Sepsis-Associated Acute Kidney Injury in the Paediatric Intensive Care Unit: Frequency and Outcomes

By Anosha Muhammad Aslam¹, Wasif Ilyas Vohra¹, Ariba Siddiqui¹, Ezza Riaz², Qalab Abbas¹, Sajid Bashir Soofi¹

Affiliations

1. Department of Paediatrics, The Aga Khan University Hospital, Karachi, Pakistan
2. Medical College, The Aga Khan University Hospital, Karachi, Pakistan

doi: 10.29271/jcpsp.2025.08.1001

ABSTRACT
Objective: To assess the frequency and short-term outcomes of padietric patients admitted with sepsis-associated acute kidney injury (S-AKI) in the paediatric intensive care unit (PICU).
Study Design: A cross-sectional study.
Place and Duration of the Study: Department of Paediatrics, The Aga Khan University Hospital, Karachi, Pakistan, from January 2021 to June 2022.
Methodology: Children aged 1 month to 18 years who were admitted to the PICU with a diagnosis of sepsis, based on the International Paediatric Sepsis Consensus (2005), were included. The p-RIFLE criteria was used to label AKI. Patients with chronic kidney disease or missing baseline creatinine at admission were excluded. The Chi-square test was used to study the association between variables. Logistic regression analysis was performed to compare AKI and non-AKI groups for different variables. Results are presented as mean with standard deviations and frequencies with percentages.
Results: During the study period, 1,114 patients were admitted to the PICU, of which 394 (35%) had sepsis. Three hundred and twenty-three patients met the inclusion criteria. The mean age of the study population was 2.49 ± 1.40 years, and 56 (17.3%) patients developed AKI. The mean length of PICU stay was 7.04 ± 6.47 days for children with AKI versus 5.24 ± 4.59 days for those without AKI. Of the 56 children with AKI, 44 (78.5%) received mechanical ventilation, and 10 (17.9%) underwent renal replacement therapy (RRT). Overall, 23.8% (n = 77) of patients expired during the study period ¾ 55 (20.59%) from the non-AKI group and 22 (39.22%) from the AKI group. Logistic regression analysis identified several factors associated with AKI, including hypotension at admission or during PICU stay (OR = 2.89, p = 0.002), oliguria (OR = 2.22, p = 0.028), raised BUN (OR = 3.51, p <0.001), and metabolic acidosis (OR = 2.79, p <0.001).
Conclusion: Patients with S-AKI, on average, had a longer PICU stay and higher odds of mortality.

Key Words: Paediatrics, Paediatric intensive care unit, Acute kidney injury, Sepsis, p-RIFLE.

INTRODUCTION

Worldwide, the overall incidence of acute kidney injury (AKI) has increased drastically over the past few decades, especially in patients in the intensive care unit (ICU).¹ Defining AKI remains challenging due to its multiple classifications and definitions, including the p-RIFLE and the Kidney Disease: Improving Global Outcomes (KDIGO) clinical guidelines.² The p-RIFLE criteria are considered more sensitive than others for diagnosing and staging AKI in critically ill children.^3,4

The reported incidence of AKI in PICU patients ranges from 20-50%.⁵ Children who develop AKI during their hospital admission are reported to have poorer outcomes, such as high mortality, increased need for mechanical ventilation, and longer hospital stays, compared to those who do not.⁶

Two of the most common causes of AKI are sepsis and shock.⁷ Sepsis-associated acute kidney injury (S-AKI) is one of the most common and life-threatening complications of sepsis. The reported incidence of AKI can be as high as 2/3^rd in patients with septic shock, increasing the in-hospital mortality rate by six to eightfold compared to patients without AKI.^8,9 Interestingly, sepsis and AKI are both risk factors for each other.¹⁰ This limitation in establishing temporality is one reason why S-AKI remains a complex and not fully understood phenomenon. Sepsis induces the widespread release of inflammatory cytokines, leading to a dysregulated immune response, which damages renal epithelial cells and causes kidney injury.¹¹ Sepsis and AKI share similar features, such as ischaemia hypoxia, inflammation, and cell death. Both conditions disrupt homeostasis and can lead to multiple organ dysfunction and failure.¹²

This study aimed to assess the frequency and short-term outcome of S-AKI and its correlation with different risk factors in children admitted to the PICU, so that early identification and instituting interventions may improve the outcomes of critically ill children.

METHODOLOGY

This was a descriptive study conducted at the Department of Paediatrics, The Aga Khan University Hospital, Karachi, Pakistan. It included patients aged 1 month to 18 years who met the diagnostic criteria of sepsis (suspected or confirmed infection with the presence of Systemic Inflammatory Response Syndrome), according to the International Paediatric Sepsis Consensus (2005).¹³ Moreover, they were admitted to the PICU from January 2021 to June 2022. Children with pre-existing chronic kidney disease, missing baseline creatinine level measured at PICU admission, or those with record of kidney transplant or renal replacement therapy (RRT) within the past year were excluded. The OpenEpi software was used to determine the sample size.

AKI was classified according to paediatric-modified RIFLE (p-RIFLE) criteria. The acronym p-RIFLE refers to Paediatric Risk, Injury, Failure, Loss, End-stage renal disease (ESRD).¹⁴ Only the creatinine clearance criteria from the p-RIFLE was used due to its feasibility and easy application in this study. Measurement of urine output prior to admission is often not possible and may be reduced for reasons unrelated to AKI, such as intravascular volume depletion or shock.³ Moreover, many patients receive diuretics before or during admission, and some may even present in the polyuric phase of AKI, which can falsely influence its diagnosis and staging.¹⁵

Data collection included demographic data, clinical variables (admitting diagnosis, urine output, blood pressures, medications used, and inotropic support), and laboratory data (serum creatinine, blood urea nitrogen, serum albumin, serum electrolytes, serum glucose, haematocrit, platelet count and proteinuria). Inotropic score was calculated using the formula described by Gaies et al. i.e. VIS = Dopamine (µg/kg/minutes) + Dobutamine (µg/kg/minutes) + 100 * Epinephrine (µg/kg/minutes) + 100 * Norepinephrine (µg/kg/minutes) + 10 * Milrinone (µg/kg/ minutes) + 10,000 * Vasopressin (Units/kg/minutes).¹⁶ Glome-rular filtration rate was estimated by Schwartz equation i.e. GFR = {Length (cm) × K (constant) / serum creatinine}.¹⁷ The use of nephrotoxic agents, such as vancomycin, amikacin, and ciprofloxacin was documented. Outcome variables — including length of hospital stay, duration and need for mechanical ventilation, re-intubation, requirement, and duration of dialysis, and mortality — were then recorded for analysis. Ethical Approval was obtained from the Ethical Review Committee of the Aga Khan University Hospital, with exemption from informed consent (ERC No. 2021-6785-19552).

Data were analysed using STATA version 7. Results are presented as mean with standard deviation (SD). The Chi-square test was used for categorical variables. Logistic regression analysis was done to explore S-AKI associated with the outcomes — such as length of hospital stay, length and need of mechanical ventilation, re-intubation, need and duration of RRT, and mortality. Odds ratios (OR) were reported with 95% confidence intervals (CI). A p-value of <0.05 was considered statistically significant.

RESULTS

During the study period, 1,114 paediatric patients were admitted to the PICU, of whom 394 (35%) had sepsis (Figure 1). A total of 323 patients met the inclusion criteria, among whom 192 (59.4%) were male (Table I). The mean age of the study population was 2.49 ± 1.40 years, and 112 (34.7%) patients were <1 year. System-wise admitting diagnosis included respiratory diseases (127 out of 323 patients, 39.3%), infectious diseases (81/323, 25.1%), central nervous system diseases (46/323, 14.2%), gastrointestinal tract diseases (22/323, 6.8%), haematology/ oncology diseases (19/323, 5.9%), cardiovascular diseases (12/323, 3.7%), and others such as vascular, metabolic, bone, renal or endocrine system related diseases (16/323, 4.9%). Out of the total 323 patients, 185 (57.3%) had culture-positive sepsis. Two hundred and forty-five (75.9%) patients had a previous hospital admission, and 146 (45.2%) had received antibiotics prior to admission. Moreover, the majority of patients received nephrotoxic drugs (80.1%) during their hospital stay. Frequency of S-AKI was 56 (17.3%) from total 323 patients during their hospital stay (Table II).

Patients with S-AKI had a significantly longer PICU stay than non-AKI patients (7.04 ± 6.47 vs. 5.24 ± 4.59, p <0.014). Moreover, these patients required aggressive interventions more often than those without AKI. Moreover, 44 (78.5%) patients with AKI required mechanical ventilation. Patients with S-AKI required invasive mechanical ventilation more frequently than patients without AKI (71.4% vs. 38.6%, p <0.001). The mean duration of mechanical ventilation use for S-AKI patients was 5.45 ± 4.31 days. Additionally, 10 (17.9%) patients with S-AKI required RRT. Patients with S-AKI required RRT more often than those without AKI (17.9% vs. 4.1%, p <0.001). The mean duration for RRT for S-AKI patients was 95.20 ± 72.57 hours. All in all, the main outcome, mortality occurred almost twice as often in S-AKI patients as opposed to non-AKI patients (39.3% vs. 20.6%, p = 0.003; Table II).

Figure  1:  Flowchart  of  the  study.

Table  I:  Patient  demographics.

Variables	Total (n = 323)
Gender (male)	192/323 (59.4%)
Age in years	-
<1 years	112/323 (34.7%)
1 to 2 years	69/323 (21.4%)
3 to 6 years	50/323 (15.5%)
7 to 12 years	56/323 (17.3%)
>12	36/323 (11.1%)
Age in months (mean ± SD)	2.49 ± 1.40
Admitting diagnosis	-
Respiratory system	127/323 (39.3%)
Infectious diseases	81/323 (25.1%)
Central nervous system	46/323 (14.2%)
Gastrointestinal tract	22/323 (6.8%)
Heme-oncology	19/323 (5.9%)
Cardiovascular system	12/323 (3.7%)
Vascular	5/323 (1.5%)
Metabolic	5/323 (1.5%)
Bone	2/323 (0.6%)
Renal system	2/323 (0.6%)
Endocrine system	2/323 (0.6%)
Previous hospital admission	245/323 (75.9%)
Antibiotics before admission	146/323 (45.2%)
Nephrotoxic drugs received	117/146 (80.1%)
Culture-positive sepsis	185/323 (57.3%)
Source of infection	-
Community-acquired	104/323 (32.2%)
Hospital acquired	81/323 (25.1%)
Not known	138/323 (42.7%)
Class of organism	-
Gram-negative rods	73/323 (22.6%)
Gram-positive cocci	71/323 (22.0%)
Virus	42/323 (13.0%)
Fungus	40/323 (12.4%)
Tuberculosis	3/323 (0.9%)
Length of PICU stay in days (mean ± SD)	5.55 ± 5.01
Length of hospital stay in days (mean ± SD)	8.69 ± 6.53
Mechanical ventilation in days (mean ± SD)	5.40 ± 4.28
Need of reintubation	12/323 (3.7%)
Need of RRT	21/323 (6.5%)
RRT in hours (mean ± SD)	81.26 ± 70.24
Mortality	77/323 (23.8%)

In the logistic regression analysis (Table III), the significant predictors for S-AKI were oliguria (OR = 2.22, p = 0.028), hypotension (OR = 2.89, p = 0.002), raised BUN (OR = 3.51, p <0.001), use of diuretics (OR = 2.52, p = 0.043), use of inotropes (OR = 4.72, p <0.001), need for blood transfusion (OR = 2.75, p = 0.002), low albumin (OR = 2.42, p = 0.021), metabolic acidosis (OR = 2.79, p <0.001), lactic acidosis (OR = 2.13, p = 0.012), hypokalaemia (OR = 2.67, p = 0.001) or hyperkalaemia (OR = 2.36, p = 0.017), hypernatraemia (OR = 2.4, p = 0.004), hyperchloraemia (OR = 2.11, p = 0.012), hyperglycaemia (OR = 2.41, p = 0.005), haematuria (OR = 2.87, p <0.001), low Hb (OR = 2.07, p = 0.032), low neutrophils (OR = 2.20, p = 0.023), low platelets (OR = 2.18, p = 0.009), high procalcitonin (OR = 2.79, p = 0.002), and culture-positive sepsis (OR = 2.33, p = 0.009).

DISCUSSION

This study showed that developing sepsis-induced S-AKI increases both morbidity and mortality among patients during their stay in PICU. Approximately one-sixth patients with sepsis developed some degree of renal injury, and the mortality rate was nearly double in those with AKI compared to those without it. Moreover, S-AKI was associated with prolonged hospital stay, hypotension, use of inotropes, low platelets or an increased need for blood transfusions.

Prolonged hospital stay has been frequently established as a likely outcome in patients with AKI during sepsis as opposed to those without it.¹⁸ Moreover, increased severity of S-AKI results in higher chances of morbidity and mortality. Fitzgerald et al. reported a two-times higher mortality or new disability rate in patients with severe AKI compared to those with no/mild AKI.¹⁹

Table II: Therapeutic interventions and outcomes based on AKI status.
 

Parameters	AKI (n = 56)	NON-AKI (n = 267)	p-values*
Patients requiring hospital stay of >7 days	30/56 (53.6%)	122/267 (45.7%)	0.280
Patients requiring PICU stay of >7 days	21/56 (37.5%)	46/267 (17.2%)	<0.001
Length of PICU stay in days (mean ± SD)	7.04 ± 6.47	5.24 ± 4.59	0.014
Patients requiring mechanical ventilation of >3 days	24/40 (60.0%)	61/106 (57.5%)	0.790
Mechanical ventilation in days (mean ± SD)	5.45 ± 4.31	5.38 ± 4.29	0.930
Mode of ventilation	-	-	-
Non-invasive	38/56 (67.9%)	219/267 (82.0%)	0.017
SIMV/conventional	40/56 (71.4%)	103/267 (38.6%)	<0.001
HFOV	4/56 (7.1%)	8/267 (3.0%)	0.140
Room air	0/56 (0.0%)	5/267 (1.9%)	0.300
Inotropic score (mean ± SD)	32.28 ± 32.53	26.35 ± 32.19	0.310
Need of reintubation	4/56 (7.1%)	8/267 (3.0%)	0.140
Need of RRT	10/56 (17.9%)	11/267 (4.1%)	<0.001
Patients requiring RRT of >72 hours	6/10 (60%)	3/11 (27%)	0.130
RRT in hours (mean ± SD)	95.20 ± 72.57	68.59 ± 68.96	0.400
Type of dialysis	-	-	0.830
CRRT	5/10 (50%)	6/11 (55%)	-
Peritoneal dialysis	5/10 (50%)	5/11 (45%)	-
Code status	-	-	0.002
Full	35/56 (62.5%)	215/267 (80.5%)	-
Withdrawal	8/56 (14.3%)	31/267 (11.6%)	-
Others	13/56 (23.2%)	21/267 (7.9%)	-
Mortality	22/56 (39.3%)	55/267 (20.6%)	0.003
*A p-value was determined using the Chi-square test. SIMV: Synchronised intermittent mandatory ventilation, SD: Standard deviation, HFOV: High frequency oscillatory ventilation, RRT: Renal replacement therapy, CRRT: Continuous renal replacement therapy.

Table III: Factors associated with AKI.

Variables	OR	95% CI	p-values*
Age in years	-	-	-
<1 years	1.04	0.44, 2.48	0.915
1 to 2 years	0.18	0.05, 0.65	0.009
3 to 6 years	0.48	0.16, 1.46	0.201
7 to 12 years	0.42	0.14, 1.27	0.129
>12	-	-	-
Haematology	-	-	-
Neutrophils (high)	1.94	0.95, 3.94	0.066
Neutrophils (low)	2.20	1.11, 4.36	0.023
Lymphocytes (high)	1.85	0.94, 3.63	0.073
Lymphocytes (low)	1.62	0.83, 3.18	0.155
Platelets (high)	0.79	0.36, 1.71	0.555
Platelets (low)	2.18	1.21, 3.91	0.009
HB low	2.07	1.06, 4.04	0.032
High HCT	0.94	0.34, 2.59	0.919
High TLC	1.97	0.99, 3.89	0.051
Low TLC	0.92	0.45, 1.85	0.818
Metabolic panel	-	-	-
Raised BUN	3.51	1.76, 7.00	<0.001
Metabolic acidosis	2.79	1.51, 5.13	<0.001
Lactic acidosis	2.13	1.18, 3.86	0.012
Hypercalcaemia	1.93	0.90, 4.13	0.09
Hypocalcaemia	1.53	0.76, 3.08	0.232
Hypokalaemia	2.67	1.47, 4.82	0.001
Hyperkalaemia	2.36	1.16, 4.78	0.017
Hyponatraemia	1.68	0.85, 3.35	0.134
Hypernatraemia	2.4	1.32, 4.36	0.004
Low bicarbonate	1.7	0.95, 3.05	0.073
Hyperchloraemia >105	2.11	1.17, 3.79	0.012
Hyperglycaemia	2.41	1.30, 4.48	0.005
Hypoglycaemia	1.75	0.84, 3.62	0.132
Blood pressure	-	-	-
Hypotension	2.89	1.47, 5.69	0.002
Hypertension	0.64	0.28, 1.43	0.281
Use of inotropes	4.72	2.42, 9.19	<0.001
Volume overload	2.52	1.03, 6.15	0.043
Low albumin	2.42	1.14, 5.14	0.021
Blood transfusion	2.75	1.47, 5.16	0.002
Need of IVIG	1.54	0.71, 3.34	0.274
Need of insulin infusion	2.51	0.82, 7.68	0.104
Urine	-	-	-
Haematuria in urine dip/DR	2.87	1.54, 5.34	<0.001
Proteinuria in urine dip/DR	1.66	0.85, 3.25	0.133
Oliguria	2.22	1.08, 4.54	0.028
Procalcitonin high	2.79	1.47, 5.29	0.002
Elevated CRP	1.82	0.99, 3.32	0.052
Culture-positive sepsis	2.33	1.23, 4.42	0.009
*Logistic regression.

Early identification of renal injury thus can have a significant impact on implementing renal protective measures and prevention of mortality. Aggressive management of sepsis by appropriate anti-microbial therapy, early correction of acidosis or electrolyte imbalances — such as hypo- or hyperkalaemia — and treating hypotension may aid in preventing kidney injury.²⁰ One retrospective study concluded similar results, with duration of severe systolic hypotension in the first 48 hours of paediatric sepsis associated with AKI incidence and duration.²¹ Moreover, Ozkaya et al. identified low platelet count as an independent risk factor for the developing S-AKI.⁴ Their study concluded that low platelet levels were significantly associated with the development of S-AKI. Other risk factors or clinical conse-quences of sepsis and AKI — such as hypovolaemia or exposure to nephrotoxic agents — can confound the relation between the two.²² Some patients in this study who did not develop AKI still required RRT, possibly due to volume overload during their PICU stay or electrolytes imbalances that necessitated prompt interventions. Previous studies have indicated that fluid overload is usually associated with poorer outcomes.²³

Limited data are available from developing countries regarding S-AKI, and this study addresses that literature gap. By identifying key clinical and biochemical risk factors linked to the development of S-AKI and associated mortality, this study offers valuable insight into the disease that can support early recognition, targeted interventions, and improved outcomes in critically ill children. However, this was a single-centre study, which may not be applicable to the general population or setting. Additionally, not all potential risk factors were evaluated, particularly patients’ volume status at admission or during PICU stay and the renal angina index, both of which are main contributors to renal injury.

The study relied exclusively on the serum creatinine-based p-RIFLE criteria, as urine output could not be incorporated due to feasibility constraints. While practical, this may have led to underdiagnosis or misclassification of AKI, especially in patients receiving diuretics or those in the polyuric phase. Furthermore, novel biomarkers — such as neutrophil gelatinase-associated lipocalin (NGAL), interleukin-8 (IL-8), kidney injury molecule-1 (KIM-1), and liver-type fatty acid-binding protein (L-FABP) — which offer earlier and more sensitive detection of renal injury, were not used due to limited resource availability.

Another limitation is the retrospective nature of the study and the absence of long-term follow-up. While short-term outcomes were assessed, the long-term renal sequelae of S-AKI—such as chronic kidney disease (CKD) or progression to ESRD — remain unexamined.

Early identification of AKI is a key in initiating appropriate supportive measures to minimise long-term sequelae of the disease. Approximately 10% of the patients who had AKI during their stay in the PICU developed CKD within 1 to 3 years post-discharge, likely due to renal inflammation and subsequent fibrosis leading to chronic dysfunction.^24,25 Targeted identification and management of modifiable risk factors can markedly reduce the incidence and severity of S-AKI in paediatric patients. Early screening, vigilant monitoring of high-risk patients, avoidance of nephrotoxic drugs, optimal fluid resuscitation, and timely treatment of underlying infections are essential strategies. Implementing these measures can mitigate complications and improve both short-term and long-term outcomes in critically ill children.

In the future, a multi-centre study would provide a more comprehensive understanding of the full scope of AKI and produce results generalisable to the broader population.

CONCLUSION

The frequency of AKI in the studied patients was 17.3%, with a higher incidence observed in infants under one year of age and a predominance among males. The development of S-AKI during sepsis was associated with nearly a two-fold increase in mortality compared to those without it. It was also linked to worse clinical outcomes ¾ including increased need for invasive mechanical ventilation, RRT, and prolonged hospital stay.

ETHICAL APPROVAL:
Ethical approval was obtained from the Ethical Review Committee of the Aga Khan University Hospital, Karachi, Pakistan (ERC No. 2021-6785-19552).

PATIENTS’ CONSENT:
Informed consent was taken from all participants of this study.

COMPETING INTEREST:
The authors declared no conflict of interest.

AUTHORS’ CONTRIBUTION:
AMA: Study conception and design, literature search, data collection, and assembly of data.
WIV: Data collection, data analysis, and interpretation.
AS: Study conception and design, data analysis and interpretation.
ER: Manuscript drafting.
SBS, QA: Manuscript drafting and critical revision.
All authors approved the final version of the manuscript to be published.

REFERENCES

1. Wang X, Jiang L, Wen Y, Wang MP, Li W, Li ZQ, et al. Risk factors for mortality in patients with septic acute kidney injury in intensive care units in Beijing, China: A multicenter prospective observational study. Biomed Res Int 2014; 2014:172620. doi: 10.1155/2014/172620.
2. Khwaja A. KDIGO clinical practice guidelines for acute kidney injury. Nephron Clin Pract 2012; 120(4):c179-84. doi: 10. 1159/000339789.
3. Usman P, Qaisar H, Haque AU, Abbas Q. Comparison of two definitions (p-RIFLE AND KDIGO) for prevalence of acute kidney injury and in hospital mortality in a paediatric intensive care unit of Pakistan. J Ayub Med Coll Abbottabad 2022; 34(1):112-7. doi: 10.55519/JAMC-01-9147.
4. Ozkaya PY, Taner S, Ersayoglu I, Turan B, Yildirim Arslan S, Karapinar B, et al. Sepsis associated acute kidney injury in paediatric intensive care unit. Ther Apher Dial 2023; 27(1): 73-82. doi: 10.1111/1744-9987.13928.
5. Hessey E, Melhem N, Alobaidi R, Ulrich E, Morgan C, Bagshaw SM, et al. Acute kidney injury in critically ill children is not all acute: Lessons over the last 5 years. Front Pediatr 2021; 9:648587. doi: 10.3389/fped.2021.648587.
6. Alkandari O, Eddington KA, Hyder A, Gauvin F, Ducruet T, Gottesman R, et al. Acute kidney injury is an independent risk factor for paediatric intensive care unit mortality, longer length of stay and prolonged mechanical ventilation in critically ill children: A two-center retrospective cohort study. Crit Care 2011; 15(3):R146. doi: 10.1186/cc10269.
7. Prowle JR. Sepsis-associated AKI. Clin J Am Soc Nephrol 2018; 13(2):339-42. doi: 10.2215/CJN.07310717.
8. Manrique-Caballero CL, Del Rio-Pertuz G, Gomez H. Sepsis-associated acute kidney injury. Crit Care Clin 2021; 37(2):279-301. doi: 10.1016/j.ccc.2020.11.010.
9. Kellum JA, Chawla LS, Keener C, Singbartl K, Palevsky PM, Pike FL, et al. The effects of alternative resuscitation strategies on acute kidney injury in patients with septic shock. Am J Respir Crit Care Med 2016; 193(3):281-7. doi: 10.1164/rccm.201505-0995OC
10. Basalely A, Menon S. Sepsis and AKI: A two-way street. Kidney360 2023; 4(3):289-90. doi: 10.34067/KID.0000000 000000106.
11. He FF, Wang YM, Chen YY, Huang W, Li ZQ, Zhang C. Sepsis-induced AKI: From pathogenesis to therapeutic approaches. Front Pharmacol 2022; 13:981578. doi: 10.3389/fphar.2022. 981578.
12. Devarajan P, Basu RK. Sepsis-associated acute kidney injury – Is it possible to move the needle against this syndrome? J Pediatr (Rio J) 2017; 93(1):1-3. doi: 10.1016/j.jped.2016.09.001.
13. Goldstein B, Giroir B, Randolph A, International Consensus Conference on Paediatric Sepsis. International paediatric sepsis consensus conference: definitions for sepsis and organ dysfunction in paediatrics. Pediatr Crit Care Med 2005; 6(1):2-8. doi: 10.1097/01.PCC.0000149131.72248.E6.
14. Sadeghi-Bojd S, Noori NM, Mohammadi M, Teimouri A. Clinical characteristics and mortality risk prediction in children with acute kidney injury. Niger Med J 2015; 56(5):327-2. doi: 10.4103/0300-1652.170381.
15. Allen JC, Gardner DS, Skinner H, Harvey D, Sharman A, Devonald MAJ. Definition of hourly urine output influences reported incidence and staging of acute kidney injury. BMC Nephrol 2020; 21(1):19. doi: 10.1186/s12882-019-1678-2.
16. Gaies MG, Gurney JG, Yen AH, Napoli ML, Gajarski RJ, Ohye RG, et al. Vasoactive-inotropic score as a predictor of morbidity and mortality in infants after cardiopulmonary bypass. Pediatr Crit Care Med 2010; 11(2):234-8. doi: 10.1097/PCC.0b013e3181b806fc.
17. Gao A, Cachat F, Faouzi M, Bardy D, Mosig D, Meyrat BJ, et al. Comparison of the glomerular filtration rate in children by the new revised Schwartz formula and a new generalized formula. Kidney Int 2013; 83(3):524-30. doi: 10.1038/ki. 2012.388.
18. Afroze M, Haider M, Arshad U, Noor N, Naqvi S, Tebha S. Frequency of acute kidney injury among septic children, admitted at a tertiary care hospital. Medical Forum Monthly 2021; 32:107-11.
19. Fitzgerald JC, Basu RK, Akcan-Arikan A, Izquierdo LM, Pineres Olave BE, Hassinger AB, et al. Acute kidney injury in paediatric severe sepsis: An independent risk factor for death and new disability. Crit Care Med 2016; 44(12): 2241-50. doi: 10.1097/CCM.0000000000002007.
20. Kumar A, Roberts D, Wood KE, Light B, Parrillo JE, Sharma S, et al. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Crit Care Med 2006; 34(6):1589-96. doi: 10.1097/01.CCM.0000217961.75225.E9.
21. Fitzgerald JC, Ross ME, Thomas NJ, Weiss SL, Balamuth F, Chilutti M, et al. Association of early hypotension in paediatric sepsis with development of new or persistent acute kidney injury. Pediatr Nephrol 2021; 36(2):451-61. doi: 10.1007/s00467-020-04704-2.
22. Perner A, Cecconi M, Cronhjort M, Darmon M, Jakob SM, Pettila V, et al. Expert statement for the management of hypovolemia in sepsis. Intensive Care Med 2018; 44(6): 791-8. doi: 10.1007/s00134-018-5177-x.
23. Payen D, de Pont AC, Sakr Y, Spies C, Reinhart K, Vincent JL. A positive fluid balance is associated with a worse outcome in patients with acute renal failure. Crit Care 2008; 12(3):R74. doi: 10.1186/cc6916.
24. Mammen C, Al Abbas A, Skippen P, Nadel H, Levine D, Collet JP, et al. Long-term risk of CKD in children surviving episodes of acute kidney injury in the intensive care unit: A prospective cohort study. Am J Kidney Dis 2012; 59(4): 523-30. doi: 10.1053/j.ajkd.2011.10.048.
25. Lewers DT, Mathew TH, Maher JF, Schreiner GE. Long-term follow-up of renal function and histology after acute tubular necrosis. Ann Intern Med 1970; 73(4):523-9. doi: 10.7326/ 0003-4819-73-4-523.