Neonatal Acute Kidney Injury: Diagnostic and Therapeutic Challenges

Ashraf Bakr, Riham Eid, Nahla Abdelrahman Allam, Hisham Saleh

Ashraf Bakr, Riham Eid, Paediatric Nephrology Unit, Mansoura University Children’s Hospital, Egypt
Nahla Abdelrahman Allam, Nora centre for pediatric kidney disease and transplant. Soba university hospital. Khartuom sudan.
Hisham Saleh, Neonatology Unit, Mansoura general hospital, Mansoura, Egypt

Conflict-of-interest statement: The author(s) declare(s) that there is no conflict of interest regarding the publication of this paper.

Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

Corresponding Author: Riham Eid, Paediatric Nephrology Unit, Mansoura University Children’s Hospital, Egypt.
Email: rihameid@mans.edu.eg
Telephone: +0020502230376

Received: October 25, 2017
Revised: December 23, 2017
Accepted: December 27, 2017
Published online: March 31, 2018


Acute kidney injury (AKI) affects more than 30% of hospitalized neonates with increased rates of mortality and longer hospital admission. While research in neonatal AKI has increased over the last few years, advances in clinical recognition, diagnosis, and supportive care for AKI in this specific age group, have lagged behind advances in pediatric patient groups. The lack of a standardized definition of AKI in neonates similar to those used in adult and pediatric patients in addition, the unique renal physiology of preterm and term infants create challenges for the use of serum creatinine as an AKI biomarker in these patients creating a challenge in diagnosis, management and even research concerning neonatal AKI. In addition nutrition as a critical item in neonatal care, the special precautions regarding drugs use in neonates and renal replacement therapy in neonates which is not only technically difficult, but also associated with high rates of complications all yields AKI management in neonates to be a great challenge.

Key words: Neonate; Acute kidney injury

© 2017 The Author(s). Published by ACT Publishing Group Ltd. All rights reserved.

Bakr A, Eid R, Allam NA, Saleh H. Neonatal Acute Kidney Injury: Diagnostic and Therapeutic Challenges. Journal of Nephrology Research 2018; 4(1): 130-134 Available from: URL: http: //www.ghrnet.org/index.php/jnr/article/view/2184


The primitive antenatal kidney appears at 3rd week of gestation[1], while the permanent kidney begins to form after the 30th day of gestation[2]. Fetal kidneys produce diluted urine forming a significant proportion of amniotic fluid[3]. Fetal urine output (UOP) rises from 15 ml/kg/ hr to 50 ml/kg/hr at 40 weeks of gestation[4]. After birth, serum creatinine reflects the maternal renal function up to 72 hours of life[5]. Glomerular filtration rate (GFR) and effective renal plasma flow are low in term and preterm infants, due to high vascular resistance in renal vessels as a result of vasoconstrictive and vasodilator renal forces, and also due to marked drop of systemic vascular resistance resulting from redistribution of blood flow at birth[6]. GFR slowly increases daily, doubles at the age of 2 weeks and reaches full maturity by age of 2 years (Table 1). The neonatal kidneys work hardly in the first few days of life to reduce the extracellular fluid content with UOP up to 10 ml/kg/hr and also to manage the large water load from breast feeding. Urine flow is regulated by tubular reabsorption in presence of low GFR and high UOP giving a picture similar to polyuric phase of acute kidney injury(AKI)[7].

Table 1 Normal GFR in neonates, Children and Adolescents[8,9].
Age Mean GFR+/- SD (ml/min/1.73m2)
29-34 weeks GA- 1 week postnatal age15+/- 5.6
29-34 weeks GA- 2-8 week postnatal age28.7+/- 13.8
29-34 weeks GA- above 8 week postnatal age51>4
1 week term males and females41+/-15
2-8 weeks term males and females66+/-25
Above 8 weeks term males and females96+/-22
2-12 years (males and females)133+/-27
13-21 years (males)140+/-30
13-21 years (females)126+/-22
GFR: glomerular filtration rate, SD: standard deviation, GA: gestational age.

Incidence, Risk factor and Etiology of AKI in neonates

The incidence of AKI in children is highly variable (25.1-82%) among pediatric intensive care unit (PICU) reports from different countries due to various inclusion criteria and profile of patients admitted to the PICU[10-15]. The incidence of neonatal AKI is also variable. Table 2 shows AKI Incidence in various neonatal populations and the AKI definition used for diagnosis. Very low birth weight, a low 5 minute APGAR score, maternal drug administration, intubation at birth, respiratory distress syndrome, patent ductus arteriosus, sepsis, phototherapy and neonatal medications (Non-steroidal anti inflammatory drugs, Antibiotics, diuretics) are the most commonly reported factor predisposing to AKI in neonates[16]. Hypernatremic dehydration is a rarer cause of AKI in neonates that may occur as a result of inadequate milk intake[17,18]. Congenital renal malformations may presents as AKI, with progressive deterioration of kidney functions. Autosomal recessive poly- cystic kidney disease may cause renal failure in the neonatal period, but only in a small proportion of patients[19].

Table 2 Acute kidney injury Incidence in various neonatal populations and the Acute kidney injury definition used for diagnosis[20].
Population AKI incidenceAKI Definition
Pre-term VLBW18%Modified KDIGO
Pre-term ELBW12.50%Modified KDIGO
Sick near-term/term18%Modified KDIGO
Asphyxiated newborn38%Modified KDIGO
ECMO71%RIFLE criteria
Cardiac surgery 62%AKIN criteria
AKI: Acute kidney injury, VLBW: very low birth weight, ELBW: extremely low birth weight, ECMO: extracorporeal membrane oxygenation, KDIGO: kidney disease improving global outcome. RIFLE: risk, injury, failure, loss, end stage. AKIN: acute kidney injury neonate.

Diagnostic and classification criteria for neonatal Acute kidney injury

Before 2005, the majority of neonatal AKI studies used a definition of AKI defined by a serum creatinine concentration (SCr) ≥ 1.5 mg/ dl. In 2012, Jetton and Askenazi[21] proposed a standardized neonatal AKI definition based on the kidney disease improving global outcome. (KDIGO) definition for adults and children (Table 3). Ackan arikan slightly modified the RIFLE criteria used for classification of adult AKI (Table 4) definition to enhance it is applicability in children, by specially assessing the change in serum creatinine and UOP. Base line serum creatinine estimation is challenging in neonates since serum creatinine rapidly decrease in the first week of life as the function of nephron mature and the lessened exposure to maternal creatinie level. UOP is the earliest clinical sign of AKI and it is the simplest method of diagnosis AKI in neonates so oligourea is considered a sensetive highly specific marker of AKI in neonates. Table 4 compares pediatric and neonatal RIFLE criteria[12].

Table 3 Neonatal acute kidney injury Kidney Disease Improving Global Outcomes(KDIGO) classification[21].
Stage Serum creatinineUrine output
0No change in sCr or rise less than 0.3 mg/dl≥ 1ml/kg/h
1sCr rise ≥ 0.3 mg/dl within 48 h or sCr rise ≥ 1.5-1.9 x reference sCr within 7 days≥ 0.5ml/kg/h and less than 1 ml/kg/h
2sCr rise ≥ 2-2.9 reference sCr≥ 0.3 ml/kg/h and less than 0.5 ml/kg/h
3sCr rise ≥ 3 x 3 reference sCr or sCr ≥ 2.5 mg/dl or receipt dialysisLess than 0.3 ml/kg/h
sCR: Serum creatinine.

Table 4 Pediatric and neonatal RIFLE criteria[22].
  Creatinine critreiaUrine out put criteria
RiskeCCL decrease by 25%?UOP<0.5ml/kg/hrx8hrUO<1.5ml/kg/hr for 24hr
Injurye CCLdecrease by50%?UOP<0.5ml/kg/hrx16hrUO<1.Oml/kg/hr for 24hr
FailureeCCL decrease by 75%oreCCL<35ml/min/1.73m2.?UOP<0.3ml/kg/hrx24hr or anuric for 12hr.UO<0.7ml/kg/hr for24hr or anuric for 12hr.
Loss of functionPersistant failure >4 Persistant failure >4Persistant failure >4Persistant failure >4
End stagePersistant failure >3monthPersistant failure >3monthPersistant failure >3monthPersistant failure >3month
eCCL: estimated creatinine Clearance.UOP: urine output. Hr: hour, Question mark ('?') is intended to mean uncertain thresholds, RIFLE: risk, injury, failure, loss. pRIFLE: pediatric RIFLE. nRIFLE: neonatal RIFLE

New biomarkers

Traditionally used biomarkers such as blood urea nitrogen (BUN) and creatinine are insensitive, non-specific and do not adequately differentiate between the different stages of AKI especially in neonates. A delay in diagnosis prevents appropriate timely patient management decisions. Early biomarkers of AKI such as Cystatin C and Beta 2 microglobulin (B2M) facilitate earlier diagnosis and specific preventative and therapeutic strategies, thus resulting in fewer complications and improved outcomes which was proved in many studies in pediatric population[23,24]. The superiority of these biomarkers to creatinine was replicated in many neonatal studies[25-27].

Management of AKI in neonates

Non-dialytic management of AKI in the newborn

Identification and management of reversible causes is crucial element in management of neonatal AKI. If urinary tract obstruction is identified, it should be relieved and urological consultation should be sought for further management[28]. Treatment of the metabolic complications of AKI involves appropriate management of fluid (This includes body weight recorded at least twice daily to facilitate early detection of fluid overload), electrolytes, and acid– base balance; provision of good nutrition; and initiation of renal replacement therapy (RRT) if conventional therapy fails. Although, newborns are able to tolerate potassium levels up to 6.5mmol/L, higher levels are characteristic of AKI[29]. Bicarbonate therapy for correction of acidosis should be restricted to severe life threatening conditions. There is disagreement on the role of rapid infusion of sodium bicarbonate in intraventricular hemorrhage in neonates by causing episodic increase in the cerebral blood flow by causing high arterial CO2 leading to cerebral vasodilation[30].

Osmotic diuretics should be avoided due to risk of intraventricular hemorrhage[28]. Loop diuretics have also been proclaimed to be renal protective due to their effects on the redistribution of the renal blood flow resulting from the changes in the prostaglandin synthesis. Loop diuretics should be used with caution due to their ototoxic potential (although reversible) and the risk of renal calculi with long-term use[31].

Dopamine is a safe and effective vasopressor agent commonly used in neonates as a first line therapy for hypotension. Dopamine also improves UOP and serum creatinine in neonates transiently[32].

Theophillin appears to have an important therapeutic effect in the prophylaxis of AKI in the post-asphyxial neonate. Theophillin, by antagonizing the adenosine receptors, is capable of contrasting renal vasoconstriction both preventively and during AKI (thus limiting injury and allowing a faster recovery)[33-35]. Despite the many and promising studies theophillin still does not have an official role in the guidelines for the treatment of AKI and its use requires further research[36].

Nutritional support is highly important during AKI management in neonate. Protein intake should be adjusted at least to meet the basal growth requirements (1-2 g/kg/day) while keeping the BUN below the threshold for causing increase in the serum osmolarity[37].

Dialysis modalities in neonates with AKI

The main indications for initiating dialysis in neonates with AKI includes: severe oligoanuria (decrease in hourly urine out put to less than 0.5 mL/kg for more than 12 hours) despite fluid therapy, diuretics, and inotropic support; hypervolemia (physical evidence of total body fluid overload, edema); hyperuricemia (≥13 mg/dL); severe metabolic acidosisdespite bicarbonate therapy and azotemia[38].

The preferential use of hemodialysis (HD) and hemofiltration by pediatric nephrologists is increasing, but those modalities are technically difficult procedures. The large extracorporeal circuit volumes, anticoagulation, and vascular access required are limiting factors, particularly in neonates. As a result, peritoneal dialysis (PD) is generally the most common form of RRT in young children, including neonates, the advantages being relative ease of access and technical simplicity[19]. A study by Bojan and colleagues stated that early initiation of PD in neonates and infants with AKI after cardiac surgery was associated with significantly lower mortality rates[39].

Peritoneal dialysis is the optimal dialysis modality for neonates. PD facilitates the slow removal of fluids and solutes, while preventing hemodynamic instability. PD is technically a simple treatment modality, which can be continuously performed in neonates, hospitalized at neonatal intensive care units (NICUs)[40]. PD is generally performed after a failed conservative treatment. Indications for dialysis include decompensated metabolic acidosis, hyperkalemia and/or progressive azotemia, hyponatremia with symptomatic volume overload, hypocalcemia, hypophosphatemia and inability to provide adequate nutrition (due to oliguria or anuria), hyperammonemia and accumulation of neurotoxic metabolites[41]. Table 5 compares advantages and disadvantages of different dialysis modalities in neonates[40].

Table 5 Advantages and Disadvantages of Different Dialysis Modalities[40].
Peritoneal dialysisNo need for vascular access or blood prime; No systemic heparinization; Slow, continuous; Less risk of hemodynamic instability Slower correction of metabolic parameters; Risk of peritonitis; Contraindicated in patients who have severe pulmonary disease and intra-abdominal processes
HemodialysisRapid correction of metabolic abnormalities ; Rapid removal of fluid or toxins; Initial modality of choice in metabolic; disorders such as hyperammonemia Vascular access; Blood prime; Risk of hemodynamic instability; Systemic heparinization; Reverse osmosis system required; Dialysis disequilibrium; Relative contraindications: severe; hemorrhage or hemodynamic instability
Hemofiltration with without dialysis Slow, continuous without dialysis; Less risk of hemodynamic instability; Citrate-based anticoagulation available at come centers; Removal of toxins, cytokines Vascular access; Blood prime; Hypotension initially with bradykinin release syndrome?; Systemic heparinization in some institutions

The first large series for neonatal HD described 33 infants weighing less than 5 kg received hemodialysis treatment between1980- 1991 in Children’s hospital, Harvard medical school with 52% survival rate at end of dialysis treatment. In 27% of these cases dialysis was performed through two single lumen catheters in umbilical artery and vein[42].

Hemodialysis is used if PD is contraindicated, failed or when rapid correction of volume overload is required, severe hyperkalemia, severe unremitting metabolic acidosis are present, and in the treatment of oxalosis and hyperammonemia. Most infants require hemodialysis four times weekly to avoid the fluid overload caused by their liquid nutrition. Neonatal blood lines have smaller internal luminal diameters. Even the pump header segment has a smaller internal luminal diameter, thus requiring a pump speed four times greater than the blood flow. Dialyzers that have smaller surface areas also are used. The surface area can be reduced by decreasing the length of the dialyzer and the number of hollow fibers within the dialyzer. Some dialyzers require a reduction in the volume of dialysate from 500 to 600 mL/min to 300 to 400 mL/min for the dialyzer/circuit set to work properly[43].

Even with neonatal blood lines and small dialyzers, most neonates weighing less than 8 kg require at least occasional blood priming. If the hemoglobin level is maintained in the high range of normal or the patient is transfused concurrently during the start of dialysis, the infant may tolerate a crystalloid or 5% albumin prime. For many neonates, warming the dialysate is insufficient to maintain normal patient temperature; returning the blood via a warming device sometimes is needed. Increasing the overhead warmer temperature is also helpful[43].

The most commonly used equations to determine the efficacy of dialysis are the Kt/V equation and peritoneal equilibration testing (PET). Studies evaluating dialysis adequacy have not been performed for neonates. PET has been used extensively in pediatric patients to determine the permeability of the peritoneal membrane. patients with hightransport membranes have excellent Kt/V values because urea and creatinine diffuse well, but have poor ultrafiltration rates because the dextrose diffuses quickly across the membrane, thereby rapidly decreasing the osmolality gradient needed for ultrafiltration. Many neonates have high-transport membranes[40].

Prognosis of neonatal AKI

There are few studies on the long-term prognosis of neonatal AKI regarding long-term kidney disturbances, such as chronic renal insufficiency, hypertension and defect in renal concentration. Therefore, it is important to emphasize the need for a prolonged and careful follow-up of all neonates who suffered from AKI, especially preterm[44]. In general AKI with conserved diuresis has better survival and long term outcome while AKI with contracted diuresis has poor outcome specially in presence of multiple organ failure[36].


1. Moritz KM, Wintour EM. Functional development of the meso and metanephros. Pediatr Nephrol 1999; 13(2): 171-178. [DOI: 10.1007/s004670050587].

2. Moritz KM, Wintour EM, Black MJ, Bertram JF, Caruana G. factors influencing mammalian kidney development: implications for health in adult life. Adv Anat Embryol Cell Biol. 2008; 196: 1-78. [PMID: 18637522].

3. Jahnukainen T, Chen M, Berg U, Cells G. Antenatal Glucocorticoids and renal function after birth. Semin Neonatal. 2001; 6(4): 351-355. [DOI: 10.1053/siny.2001.0070]

4. Rabinowitz R, Peters MT, Vyas S, Campbell S, Nicolaides KH. Measurment of fetal urine production in normal pregnancy by real time ultrasonography. Am J Obstet Gynecol. 1989; 161(5): 1264- 1266. [PMID: 2686448].

5. Filler G, Lopes L, Harrold J, Bariciak. Beta trace protein may be a more suitable marker of neonatal renal function. Clin Nephrol. 2014; 81(4): 269-276. [DOI: 10.5414/CN108089].

6. Toth-Heyn P, Drukker A, Guignard JP. The stressed Neonatal Kidnet: from pathophysiology to clinical management of neonatal vasomotor nephropathy. Pediatr Nephrol. 2000; 14(3): 227-239. [PMID: 10752764]

7. Tripepi G, Benedetto FA, Mallamaci F, Tripepi R, Malatino L, Zoccali C. Left atrial volume in end-stage renal disease: a prospective cohort study. J Hypertens. 2006; 24(6): 1173-1180. [DOI: 10.1097/01.hjh.0000226208.11184.bb]

8. Hogg RJ, Tripepi R, Malatino L, Zoccali C, et al. National kidney foundation’s kidney Disease outcome quality initiative clinical practice guidelines for chronic kidney disease in children and adolescents: evaluation, classification, and stratification. Pediatrics. 2003; 111(6): 1416-1421. [PMID: 12777562]

9. Schwartz Gj, Brian LP and Spitzer A. The use of plasma creatinine concentration for estimating glomerular filtration rate in infants, children and adolescent. Pediatrics Cain North Am. 1987; 34(3): 571-590. [DOI: 10.1016/S0031-3955(16)36251-4].

10. Mehta P, Sinha A, Sami A, et al. Incidence of acute kidney injury in hospitalized children. Indian Pediatr. 2012; 49(7): 537-542. [PMID: 22317984]

11. Ostermann M, Chang RW. Acute kidney injury in the intensive care unit according to RIFLE. Crit Care Med. 2007; 35(8): 1837-1843. [DOI: 10.1097/01.CCM.0000277041.13090.0A]

12. Akcan-Arikan A, Zappitelli M, Loftis LL, Washburn KK, Jefferson LS, Goldstein SL. Modified RIFLE criteria in critically ill children with acute kidney injury. Kidney Int. 2007; 71(10): 1028-1035. [DOI: 10.1038/sj.ki.5002231].

13. Bagshaw SM, George C, Dinu I, Bellomo R. A multi-centre evaluation of the RIFLE criteria for early acute kidney injury in critically ill patients. Nephrol Dial Transplant. 2008; 23(4): 1203–1210. [DOI: 10.1093/ndt/gfm744].

14. Freire KM, Bresolin NL, Farah AC, Carvalho FL, Góes JE. Acute kidney injury in children: Incidence and prognostic factors in critical ill patients. Rev Bras Ter Intensiva. 2010; 22(2): 166-174. [DOI: 10.1590/S0103-507X2010000200011]

15. Krishnamurthy S, Mondal N, Narayanan P, Biswal N, Srinivasan S, Soundravally R. Incidence and etiology of acute kidney injury in Southern India. Indian J Pediatr. 2013; 80 (3): 183-189. [DOI: 10.1007/s12098-012-0791-z].

16. Cataldi L, Leone R, Moretti U, et al. Potential risk factors for the development of acute renal failure in preterm newborn infants: a case-control study. Arch Dis Child Fetal Neonatal Ed. 2005; 90(6): F514-519. [DOI: 10.1136/adc.2004.060434].

17. Moritz ML, Manole MD, Bogen DL, Ayus JC. Breastfeeding- associated hypernatremia: are we missing the diagnosis. Pediatrics 2005; 116(3): e343-347. [DOI: 10.1542/peds.2004-2647].

18. Manganaro R, Mamì C, Marrone T, Marseglia L, Gemelli M. Incidence of dehydration and hypernatremia in exclusively breast-fed infants. J Pediatr. 2001; 139(5): 673-675. [DOI: 10.1067/mpd.2001.118880].

19. Haycock GB. Management of acute and chronic renal failure in the newborn. Semin Neona-tol. 2003; 8(4): 325-334. [DOI: 10.1016/S1084-2756(03)00044-7]

20. Selewski DT, Charlton JR, Jetton JG, et al. Neonatal acute kidney injury. Pediatrics. 2015; 136(2): e463-473. [DOI: 10.1542/peds.2014-3819]

21. Jetton JG, Askenazi DJ. Update on acute kidney injury in the neonate. Curr Opin Pediatr. 2012; 24(2): 191-196. [DOI: 10.1097/MOP.0b013e32834f62d5]

22. Ricci Z, Ronco C. Neonatal RIFLE. Nephrol Dial Transplant. 2013; 28(9): 2211-2214. [DOI: 10.1093/ndt/gft074]

23. Vaidya VS, Ferguson MA, Bonventre JV. Biomarkers of acute kidney injury. Annu Rev Pharmacol Toxicol. 2008; 48: 463-493. [DOI: 10.1146/annurev.pharmtox.48.113006.094615].

24. Askenazi DJ, Ambalavanan N, Goldstein SL. Acute kidney injury in critically ill newborns: What do we know? What do we need to learn?. Pediatr Nephrol. 2009; 24(2): 265-274. [DOI: 10.1007%2Fs00467-008-1060-2].

25. El-Frargy MS, El-Refaey AM, Eid R, Hussien MA. Serum cystatin-C and BETA 2microglobulin as accurate markers in the early diagnosis of kidney injury in neonates: A single center study.Saudi J Kidney Dis Transpl. 2015; 26 (4): 712-717. [DOI: 10.4103/1319-2442.160151]

26. Kandasamy Y, Smith R, Wright IM. Measuring cystatin C to determine renal function in neonates. Pediatr Crit Care Med. 2013; 14(3): 318-322. [DOI: 10.1097/PCC.0b013e318271f4a5]

27. Filler G, Grimmer J, Susan Huang SH, Bariciak E. Cystatin C for the assessment of GFR in neonates with congenital renal anomalies. Nephrol Dial Transplant. 2012; 27 (9): 3382-3384. [DOI: 10.1093/ndt/gfs253].

28. Chua AN, Sarwal MM. Acute renal failure management in the neonate. NeoReviews. 2005; 6(8): e369-e76. [DOI: 10.1542/neo.6-8-e369].

29. Gouyon JB, Guignard JP. Management of acute renal failure in newborns. Pediatr Nephrol. 2000; 14(10-11): 1037-1044. [PMID: 10975322].

30. Ballabh P. Intraventricular Hemorrhage in Premature Infants: Mechanism of Disease. Pediatric research. 2010; 67(1): 1-8. [DOI: 10.1203/PDR.0b013e3181c1b176].

31. Bagshaw SM, Delaney A, Haase M, Ghali WA, Bellomo R. Loop diuretics in the management of acute renal failure: a systematic review and meta-analysis. Crit Care Resusc. 2007; 9(1): 60-68. [PMID: 17352669].

32. Friedrich JO, Adhikari N, Herridge MS, Beyene J. Meta- analysis: low-dose dopamine increases urine output but does not prevent renal dysfunction or death. Ann Intern Med. 2005; 142(7): 510-524. [PMID: 15809463].

33. Bhat MA, Ahah ZA, Makhdoomi MS, Mufti MH. Theophylline for renal function in term neonates with perinatal asphyxia: a randomized, placebo-controlled trial. J Pediatr. 2006; 149(2): 180-184. [DOI: 10.1016/j.jpeds.2006.03.053]

34. Cattarelli D, Spandrio M, Gasparoni A, Bottino R, Offer C, Chirico G. A randomised, double blind, placebo controlled trial of the effect of theophylline in prevention of vasomotor nephropathy in very preterm neonates with respiratory distress syndrome. Arch Dis Child Fetal Neonatal Ed. 2006; 91(2): F80-84. [DOI: 10.1136/adc.2005.073650].

35. Eslami Z, Shajari A, Kheirandish M, Heidary A. Theophylline for prevention of kidney dysfunction in neonates with severe asphyxia. Iran J Kidney Dis. 2009; 3(4): 222-226. [https://pdfs.semanticscholar.org/4b54/25e63f900934f154ae430ec706d7e56530a0.pdf]

36. Ottonello G, Dessì A, Neroni P, Trudu ME, Manus D, Fanos V. Acute kidney injury in neonatal age. J Pediatr Neonat Individual Med. 2014; 3(2): e030246). [DOI: 10.7363/030246].

37. Pandey V, Kumar D, Vijayaraghavan P, Chaturvedi T, Raina R. Non-dialytic management of acute kidney injury in newborns. J Renal Inj Prev. 2017; 6(1): 1-11. [DOI: 10.15171/jrip.2017.01].

38. Yildiz N, Erguven M, Yildiz M, Ozdogan T, Turhan P. Acute Peritoneal Dialysis in Neonates with Acute Kidney Injury and Hypernatremic Dehydration. Perit Dial Int. 2013; 33(3): 290-296. [DOI: 10.3747/pdi.2011.00211].

39. Bojan M, Gioanni S, Vouhe PR, Journois D, Pouard P. Early initiation of peritoneal dialysis in neonates and infaqnts with acute kidney injury following cardiac surgery is associated with a significant decrease in mortality. Kidney Int. [DOI: 10.1038/ki.2012.172]

40. Lee MM, Chua AN, Yorgin PD. Neonatal Peritoneal Dialysis. NeoReviews. 2005; 6(8): 384-391. [Downloaded from http://neoreviews.aappublications.org/ at USUHS LRC on June 6, 2013]

41. Osichenko A, Maslarska R, Anadoliyski K. Application of peritoneal dialysis in the neonatal period-A clinical case. J Clin Med. 2011; 4(1): 72-75.

42. Sadowski RH, Harmon WE, Jabs K. Acute hemodialysis of infants weighing less than five kilo-grams. Kidney Int. 1994; 45(3): 903-906. [DOI: 10.1038/kisup.2012.1]

43. Yorgin PD, lee M. Neonatal Hemodialysis and Continuous Renal Replacement Therapy. NeoReviews. 2005; 6(8): e377. [DOI: 10.1542/neo.6-8-e377]

44. Polito C, Papale MR, La Manna A. Long-term prognosis of acute renal failure in the full-term neonate. Clin Pediatr (Phila). 1998; 37(6): 381-385. [DOI: 10.1177%2F000992289803700609].

Peer Reviewer: Monchai Siribamrungwong


  • There are currently no refbacks.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.