (15-25ml/kg/d in term infants, up to 80ml/kg/d in preterms with birth weight below 1000g [12]). If systemic hypotension develops, despite adequate volume administration, early initiation of dopamine with the subsequent normalization of blood pressure can ensure appropriate renal perfusion [11].

Management of obstruction

Management of obstructive ARF centers around the immediate relief of the obstruction before intrinsic renal failure initiates. Polyuria with severe electrolyte disturbances may occur following the relief of the obstruction, therefore close monitoring of serum electrolytes and appropriate fluid and electrolyte replacement therapy are necessary.

Intrinsic AFR, multidimensional challenge

There is still no accepted specific clinical therapy for intrinsic ARF. Aggressive management of complications of neonatal intrinsic ARF, including fluid overload, hypertension, electrolyte disturbances, nutritional deficiency, metabolic acidosis and sepsis is still the main target. Fluid restriction that limits intake to insensible and gastrointestinal and renal losses is required to avoid fluid overload, which can lead to pulmonary edema, congestive heart failure, hypertension and hyponatremia.

Hyponatremia occurs during intrinsic ARF primarily from excess free water due to fluid overload and frequently in association with increased antidiuretic hormone production. In case of non symptomatic hyponatremia (serum sodium usually between 120-130 mEq/l), further restriction of free water is recommended.

If hyponatremia is symptomatic (lethargy, seizures), sodium replacement can be started according to the formula published by Karlowicz and Adelman [12]. Hypertonic saline should be used very cautiously, and infusion time may need to be more than 2 hours, because the potential complications include congestive heart failure, pulmonary edema, hypertension and intraventricular brain hemorrhage.

Hyperkalemia is a common complication in patients with ARF, regardless of age. This is a medical emergency as it may cause lethal cardiac arrhythmias. Hypocalcemia and hypomagnesemia, both common in ARF, can bring about hyperkalemia [12]. Temporary interventions such as glucose and insulin infusions, intravenous salbutamol or intravenous sodium bicarbonate can shift potassium from the ECF into cells, but these do not eliminate potassium from the body. These measures allow time to prepare for dialysis. Oral/rectal cation-exchange resins, for example calcium polystyrene sulfate (Resonium), are effective in the permanent removal of potassium from the body but may cause complications like bowel obstructions and perforation and should preferably not be used in newborns.

Hyperphosphatemia is a common and frequently overlooked problem in ARF and should be managed by the addition of oral calcium carbonate to feeds. Hyperphosphatemia is usually accompanied by hypocalcemia. If ionized calcium is decreased and the newborn is symptomatic, a weight adjusted dose of calcium gluconate should be infused over 10 to 20 minutes. In non symptomatic infants, calcium should not be given until the plasma phosphate level has been reduced to normal, otherwise ectopic calcification may occur.

Metabolic acidosis can be treated with sodium bicarbonate in a dose sufficient to normalize the plasma pH and bicarbonate levels.


Nutrition considerations

Nutrition is an important consideration in ARF and may be severely limited by the imposed fluid restriction. An inability to meet the baby´s nutritional needs because of fluid restrictions is an indication for dialysis. The nutritional goal in anuric neonates should be to provide about 100 kcal/kg with fat and carbohydrates. About 1-2 g/kg/d of high biologic value protein or an amino acid equivalent should be provided [11].

 

Peritoneal dialysis preferred in newborns

When conservative supportive therapy of acute renal failure is unsuccessful, dialysis should be considered. It should be started when the newborn still is hemodynamically stable, so that morbidity and mortality from ARF can be reduced.

Main indications for dialysis in ARF

  • Volume overload
  • Hyperkalemia
  • Severe metabolic acidosis
  • Hyperphosphatemia / hypocalcemia
  • To make space for nutrition and drug administration
  • Failure to improve with conservative management


Choice of dialysis method

By definition, dialysis means removal of small solutes across a semi permeable membrane by diffusion down their concentration gradient.
In hemodialysis, blood and dialysis fluid are pumped on opposite sides of a synthetic membrane. Peritonium can also be used as a semi permeable membrane, as it can separate blood in the splanchnic capillaries from dialysis fluid within the peritoneal cavity.

Both peritoneal and hemodialysis are possible in infants weighing less than 1 kg [9]. For the newborns, peritoneal dialysis may be preferred over hemodialysis, as the former is similarly effective, probably safer, and technically less demanding [9].

 

Long-term effects

Importance of early treatment

The mortality rate of newborns with ARF caused by congenital malformations or acquired diseases is around 50% [12], but nonoliguric renal failure has a much better prognosis [1]. The long-term effects of neonatal ARF include reduced GFR in cases with excessive nephron losses and tubular dysfunction. GFR remains decreased in approximately 40% of newborns with both acquired oliguric and nonoliguric ARF [1,2].

The earliest possible detection and adequate treatment of acute renal failure in the newborn is of extreme importance. In preterm and or low birth weight infants, kidney growth can already be impaired. Fewer nephrons, coupled with subsequent hyperperfusion and glomerulosclerosis in the remaining nephrons, can cause accelerated ageing and early loss of renal function. These infants, being already at high risk, need the most meticulous care available to prevent long term effects from ARF.

 

References

1. Chevalier RL, Campbell F, Brenbridge AN (1984) Prognostic factors in neonatal acute renal failure. Pediatrics 74: 265-72

2. Stapleton FB, Jones DP, Green RS (1987) Acute renal failure in neonates: incidence, etiology and outcome. Pediatr Nephrol 1: 314-320

3. Gouyon JB, Guignard JP (2000) Management of acute renal failure in newborns. Pediatr Nephrol 14: 1037-1044

4. Guinard JP, Drucker A (1999) Why do newborn infants have a high plasma creatinine? Pediatrics 103: 49

5. Svenningsen NW, Aronson AS (1974) Postnatal development of renal concentration capacity as estimated by DDAVP-test in normal and asphyxiated neonates. Biol Neonate 25: 230-41

6. Norman ME, Assadi FK (1979) A prospective study of acute renal failure in the newborn infant. Pediatrics 63: 475-479

7. Hentschel R, Lodige B, Bullas M (1996) Renal insufficiency in the neonatal period. Clin Nephrol 46: 54-58

8. Guignard J-P, Gillieron P (1997) Effect of modest hypothermia on the immature kidney. Acta Paediatr 86: 1040-1041
9. Haycock GB (2003) Management of acute and chronic renal failure in the newborn Seminars in Neonataology 8: 325-334

10. Shaffer SE, Norman ME (1989) Renal function and renal failure in the newborn. Clin Perinatol 16: 199-218

11. Seri I, Rudas G, Bors ZS (1993) The effect of dopamine on renal function: cerebreal blood flow and plasma cathecholamine levels in sick preterm newborns. Ped Res 34: 742

12. Karlowicz MG, Adelman RD (1992) Acute renal failure in the newborn. Clin Perinatol 19: 139

Clinical Window Web Journal #25: Acute renal failure in the newborn (Part II): Care and outcome (November 2008). ISSN 1795-6269.

© 2006-2008 GE Healthcare Finland Oy doing business as GE Healthcare. All rights reserved. The copyright, any and all trademarks and trade names and other intellectual property rights subsisting in or used in connection with and related to this publication are, unless another owner is specified, the property of GE Healthcare. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording or otherwise, without the prior written permission of GE Healthcare.


Last updated: 30 November 2008
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