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Neonatology
Original research
Effectiveness and feasibility of continuous renal replacement therapy for acute kidney injury in neonates weighing 3 kg or less: a two-centre, retrospective study
  1. Yifan Sun1,
  2. Jinglin Xu2,
  3. Xiaoyun Chu1,
  4. Weifeng Zhang2,
  5. Xiaohui Gong1,
  6. Dongmei Chen2,
  7. Cheng Cai1
  1. 1Department of Neonatology, Shanghai Children’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China
  2. 2Department of Neonatology, Quanzhou Maternity and Children’s Hospital, Quanzhou, Fujian Province, China
  1. Correspondence to Dr Cheng Cai; caicheng2004{at}163.com

Abstract

Background Continuous renal replacement therapy (CRRT) is commonly used for the treatment of acute kidney injury (AKI) in critically ill neonates. This study investigated the effectiveness and feasibility of CRRT for AKI in neonates who weigh ≤3 kg.

Methods Data from 19 neonates with a weight ≤3 kg and AKI who underwent CRRT at two centres between January 2015 and October 2021 were collected retrospectively. Kidney function, circulatory function, complications and clinical outcomes were recorded. Repeated-measures analyses of variance, t-tests and non-parametric tests were conducted.

Results The median patient age at CRRT initiation was 3 days (IQR: 1–7 days). The median patient weight at CRRT initiation was 2.67 kg (IQR: 2.20–2.85 kg). The median CCRT duration was 46 hours (IQR: 32–72 hours). The serum creatinine and blood urea nitrogen levels decreased significantly, and the mean arterial pressure increased significantly after 12 hours of CRRT and at the end of CRRT. The urinary output was significantly increased at the end of CRRT. 11 patients had thrombocytopaenia, 6 had electrolyte disorders and 3 had blocked tubes. Five patients were discharged, six died after their parents chose to discontinue treatment and eight died after active treatment. Weight at CRRT initiation and urinary output at the end of CRRT were significantly lower among patients who died than among patients who survived.

Conclusions CRRT is feasible and effective for AKI in neonates who weigh ≤3 kg when accompanied by elaborate supportive care. Lower body weight and persistent oliguria may be correlated with an increased risk of poor clinical outcomes.

  • Neonatology
  • Infant
  • Nephrology

Data availability statement

Data are available on reasonable request. Data from this study can be obtained from the corresponding authors on reasonable request.

http://creativecommons.org/licenses/by-nc/4.0/

This is an open access article 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, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

https://doi.org/10.1136/bmjpo-2023-002241

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    WHAT IS ALREADY KNOWN ON THIS TOPIC

    • Continuous renal replacement therapy (CRRT) is a favoured renal replacement modality for acute kidney injury (AKI) in critically ill neonates. The application of CRRT in neonates weighing ≤3 kg is challenging and clinical evidence for this patient population is lacking.

    WHAT THIS STUDY ADDS

    • CRRT is feasible and effective for AKI in neonates who weigh ≤3 kg. Lower body weight and persistent oliguria may be associated with an increased risk of poor clinical outcomes.

    HOW THIS STUDY MIGHT AFFECT RESEARCH, PRACTICE OR POLICY

    • The present study provides evidence supporting the application of CRRT for AKI in neonates who weigh ≤3 kg. However, studies with larger samples are necessary to elucidate the precise appropriate treatment.

    Introduction

    Acute kidney injury (AKI) is one of the most common critical illnesses experienced by neonates and has an incidence rate of 6%–24% among this population.1 2 It is characterised by a sudden decrease in kidney function with oliguria or anuria, oedema, electrolyte disturbances and increased metabolite levels.3 4 Risk factors for neonatal AKI include low birth weight (BW), perinatal events (such as asphyxia and infections), medicine use (such as aminoglycoside antibiotics and loop diuretics), blood clots and congenital developmental abnormalities.2 5 Peritoneal dialysis (PD) or continuous renal replacement therapy (CRRT) is conducted when medical therapy fails to correct electrolyte and/or metabolic disturbances and maintain fluid balance.2 4 However, PD is difficult to perform in haemodynamically unstable infants, those with a history of abdominal surgery or necrotising enterocolitis (NEC), and those who require strict control of the volume status.1 6 Therefore, CRRT is a favoured treatment modality for the treatment of AKI in critically ill neonates.1 6 Immaturity of the thermoregulatory centre, catheterisation difficulties and relatively large extracorporeal volumes create challenges in the application of CRRT for neonates, and especially for those weighing ≤3 kg.7–9 Clinical evidence regarding the application of CRRT for this patient population is lacking, although the successful application of CRRT for neonates weighing ≤3 kg has been reported.7 10 11 Therefore, during this study, the clinical data of neonates weighing ≤3 kg with AKI were retrospectively analysed to provide more evidence to support the application of CRRT for this patient population.

    Methods

    Study design and patient population

    This study was conducted in the neonatology departments of two hospitals between January 2015 and October 2021. The clinical data were collected retrospectively from neonates weighing ≤3 kg with AKI. Inclusion criteria were as follows: treated with CRRT; admitted within 28 days after birth; met the diagnostic criteria for AKI in neonates with one of the following manifestations: haemodynamic disturbance, increased intracranial pressure or cerebral oedema, cardiac insufficiency, hypercatabolism, severe fluid overload or pulmonary oedema (table 1)4 12; and weight ≤3 kg at CRRT initiation. Exclusion criteria were as follows: the presence of severe congenital kidney abnormalities; lack of informed consent from families or incomplete clinical data. 60 neonates were treated with CRRT over the study period. According to the inclusion and exclusion criteria, 19 patients were ultimately included in the study (figure 1).

    Figure 1
    Figure 1

    Flow chart of the procedure to enrol neonates in the study. AKI, acute kidney injury; CRRT, continuous renal replacement therapy.

    View this table:
    Table 1

    Neonatal AKI KDIGO classification

    CRRT treatment

    Equipment

    The Plasauto iQ21 (Asahi Kasei Corporation, Tokyo, Japan) and Multi Filtrate (Fresenius, Bad Homburg, Germany) were used. The CRRT instrument consists of a filter and external blood circulation. The AEF 03 (26 mL) filter with a blood circulation volume of 47 mL and Ultraflux AV Ped (18 mL) filter with a blood circulation volume of 52 mL were used during this study.

    Mode

    Depending on the molecular weight of the solute that was removed, continuous venovenous haemofiltration (CVVH) or continuous venovenous haemodiafiltration (CVVHDF) was performed.

    Vascular access location and size

    Venous catheterisation was performed by the attending physicians. Puncture sites included the femoral, internal jugular and umbilical veins. A 4 Fr or 5 Fr two-lumen central venous catheter (Arrow International, Cleveland, Ohio, USA) was used.

    Prefill

    Heparin saline was used to prefill the filter and external blood circulation before an erythrocyte suspension was used.

    Parameters

    The initial flow rate of the blood pump was 3 mL/kg/min, which was increased to 5 mL/kg/min according to the blood pressure. The flow rate of the replacement fluid was 20–30 mL/kg/hour. The flow rate of the dialysate was 15–25 mL/min/m2. Dehydration was dynamically adjusted according to the kidney and circulatory functions.

    Anticoagulation

    Heparin anticoagulation was used to maintain a prothrombin time of 25–40 s and an activated partial thromboplastin time of 80–120 s. The initial dose of heparin was typically 10–20 U/kg/hour.4

    Variables

    The curative effect of CRRT was evaluated based on the changes in serum creatinine (SCr), blood urea nitrogen (BUN), urinary output, blood pH, Vasoactive-Inotropic Score (VIS) and mean arterial pressure (MAP) before CRRT, 12 hours after CRRT initiation and at the end of CRRT. Improvements in these variables were interpreted as effective CRRT. The safety of CRRT was evaluated based on the occurrences of hypotension, hypothermia, thrombocytopaenia, bleeding or thrombosis, catheter-related infections and electrolyte disturbances during treatment. Data collection and evaluation were completed by more than three attending physicians.

    Statistical analysis

    Statistical software (SPSS V.22.0; IBM) was used to analyse the data. Normally distributed data are expressed as mean±SD and were analysed using a repeated-measures analysis of variance or t-test. Non-normally distributed data are expressed as median and IQR and were analysed using non-parametric tests (Friedman or Mann-Whitney U tests). Count data were expressed as the number of cases and percentages, and the chi-square test was used. Statistical significance was set at p<0.05.

    Results

    Demographic characteristics

    19 neonates with AKI who underwent CRRT and were admitted between January 2015 and October 2021 were included (13 male neonates and 6 female neonates). The mean gestational age was 36.71±3.20 weeks. The median BW was 2.66 kg (IQR: 2.00–2.87 kg). The mean Apgar score at 5 min was 5.05±3.33. The primary diseases included asphyxia (n=11), metabolic diseases (n=2), NEC (n=2), congenital gastrointestinal malformation (n=2), congenital cardiac malformation (n=1) and sepsis (n=1). The median age at CRRT initiation was 3 days (IQR: 1–7 days). The median weight at CRRT initiation was 2.67 kg (IQR: 2.20–2.85 kg). The median CRRT duration was 46 hours (IQR: 32–72 hours) (table 2).

    View this table:
    Table 2

    Demographic characteristics

    Changes in indicators of the kidney function and circulatory function

    The SCr levels at 12 hours after CRRT initiation (p=0.001) and at the end of CRRT (p=0.000) were significantly decreased compared with those before CRRT (figure 2A, table 3). Significantly decreased levels of BUN were detected at 12 hours after CRRT initiation (p=0.000) and at the end of CRRT (p=0.005) compared with those before CRRT (figure 2B, table 3). The increase in the urinary output at 12 hours after CRRT initiation was not statistically significant (p=0.991). However, the urinary output was significantly increased at the end of CRRT (p=0.011) compared with that before CRRT (figure 2C, table 3). No significant differences in serum sodium levels were observed during CRRT (figure 2D, table 3). The serum potassium levels were significantly decreased at 12 hours after CRRT initiation compared with those before CRRT (p=0.049), although they were not significantly different at the end of CRRT (p=0.079) (figure 2E, table 3).

    Figure 2
    Figure 2

    Changes of laboratory values during CRRT. (A) SCr; (B) BUN; (C) urine output; (D) serum Na+; (E) serum K+; (F) blood PH; (G) VIS; (H) MAP. The SCr, BUN, urine volume and MAP were significantly different before and after CRRT. BUN, blood urea nitrogen; CRRT, continuous renal replacement therapy; K+, serum potassium; MAP, mean arterial pressure; Na+, serum sodium; SCr, serum creatinine; VIS, Vasoactive-Inotropic Score.

    View this table:
    Table 3

    Changes of kidney function variables before and after CRRT therapy

    The blood pH increased during CRRT, but the differences were not statistically significant (figure 2F, table 4). No significant differences were observed in VIS at different time points (figure 2G, table 4). The MAP was significantly higher at 12 hours after CRRT initiation (p=0.002) and at the end of CRRT (p=0.030) than before CRRT (figure 2H, table 4).

    View this table:
    Table 4

    Changes of circulatory function variables before and after CRRT therapy

    Complications and clinical outcomes

    Venous catheterisation was successfully performed for all 19 neonates. Thrombocytopaenia was observed in 11 patients. Electrolyte disturbances, including hyponatraemia, hypokalaemia or hypophosphataemia, occurred in six patients. Hypotension was observed in five patients, and catheter blockage caused by blood clots was observed in three patients. One patient developed a left intraventricular haemorrhage 72 hours after CRRT. No patient developed hypothermia.

    Of the 19 neonates, 5 were discharged with improved kidney function and stable circulation, indicating a survival rate of 26.3%. Six patients died because their parents withdrew all treatment measures because of the poor long-term prognosis and/or economic factors. The kidney function of the remaining eight patients improved slightly with aggressive treatment. However, severe disseminated intravascular coagulation (DIC), heart failure or haemorrhage developed, and these patients eventually died.

    Comparison of indicators of the survival and death groups

    The neonates were divided into the survival group (n=5) and death group (n=14). The primary diagnoses of neonates in the survival group were asphyxia (n=2), NEC (n=1), congenital gastrointestinal malformation (n=1) and sepsis (n=1). The primary diagnoses of neonates in the death group were asphyxia (n=9), metabolic diseases (n=2), NEC (n=1), congenital gastrointestinal malformation (n=1) and congenital cardiac malformation (n=1). Neonate weight at CRRT initiation (p=0.047) and urinary output at the end of CRRT (p=0.000) were significantly lower among patients who died than among those who survived. Apgar scores at 5 min, neonate age at CRRT initiation, sex, AKI stage, CRRT duration, SCr at the end of CRRT and the complication rate were not significantly different between the two groups (table 5).

    View this table:
    Table 5

    Comparison of variables between survival and death groups

    Discussion

    AKI is an independent risk factor for a poor clinical prognosis, prolonged hospital stay and increased mortality among critically ill neonates.1 4 6 13 14 The application of CRRT for neonatal AKI has become a favourable treatment modality for critically ill neonates.6 Neonates weighing ≤3 kg represent an important proportion of neonates with AKI, but there have been limited studies of the treatment of AKI with CRRT among this population. The findings of our study demonstrated that the kidney function and circulatory function improved after CRRT treatment for AKI in neonates weighing ≤3 kg. Complications detected during this study were manageable. In addition, lower body weight and persistent oliguria were observed in the death group.

    The mechanisms for CRRT that eliminate solutes and water include ultrafiltration, diffusion, convection and adsorption.15 16 CRRT modes include CVVH, continuous venovenous haemodialysis, CVVHFD and slow continuous ultrafiltration.4 CVVH and CVVHDF were performed during our study. The mechanism of CVVH is convection-based solute and water elimination, whereas that of CVVHDF is convection and diffusion-based solute and water elimination.7 16

    Well-functioning vascular access is essential for the provision of adequate CRRT.17 18 Catheterisation difficulties often limit the use of CRRT for low-weight infants. During this study, 4 Fr or 5 Fr two-lumen central venous catheters were used for CRRT in neonates with AKI who weighed ≤3 kg, and the puncture sites included the femoral, internal jugular and umbilical veins. Hackbarth et al reported that larger catheter diameters and the use of the internal jugular vein were beneficial for maintaining a functional CRRT circuit and that a catheter with the largest diameter appropriate for patients should be selected when the puncture site is a vessel other than the internal jugular vein.18 The successful application of 4 Fr or 5 Fr double or single-lumen central venous catheters for neonatal CRRT has been reported.19 20 Onwubiko et al compared the clinical outcomes of the use of standard haemodialysis catheters or 6 Fr central venous catheters during neonatal CRRT and found that the use of 6 Fr catheters resulted in fewer catheter revisions and provided longer-lasting vascular access.17 Therefore, the appropriate catheter size and location for CRRT in neonates ≤3 kg must be determined in future studies.

    During our study, the kidney function was significantly improved, and MAP was significantly higher at the end of CRRT treatment than those before CRRT. Erkol et al reported that CRRT effectively improved the kidney function and reduced the fluid load of critically ill children with AKI and fluid overload.21 Cai et al also found that CRRT had a positive effect on the cardiopulmonary function, kidney function and electrolyte disturbances of neonates with sepsis-associated AKI.20 Sohn et al confirmed the significant effect of CRRT on improving kidney function and metabolite clearance in neonates weighing <3 kg.10 These findings suggest that CRRT allows for the dialysis of excess water, removes inflammatory mediators and metabolites and promotes the recovery of the kidney function of neonates with AKI. In addition, fluid overload, inflammatory factors and metabolite accumulation can cause cardiovascular dysfunction and pulmonary oedema, resulting in or aggravating pre-existing hypotension and hypoxaemia. Therefore, CRRT can improve tissue oxygenation and stabilise the internal environment and haemodynamics.

    CRRT complications, including hypotension at CRRT initiation, catheter-related problems, bleeding and electrolyte disturbances, occur more frequently in paediatric patients.2 7 22 23 During this study, the most common complication was thrombocytopaenia (11/19 patients). Contact between blood and the extracorporeal circuit activates the coagulation pathway and platelets, resulting in fibrin deposition and filter clotting.24 Heparin, a common anticoagulant used for CRRT, can lead to heparin-induced thrombocytopaenia and increase the risk of haemorrhage.24 Therefore, thrombocytopaenia may be related to the extracorporeal circuit, filtration membrane, heparin anticoagulation and DIC. A new intraventricular haemorrhage was observed in one patient. The causes of intraventricular haemorrhage were complex. In this patient, coagulation dysfunction caused by the patient’s primary disease, heparin anticoagulation and thrombocytopaenia occurring during CRRT may all have contributed to the intraventricular haemorrhage. This indicates that the management of coagulation functions and an appropriate balance between procoagulation and anticoagulation are very important during CRRT. Electrolyte disturbances occurred in six patients and improved rapidly after active treatment, suggesting that electrolyte disturbances are common but manageable. The incidence of hypotension in this study (5/19 patients) was consistent with that reported previously.10 22 25 The incidence of hypotension in neonates during CRRT was not significantly different than that of children, suggesting that hypotension is not a limitation for the application of CRRT in neonates.10 22 25 Hypotension in neonates during CRRT is mainly affected by the volume of systemic circulation and the extracorporeal circuit.25 Dilution of the vasoactive drug concentration or binding of catecholamines to the extracorporeal circuit may be associated with hypotension at the initiation of CRRT.26 The use of an erythrocyte suspension prefilled with external blood circulation or the adjustment of the vasoactive drug dose at CRRT initiation can help prevent hypotension. Catheter blockage, which occurred in three patients, may be related to haemodynamic instability, slow blood flow settings or failure to achieve coagulation within the target ranges. This problem was solved by regulating the dosage of heparin or replacing catheters. Therefore, the identification of a more appropriate extracorporeal circuit, timely adjustment of vasoactive drugs and monitoring of the coagulation function and internal environment have important roles in CRRT for low-weight patients.

    During this study, the survival rate was 26.3% (5/19 patients). Patients who died had lower weight at CRRT initiation and lower urine output at the end of CRRT than patients who survived. The reported survival rate of infants treated with CRRT ranges from 35% to 44%; this range is similar to that of older paediatric patients.11 25 27–29 However, the survival rate of patients weighing ≤3 kg (25%) is lower than that of patients weighing >3 kg (41%).11 25 27–29 Urinary output and total body water of neonates are higher than those of children and adults, and there is a correlation between decreased urinary output after CRRT, mortality and kidney function recovery. Therefore, persistent oliguria after CRRT may be a marker of mortality for neonates undergoing CRRT.6 During this study, there was no significant difference in the age at CRRT initiation or AKI stage between patients who survived and those who died. No consensus regarding the optimal timing of CRRT initiation has been reached.7 However, retrospective cohort studies have reported that early initiation of CRRT is associated with improved survival of paediatric patients.10 26 30 Improving the survival of low-weight patients treated with CRRT should be a priority for future studies.

    This study is a two-centre retrospective study. Its limitations include the small sample size, potential regional differences and the effects of economic level. Long-term follow-up data of patients were also lacking.

    In conclusion, CRRT is feasible and effective for AKI in neonates who weigh ≤3 kg. The complications are manageable despite their frequent occurrence. Lower body weight and persistent oliguria may be correlated with an increased risk of mortality. Larger multicentre studies of the application of CRRT for AKI in neonates weighing ≤3 kg are needed to elucidate the precise appropriate treatment.

    Data availability statement

    Data are available on reasonable request. Data from this study can be obtained from the corresponding authors on reasonable request.

    Ethics statements

    Patient consent for publication

    Ethics approval

    This study involves human participants and was approved by the Ethics Committee of Shanghai Children’s Hospital (2020R064-E02). Participants gave informed consent to participate in the study before taking part.

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    Footnotes

    • YS and JX contributed equally.

    • Contributors YS, JX, DC and CC conceptualised the study. YS, JX, XC, WZ and XG collected and analysed the data. YS and JX prepared the first draft. XG, DC and CC reviewed and edited the manuscript. All authors approved the final manuscript. CC is responsible for the overall content as guarantor

    • Funding This work was supported by the Science and Technology Innovation Plan Of Shanghai Science and Technology Commission in 2020 (20Y11907000).

    • Competing interests None declared.

    • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

    • Provenance and peer review Not commissioned; externally peer reviewed.