Quick Search
  Home Journal Information Current Issue Past Issues Services Contact Us  
Acute kidney injury in a single neonatal intensive care unit in Turkey 
Acute kidney injury in a single neonatal intensive care unit in Turkey
  Fatih Bolat, Serdar Comert, Guher Bolat, Oznur Kucuk, Emrah Can, Ali Bulbul, Hasan Sinan Uslu, Asiye Nuhoglu
 [Abstract] [Full Text] [PDF]   Pageviews: 11806 Times

Acute kidney injury in a single neonatal intensive care unit in Turkey

Fatih Bolat, Serdar Comert, Guher Bolat, Oznur Kucuk, Emrah Can, Ali Bulbul, Hasan Sinan Uslu, Asiye Nuhoglu

Istanbul, Turkey

Author Affiliations: Department of Pediatrics, Division of Neonatology, Faculty of Medicine, Cumhuriyet University, Sivas (Bolat F); Department of Pediatrics, Division of Neonatology, Sisli Children Hospital, Istanbul (Bolat F, Comert S, Can E, Bulbul A, Uslu HS, Nuhoglu A); Goztepe Training and Research Hospital, Istanbul (Bolat G); Department of Pediatrics, Medical Faculty, Yeditepe University, Istanbul, Turkey (Kucuk O).

Corresponding Author: Fatih Bolat, MD, Cumhuriyet Üniversitesi, Tıp Fak¨¹ltesi, Çocuk Sağlığı ve Hastalıkları Yenidoğan Kliniği, Sivas, T¨¹rkiye (Tel: 90-03462581171; Fax: 90-03462581305; Email: fatihbolat74@gmail.com)


Background: Although advances in perinatal medicine have increased the survival rates of critically ill neonates, acute kidney injury (AKI) is still one of the major causes of mortality and morbidity in neonatal intensive care units. This study aimed to determine the prevalence of AKI and analyze demographic data and risk factors associated with the mortality or morbidity.

Methods: Of 1992 neonates hospitalized between January 2009 and January 2011, 168 with AKI were reviewed in the study. The diagnosis of AKI was based on plasma creatinine level >1.5 mg/dL, which persists for more than 24 hours or increases more than 0.3 mg/dL per day after the first 48 hours of birth while showing normal maternal renal function.

Results: The prevalence of AKI was 8.4%. The common cause of AKI was respiratory distress syndrome, followed by sepsis, asphyxia, dehydration, congenital anomalies of the urinary tract, congenital heart disease, and medication. The prevalence of AKI in neonates with birth weight lower than 1500 g was about three-fold higher than in those with birth weight higher than 1500 g (P<0.05). Pregnancy-induced hypertension, preterm prolonged rupture of membranes, and administration of antenatal corticosteroid were associated with increased risk of AKI (P<0.05). Umbilical vein catheterization, mechanical ventilation and ibuprofen therapy for patent ductus arteriosus closure were found to be associated with AKI (P<0.05). The overall mortality rate was 23.8%. Multivariate analysis revealed that birth weight less than 1500 g, mechanical ventilation, bronchopulmonary dysplasia, anuria, and dialysis were the risk factors for the mortality of infants with AKI.

Conclusions: Prenatal factors and medical devices were significantly associated with AKI. Early detection of risk factors can reduce the mortality of AKI patients.

Key words: acute kidney injury; mortality; neonatal intensive care unit; prevalence; risk factors

World J Pediatr 2013;9(4):323-329


Acute kidney injury (AKI) is a frequently encountered problem in tertiary level neonatal intensive care units (NICUs). It is usually a potentially reversible syndrome characterized by an abrupt reduction in glomerular filtration rate. AKI develops in approximately 8%-24% of all neonates admitted to NICUs, mostly secondary to hypovolemia, hypoxemia and hypotension.[1,2] Over 70% of these cases represent prerenal AKI. Since AKI in newborns is usually asymptomatic, many such cases will be missed if relevant investigations are not conducted.[3,4] Therefore, it is important to assess the predisposing factors and early subclinical findings of AKI to improve the treatment results of the disease.

Although several studies have shown that AKI is common in the NICUs, the precise prevalence of AKI are still unknown.[5] Many studies have been carried out in adults and children, but only limited data are available on the etiology and prognosis of neonatal AKI in Turkish NICUs.

The aim of this study was to determine the prevalence AKI and to evaluate the risk factors in predicting mortality and short term outcome in our NICU.


Study population

This retrospective study was conducted at the NICU of Sisli Etfal Education and Research Hospital between January 2009 and January 2011. All neonates admitted to the NICU during the period were included, but those who died in the first 48 hours after birth and those with a maternal history of renal failure were excluded. The study protocol was approved by the institutional ethics committee of the hospital.

Renal function

For the term and late preterm neonates, the diagnosis of AKI was made on the basis of serum creatinine levels >1.5 mg/dL at any time after first 48 hours of life with normal maternal serum creatinine levels, or creatinine level that increased at the rate of 0.3 mg/dL per day 48 hours after birth with oligo or anuria.[4,6-10] Since the creatinine levels of preterm neonates (<34 weeks) were high in the first 3-5 days of life, serum levels were measured serially for 48 to 72 hours to diagnose AKI.[11] The assessment of oliguria and anuria was based on urine flow of <1 mL/kg per hour and <0.5 mL/kg per hour 48 hours after birth.[3,12] Urine output was measured every day by collecting urine in adhesive bags in an 8-hour interval.

Glomerular filtration rate was estimated using Schwartz formula (k ¡Á height [cm]/plasma creatinine [mg/dL]). The constant k was 0.33 for infants born after gestation for less than 38 weeks and 0.45 for those born after gestation for more than or equal to 38 weeks.[13,14] Renal impairment was grouped into three categories based on the site involved: pre-renal, renal and post-renal AKI. Differentiation of pre-renal and renal failure was based on urine sodium and creatinine levels and fractional excretion of sodium (FENa).[9,10] Fractional excretion of sodium more than 2.5%-3.0% was considered as intrinsic AKI at a gestational age of less than or equal to 32 weeks. FENa less than 6% was used to define intrinsic AKI in babies born after less than 32 weeks of gestation.[15,16] Renal failure index (RFI) may sometimes be used as an alternative to FENa. However, there is no good reason to prefer one over the other since both provide the same information.[9] We did not calculate RFI in all of the infants. Those who had urinary tract obstruction diagnosed with ultrasonography, or renal scintigraphy were considered as having postrenal failure.[9,10]

Definition of variables

Gestational age of the infants was determined by early fetal ultrasound and new Ballard score after birth. Prematurity was defined as birth at less than 37 weeks of gestation. Premature rupture of membranes was defined as membrane rupture before the onset of labor.[17] Asphyxia was diagnosed when patients met the following criteria: (1) metabolic or severe, combined acidemia (pH less than 7.0) in arterial umbilical cord blood; (2) Apgar score of 0-3 for more than 5 minutes; (3) neonatal neurological manifestations (seizures, coma or hypotonia); (4) multisystemic dysfunction of organs, i.e. cardiovascular, gastrointestinal, hematological, pulmonary or renal systems).[18] All neonates with clinical features of asphyxia were staged by the Sarnat and Sarnat scoring system.[19] Dehydration was defined as a weight loss of more than 10% of the birth weight at the end of the 1st week of life or clinical findings of dehydration with hypernatremia.[20] Respiratory distress syndrome was defined on the basis of clinical, laboratory and radiological findings and respiratory support for ¡Ý6 hours within the first 24 hours after birth. Sepsis was defined as a positive blood culture or urine culture along with clinical signs of infection.[21,22] Metabolic acidosis was diagnosed if blood pH <7.20 and HCO3 ¡Ü12 mmol/L or base excess ¡Ü-6. Hypernatremia and hyponatremia were defined as serum sodium concentration >150 mmol/L and <130 mmol/L, respectively.[20] Hyperkalemia was defined as serum potassium level >7.5 mmol/L in the first day of life and >6.5 mmol/L in the remaining days.[23] Hypertension was diagnosed with systolic and diastolic blood pressures curves described by Zubrow et al.[24] Liver failure was defined by the elevated levels of aspartate aminotransferase and alanine aminotransferase that were three times higher than the upper limit of normal values.[8]


The infants who developed AKI were treated according to the standard protocol: ensuring adequate hydration [insensible loss (mL) + urine (mL)], maintaining optimal fluid-electrolyte balance (serial measurement of electrolytes), normalizing arterial blood pressure, and minimizing nephrotoxin exposure. As the levels of nephrotoxic agents were not routinely monitored, we adjusted the doses of the agents and dosing intervals according to the calculated glomerular filtration rate so as to minimize the exposure of nephrotoxin or withdraw the agents if possible. We checked fluid/electrolyte requirement every 8 hours. Infants with AKI are not treated routinely with a low dose of dopamine at our unit.

In patients with no response to treatment (severe metabolic acidosis, persistent hyperkalemia, fluid overload with evidence of hypertension and/or pulmonary edema refractory to diuretic therapy, neurologic symptoms and calcium/phosphate imbalance with hypocalcemic tetany), peritoneal dialysis was performed. Hemodialysis facility was not available in our center.

Data collection

Detailed maternal and neonatal information about age, gender, gestational age, prenatal history, maternal and neonatal medical diseases, Apgar score at five minutes, use of medical devices (central venous catheter, umbilical catheter, percutaneous catheter, mechanical ventilation), other relevant medical conditions and laboratory results, treatment modality and outcomes  were collected for each infant.

Statistical analysis

Statistical analyses were performed by SPSS version 15 (SSPS Inc, Chicago, USA). Univariate analysis was performed to identify differences between infants with and without AKI; the Chi-square test and Fisher's exact test were used to compare categorical variables and Student's t test was used to analyze continuous variables. Significant variables were identified by univariate analysis and entered into a stepwise logistic regression analysis. A P value less than 0.05 was considered statistically significant.


In 2028 infants hospitalized during the study period, 36 were excluded. In the remaining 1992 infants, 168 (133 pre-term, 35 term infants) developed AKI, with a prevalence of 8.4%. In these infants with AKI, 88.2% were inborns, 11.8% outborns (born at other hospitals). The mean gestational age and birth weight of infants with AKI were 32¡À2.1 weeks and 1350¡À450 g, respectively. Very low birth weight (VLBW)  infants (<1500 g) accounted for 34.5% (58/168) of the infants with AKI. Their prevalence of AKI was three times higher than that of those infants with birth weight lower than 1500 g (20% vs. 7%, P<0.05).  The prevalence of AKI according to birth weight was 6% in infants of 1500-2500 g and 8% in infants more than 2500 g. Seventy-three infants (43.5%) developed AKI within the first week of life, 52 (31.0%) within 8-14 days and 43 (25.5%) after two weeks. Demographic characteristics of the infants are shown in Table 1. Univariate analysis showed that pregnancy-induced hypertension, preterm prolonged rupture of membrane (PPROM), administration of antenatal corticosteroid, small gestational age and birth weight less than 1500 g were associated with the increased risk of AKI (P<0.05). Unfortunately, we could not collect information about intrauterine exposure to nonsteroidal anti-inflammatory agents during the prenatal period in this study. Therefore, we were unable to determine their relationship with the disease or other causes.

Endotracheal intubation at birth, umbilical vein catheterization, mechanical ventilation and ibuprofen therapy for patent ductus arteriosus closure were found to be significantly associated with AKI (P<0.05) (Table 2). The duration of mechanical ventilation was longer in the infants with AKI (12¡À4.8 vs. 5.2¡À2.1 days, P=0.001). Also, the duration of nephrotoxic antibiotic exposure was found to be longer in infants with AKI (13.4¡À2.5 vs. 6.4¡À2.1 days, P=0.001) despite there was no difference in the types of nephrotoxins exposured.

According to the primary site of the disease, 82 (48.8%) of the infants had prerenal failure, 78 (46.4%) had renal failure, and 8 (4.8%) had postrenal failure. The etiologic factors and site of occurrence of AKI are shown in Table 3. The most common causes of AKI were respiratory distress syndrome and neonatal sepsis. The most frequently isolated organism was Klebsiella pneumonia (n=24). Of 26 asphyxiated babies, 16 had mild-moderate asphyxia and 10 had severe asphyxia.

In 48 infants (28.6%) with hypotension receiving inotropic support, 36 were given dopamine, and 12 received dopamine and dobutamine in combination. Only two infants had systemic hypertension, none of the 48 infants received antihypertensive agents.

In 115 infants with metabolic acidosis, 25 were treated by infusion of 8.4% sodium bicarbonate. In 20 infants with hyperkalemia (two infants with acute cardiac arrhythmias), 12 were treated with calcium gluconate, sodium bicarbonate and insulin infusion. Thirty-six infants developed hyponatremia, and 8 hypernatremia. Hyponatremia or hypernatremia was managed according to the underlying conditions. Ten infants were treated by peritoneal dialysis.

The overall mortality rate was 23.8% in infants with AKI during their hospitalization. The most common cause of death was multiple-organ failure secondary to the underlying diseases rather than renal failure. The proportion of infants with hyponatremia was higher in non-survivors (70% vs. 12.5%, P=0.001). The presence of respiratory problem requiring  mechanical ventilation is a risk factor for mortality, the duration of which was significantly longer in the non-survivors  (7¡À2.1 vs. 3¡À1.2 days, P<0.05).  The duration of dialysis was also longer in the non-survivors [5 (3-9) vs. 3 (2-5) days, P=0.001].

We found that VLBW, bronchopulmonary dysplasia, antenatal steroid, high creatinine level, blood urea nitrogen and potassium, low serum sodium level,  anuria, dialysis and mechanical ventilation, hypotension requiring inotropic support were significantly associated with the mortality of the infants (P<0.05) (Table 4).

All factors associated with the mortality of the infants were assessed by stepwise logistic regression analysis. VLBW, bronchopulmonary dysplasia, mechanical ventilation, anuria and dialysis were the important determinants of mortality in neonates with renal failure (P<0.05) (Table 5).

In this study, the infants with AKI were hospitalized for a longer duration (32¡À8.4 vs. 20¡À10.2 days, P<0.05). Unfortunately, follow-up information about renal outcome could not be collected from most of the infants possibly because of low socioeconomic status or illiteracy of their parents. The infants mostly came from families of low socioeconomic status in economically deprived parts of Istanbul. This may explain why they were lost to follow up. Only 20 infants were followed up until their age of one year. Of 8 infants with postrenal AKI, 3 were diagnosed with chronic renal failure at the time of discharge. Serum creatinine levels of 5 infants normalized and remained in the normal range within a year. Three infants with chronic renal failure were referred to and followed up by the pediatric nephrology department of the hospital. None of 17 infants showed deterioration of renal function at the end of the first year.


Despite recent advances in neonatology, mortality and morbidity related to AKI pose a significant problem. This study provided a descriptive overview of AKI in newborns who had been admitted to our NICU. We found that the prevalence of AKI in newborn infants was 8.4% during the study period. Since the prevalence depends on the populations studied, literature searching reveals a wide range from 2.5% to 82%.[6,25,26] But it is reported to be as high as 75% in VLBW infants and is strongly significant in smaller and sicker infants.[8,27] In contrast to some studies, we found that the rate of AKI in newborns with VLBW was much lower than that previously reported.[6] However,  it was higher than we reported as some neonates were underestimated because of nonoliguric renal failure.[28] Obviously, gestational age and birth weight are the most important factors determining the prevalence of AKI.

There are several reasons for the high risk of renal failure in premature infants. First, these infants may suffer from insults during intrauterine life because of infections, intrauterine growth retardation, placental insufficiency or maternal medication. Second, the postnatal course of premature infants is often complicated by hypovolemia, sepsis, hypotension and ischemia.[1,2,12] These factors would make preterm infants more vulnerable to renal failure. Fetal programming hypothesis suggests that an adverse intrauterine milieu causes structural, hormonal and metabolic adaptations in the fetus.[29] In the present study, we observed that pregnancy-induced hypertension, preterm prolonged rupture of membranes, antenatal steroid, and birth weight <1500 g were significantly correlated with AKI development. Adverse intrauterine environment may produce renal damage in the neonatal period. Antibiotic use during pregnancy was reported to have adverse effects on neonatal renal function.[27] The present study revealed that PPROM treatment with antibiotics during pregnancy may contribute to exposure of newborns to nephrotoxic agents. Also, PPROM itself is an intrauterine insult.

It is well known that prenatal steroids may lead to low birth weight and compromise organogenesis, but its effects on nephrogenesis have not yet been investigated extensively.[30,31] Finken et al[32] found that the subjects who were exposed antenatally to betamethasone had a lower glomerular filtration rate. An animal study[33] suggested that pups whose mothers were treated with dexamethasone had a lower kidney weight and a lower number of glomeruli. The results of investigations indicated that measures should be taken to prevent AKI and promote the development of renal tissue in the early fetal life.

AKI is often difficult to diagnose clinically because there is no consensus on what caused AKI. So far, few prospective epidemiological studies have been reported to profile the occurrence and outcome of AKI.[3,34] Studies[35,36] found the relationship of high levels of serum creatinine with neonatal AKI, which leads to misdiagnosis of a significant number of infants according to the current definitions in adults and pediatric populations. In our study, biochemical indices (blood urea nitrogen, creatinine level), urine output, and underlying etiology before the diagnosis of AKI were evaluated. In the diagnosis of AKI in VLBW neonates, we should be aware of the fact that serum creatinine level may increase and be stable during the early neonatal period in infants of less than 1000 g compared with those of 1000 to 1500 g. VLBW neonates have high FENa even without any sign of AKI.[11] This is a challenge of the diagnosis of AKI.

Mechanical ventilation is a life-saving method for patients with acute respiratory failure. In the present study, AKI was found to be associated with mechanical ventilation after birth. Evidence has shown that mechanical ventilation may contribute to the pathogenesis of AKI.  AKI is caused by several mechanisms rather than by a single one.[37,38] One possible mechanism is the compromise of renal blood flow by hypercapnia or hypoxemia, which may affect vascular dynamics via activation or inactivation of vasoactive factors such as nitric oxide, angiotensin II, endothelin, and bradykinin. Another possibility is a pulmonary inflammatory reaction in response to barotrauma, with the release of inflammatory mediators and the induction of a systemic inflammatory reaction.[39-41]

AKI in NICUs mostly occurs as a result of perinatal conditions such as placental insufficiency, congenital anomalies etc. A few of infants have primary renal disease. Studies[6,9,10,23,27,42] found that the predisposing causes of AKI vary widely.  Asphyxia is the most common cause of AKI[6,43] followed by sepsis.[44] Predisposing factors of AKI in our patients, according to the order of frequency, were respiratory distress syndrome, sepsis and asphyxia. Other factors such as drugs and patent ductus arteriosus may also contribute to the development of AKI.

To date, various prognostic factors have been used in predicting mortality in cases of neonatal AKI. Risk factors, including birth weight, extrarenal diseases, sepsis, septic shock, multiorgan failure, oligo-anuria, hypotension, vasopressors and mechanical ventilation, have also been used in detecting mortality of AKI cases in the NICU.[8,23] Gupta et al[28] observed that abnormal renal sonographic scan and hyponatremia were associated with poor prognosis in newborns with AKI who had asphyxia. A national study[23] conducted in Turkey showed that hypoxia, metabolic acidosis, hypervolemia and dialysis were significantly associated with the mortality of children with AKI. In our study, multivariate analysis demonstrated that VLBW, mechanical ventilation, anuria, bronchopulmonary dysplasia, and dialysis were significantly associated with the mortality of infants. Critically ill infants are more likely to die from multi-organ failure rather than from renal failure.

There are some limitations in this study. First, our study is a retrospective one based on chart review which did not contain all the information we needed. Second, long-term outcomes and delayed renal squeal in survivors could not be assessed because their families could not be followed up. Third, we measured serum creatinine levels at intervals of 48-72 hours, which may be related to the high prevalence of AKI in neonates, especially in those with VLBW.

In conclusion, this study demonstrates that AKI is still an important problem despite advances in neonatal intensive care. Prenatal factors include pregnancy-induced hypertension, preterm prolonged rupture of membranes, and antenatal steroid are significantly associated with AKI after birth of infants. VLBW, mechanical ventilation, anuria, bronchopulmonary dysplasia and dialysis are risk factors for the mortality of newborns with AKI. Further studies are required to develop preventive strategies for AKI in high-risk neonates.


We would like to thank the doctors and nurses in the NICU of the hospital for their assistance in the evaluation and management of the patients.

Funding: None.

Ethical approval: This study was approved by the ethics committees of the institutions involved in the study.

Competing interest: The authors have no financial relations with other parties.

Contributors: Bolat F, Comert S, Bolat G were responsible for study idea, design, data collection and analysis. Kucuk O, Can E, and Bulbul A performed data collection and analysis. Bolat F, Uslu HS edited the manuscript. Bolat F and Nuhoglu A supervised, reviewed and edited the manuscript. All authors approved the final version of the manuscript.


1   Hentschel R, Lödige B, Bulla M. Renal insufficiency in the neonatal period. Clin Nephrol 1996;46:54-58.

2   T¨®th-Heyn P, Drukker A, Guignard JP. The stressed neonatal kidney: from pathophysiology to clinical management of neonatal vasomotor nephropathy. Pediatr Nephrol 2000;14:227-239.

3   Ogunlesi TA, Adekanmbi F. Evaluating and managing neonatal acute renal failure in a resource-poor setting. Indian J Pediatr 2009;76:293-296.

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

5   Moghal NE, Embleton ND. Management of acute renal failure in the newborn. Semin Fetal Neonatal Med 2006;11:207-213.

6   Agras PI, Tarcan A, Baskin E, Cengiz N, G¨¹rakan B, Saatci U. Acute renal failure in the neonatal period. Ren Fail 2004;26:305-309.

7   Friedlich PS, Evans JR, Tulassay T, Seri I. Acute and chronic renal failure. In: Taeusch HW, Ballard RA, Gleason CA eds. Avery's diseases of the newborn. 8th ed. Philadelphia: Elsevier Saunders Company, 2005: 1298-1305.

8   Csaicsich D, Russo-Schlaff N, Messerschmidt A, Weninger M, Pollak A, Aufricht C. Renal failure, comorbidity and mortality in preterm infants. Wien Klin Wochenschr 2008;120:153-157.

9   Haycock G. Disorders of the kidney and urinary tract. In: Rennie JM, ed. Roberton's textbook of neonatology. 4th ed. Oxford: Elsevier, 2005: 936-937.

10 Beth AV, Katherine MD. Acute kidney injury. In: Martin RJ, Fanaroff AA, Walseh MC, eds. Fanaroff and Martin's neonatal-perinatal Medicine: Diseases of the fetus and infant. 9th ed. Philadelphia (PA): Mosby-Elsevier, 2011: 1689-1691.

11 Auron A, Mhanna MJ. Serum creatinine in very low birth weight infants during their first days of life. J Perinatol 2006;26:755-760.

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

13 Schwartz GJ, Haycock GB, Edelmann CM Jr, Spitzer A. Late metabolic acidosis: a reassessment of the definition. J Pediatr 1979;95:102-107.

14 Brion LP, Fleischman AR, McCarton C, Schwartz GJ. A simple estimate of glomerular filtration rate in low birth weight infants during the first year of life: noninvasive assessment of body composition and growth. J Pediatr 1986;109:698-707.

15 Ishizaki Y, Isozaki-Fukuda Y, Kojima T, Sasai M, Matsuzaki S, Kobayashi Y. Evaluation of diagnostic criteria of acute renal failure in premature infants. Acta Paediatr Jpn 1993;35:311-315.

16 Mathew OP, Jones AS, James E, Bland H, Groshong T. Neonatal renal failure: usefulness of diagnostic indices. Pediatrics 1980;65:57-60.

17 Dilenge ME, Majnemer A, Shevell MI. Long-term developmental outcome of asphyxiated term neonates. J Child Neurol 2001;16:781-792.

18 American Academy of Pediatrics, American College of Obstetricians and Gynecologists. Intrapartum care. In:  Guidelines for Perinatal Care, 4th ed. Washington, DC: American College of Obstetricians and Gynecologists, 1997: 93-125.

19 Sarnat HB, Sarnat MS. Neonatal encephalopathy following fetal distress. A clinical and electroencephalographic study. Arch Neurol 1976;33:696-705.

20 Dell KR. Fluid, electrolytes, and acid-Base Homeostasis. In: Martin RJ, Fanaroff AA, Walseh MC, eds. Fanaroff and Martin's neonatal-perinatal Medicine: Diseases of the fetus and infant. 9th ed. Philadelphia: Mosby-Elsevier, 2011: 1689-1691.

21 Vergnano S, Sharland M, Kazembe P, Mwansambo C, Heath PT. Neonatal sepsis: an international perspective. Arch Dis Child Fetal Neonatal Ed 2005;90:F220-224.

22 Goldstein B, Giroir B, Randolph A; International Consensus Conference on Pediatric Sepsis. International pediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in pediatrics. Pediatr Crit Care Med 2005;6:2-8.

23 Duzova A, Bakkaloglu A, Kalyoncu M, Poyrazoglu H, Delibas A, Ozkaya O, et al. Etiology and outcome of acute kidney injury in children. Pediatr Nephrol 2010;25:1453-1461.

24 Zubrow AB, Hulman S, Kushner H, Falkner B. Determinants of blood pressure in infants admitted to neonatal intensive care units: a prospective multicenter study. Philadelphia Neonatal Blood Pressure Study Group. J Perinatol 1995;15:470-479.

25 Medina Villanueva A, L¨®pez-Herce Cid J, L¨®pez Fern¨¢ndez Y, Ant¨®n Gamero M, Concha Torre A, Rey Gal¨¢n C, et al. Acute renal failure in critically-ill children. A preliminary study. An Pediatr (Barc) 2004;61:509-514. [in Spanish]

26 Krzemie¨½ G, Szmigielska A, Bieroza I, Roszkowska-Blaim M. Complex etiology of acute renal failure in a newborn. Pol Merkur Lekarski 2008;24:138-140. [in Polish]

27 Cataldi L, Leone R, Moretti U, De Mitri B, Fanos V, Ruggeri L, 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:F514-519.

28 Gupta BD, Sharma P, Bagla J, Parakh M, Soni JP. Renal failure in asphyxiated neonates. Indian Pediatr 2005;42:928-934.

29 Dyer JS, Rosenfeld CR. Metabolic imprinting by prenatal, perinatal, and postnatal overnutrition: a review. Semin Reprod Med 2011;29:266-276.

30 Gubhaju L, Sutherland MR, Yoder BA, Zulli A, Bertram JF, Black MJ. Is nephrogenesis affected by preterm birth? Studies in a non-human primate model. Am J Physiol Renal Physiol 2009;297:F1668-1677.

31 Figueroa JP, Rose JC, Massmann GA, Zhang J, Acuña G. Alterations in fetal kidney development and elevations in arterial blood pressure in young adult sheep after clinical doses of antenatal glucocorticoids. Pediatr Res 2005;58:510-515.

32 Finken MJ, Keijzer-Veen MG, Dekker FW, Frölich M, Walther FJ, Romijn JA, et al. Antenatal glucocorticoid treatment is not associated with long-term metabolic risks in individuals born before 32 weeks of gestation. Arch Dis Child Fetal Neonatal Ed 2008;93:F442-447.

33 Celsi G, Kistner A, Aizman R, Eklöf AC, Ceccatelli S, de Santiago A, et al. Prenatal dexamethasone causes oligonephronia, sodium retention, and higher blood pressure in the offspring. Pediatr Res 1998;44:317-322.

34 Hsu CW, Symons JM. Acute kidney injury: can we improve prognosis? Pediatr Nephrol 2010;25:2401-2412.

35 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;24:265-274.

36 Hoste EA, Kellum JA, Katz NM, Rosner MH, Haase M, Ronco C. Epidemiology of acute kidney injury. Contrib Nephrol 2010;165:1-8.

37 Vieira JM Jr, Castro I, Curvello-Neto A, Demarzo S, Caruso P, Pastore L Jr, et al. Effect of acute kidney injury on weaning from mechanical ventilation in critically ill patients. Crit Care Med 2007;35:184-191.

38 Lee WL, Slutsky AS. Ventilator-induced lung injury and recommendations for mechanical ventilation of patients with ARDS. Semin Respir Crit Care Med 2001;22:269-280.

39 Kuiper JW, Plötz FB, Groeneveld AJ, Haitsma JJ, Jothy S, Vaschetto R, et al. High tidal volume mechanical ventilation-induced lung injury in rats is greater after acid instillation than after sepsis-induced acute lung injury, but does not increase systemic inflammation: an experimental study. BMC Anesthesiol 2011;11:26.

40 Hoke TS, Douglas IS, Klein CL, He Z, Fang W, Thurman JM, et al. Acute renal failure after bilateral nephrectomy is associated with cytokine-mediated pulmonary injury. J Am Soc Nephrol 2007;18:155-164.

41 Kim do J, Park SH, Sheen MR, Jeon US, Kim SW, Koh ES, et al. Comparison of experimental lung injury from acute renal failure with injury due to sepsis. Respiration 2006;73:815-824.

42 Viswanathan S, Manyam B, Azhibekov T, Mhanna MJ. Risk factors associated with acute kidney injury in extremely low birth weight (ELBW) infants. Pediatr Nephrol 2012;27:303-311.

43 Abu-Haweleh AF. Acute renal failure in newborn: etiology and mortality rate in jordan patients. Saudi J Kidney Dis Transpl 1998;9:18-21.

44 Mathur NB, Agarwal HS, Maria A. Acute renal failure in neonatal sepsis. Indian J Pediatr 2006;73:499-502.

Received April 3, 2012 Accepted after revision August 15, 2012

  [Articles Comment]

  title Author The End Revert Time Revert / Count

  Comment Title: 


World Journal of Pediatric Surgery

roger vivier bags 美女 美女

Home  |  Journal Information  |  Current Issue  |  Past Issues  |  Journal Information  |  Contact Us
Children's Hospital, Zhejiang University School of Medicine, China
Copyright 2007  www.wjpch.com  All Rights Reserved Designed by eb