Jurnal Nefro 12
Jurnal Nefro 12
Jurnal Nefro 12
Background: There is a paucity of data on long term-outcomes of children who undergo acute peritoneal dialysis (PD)
in resource-limited settings. We reviewed the outcomes of children who underwent PD after 18 months of follow-up.
Methods: We conducted a prospective cohort study in children with acute kidney injury (AKI) who underwent PD.
Diagnosis of AKI was based on the 2012 Kidney Disease: Improving Global Outcomes definition. We assessed
outcomes of in-hospital mortality, 18-month post-dialysis survival, factors associated with survival, and progression
to chronic kidney disease (CKD).
Results: Twenty-nine children with a median age of 6 (3 to 11) years underwent acute PD. In-hospital mortality was
3/29 (10.3%) and rose to 27.6% during follow-up. Seven (24.1%) children were lost to follow-up. Of the 14 remaining
children, six (42.9%) experienced full recovery of renal function, while eight (57.1%) progressed to CKD. Among those
who experienced full recovery, median (interquartile range) estimated glomerular filtration rate (eGFR) rose from
12.67 (7.05, 22.85) mL/min/1.73 m2 to 95.56 (64.50, 198.00) mL/min/1.73 m2, P = 0.031. No significant changes
in median eGFR from baseline were observed among those who progressed to CKD (P = 0.383) or in non-survivors (P =
0.838). According to Kaplan-Meier curve analyses, 18-month survival during follow-up was 66.0% (95% CI, 45.0%
to 86.5%). Age < 5 was associated with greater likelihood of survival (OR, 3.217; 95% CI, 1.240 to 8.342).
Conclusion: Progression of post-PD AKI to CKD occurred in more than half of survivors. Age < 5 was associated with
greater likelihood of survival.
Keywords: Acute kidney injury, Child, Chronic kidney disease, Peritoneal dialysis, Survival
Introduction
Received April 8, 2020; Revised June 7, 2020; Acute kidney injury (AKI) is a sudden decline in renal
Accepted July 2, 2020 function that is characterized by retention of nitrogenous
Editor: Hee Gyung Kang, Seoul National University, Seoul, Republic
of Korea waste products [1]. Globally, it is one of the leading
Correspondence: Olayinka Rasheed Ibrahim causes of childhood death, with varying incidence, eti-
Department of Paediatrics, Federal Medical Centre, Along Jibya ologies, and outcomes [2]. The pooled global incidence
Bypass Road, Katsina 820241, Nigeria. E-mail: ibroplus@gmail.com
of pediatric AKI is estimated at 33.7% (95% confidence
Copyright © 2020 by The Korean Society of Nephrology
interval [CI], 26.9 to 41.3) [3]. However, the incidence of
CC
This is an open-access article distributed under the terms of the Creative
Commons Attribution Non-Commercial License (http://creativecommons. pediatric AKI varies from less than 1% to as high as 60%
org/licenses/by-nc-nd/4.0/), which permits unrestricted non-commercial
use, distribution, and reproduction in any medium, provided the original work depending on the population [4,5], and low middle-
is properly cited. income countries (LMIC) have higher prevalence and
Kidney Res Clin Pract Vol. 39, No. 4, December 2020
poorer outcomes compared with high-income countries AKI from the final data analysis. Children with end stage
[6-8]. A number of factors underlies the high morbid- renal disease that required continuous renal replacement
ity and mortality of pediatric AKI in LMIC, including therapy were also excluded. All patients with AKI were
the predominance of infection-related causes, delayed admitted to the emergency pediatric unit of the hospital.
presentation, inadequate access to specialist care, lack of A Microsoft Excel spreadsheet was used to capture data
access to renal replacement therapy (RRT), and paucity for children who had AKI including acute PD during
of data, especially from Africa. When data are available, hospital admission. The spreadsheet captured detailed
they are mainly from tertiary health facilities that treat history and physical examination data for each child
relatively few patients [7-10]. at admission. Anthropometric data including weight,
Despite the challenges in caring for children with AKI height, body mass index, and body surface area were also
in developing countries, there has been recent progress documented for each patient. Upon admission, data for
in some tertiary health facilities in LMIC that now of- complete blood count, peripheral blood film appear-
fer acute peritoneal dialysis (PD) using adaptable tech- ance, blood film for the malaria parasite, urinalysis and
niques [11-13]. This pragmatic approach utilizes impro- urine microscopy, electrolytes, urea, creatinine, calcium,
vised PD catheters and locally constituted PD fluids. PD phosphate, and abdominal ultrasound were obtained
exchange procedures are performed manually at bedside for all patients. We also recorded information for blood
[14]. There are some data regarding treatment and out- cultures, hemoglobin genotyping, bleeding time, pro-
comes of children with AKI and acute PD in LMIC, espe- thrombin time, activated partial thromboplastin time,
cially Nigeria [15-17]. However, these studies are limited renal biopsy (where indicated), complement C3 and C4,
to analyses of procedure complications and in-hospital anti-double stranded DNA, and antinuclear antibody test
mortality. Very few studies include outcomes measured for some patients as clinically indicated. For the recruited
as long as three months after onset of AKI [12,17]. Thus, children, serum creatinine, urea, and electrolyte studies
the long term-outcomes of children who undergo acute were repeated, and clinical details were updated upon
PD for AKI in developing countries remain largely un- follow-up. Estimated glomerular filtration was calculated
known. Therefore, in this study, we determined the using the original Schwartz formula (estimated glomeru-
outcomes of children with acute PD for AKI who were lar filtration rate, eGFR = k × L/Scr, mL/min/1.73 m2, L
treated at a faith-based hospital in southwest Nigeria. was height in c, Scr was serum creatinine mg/dL, and k
The outcomes assessed were in-hospital mortality, pro- was the constant) [18]. The values of K used were 0.45 for
gression to chronic kidney disease (CKD), mortality rate infants, 0.55 for children and females, and 0.7 for males’
on follow-up, and factors associated with survival. adolescents.
The indications for RRT included the presence of one
Methods or more of the following features: uremic syndrome, poor
response to medical treatment for severe or rapidly rising
We conducted this study at Bowen University Teaching azotemia, hyperkalemia (serum potassium > 6.5 mmol/L),
Hospital (BUTH) Ogbomosho, southwest Nigeria, which severe metabolic acidosis (serum bicarbonate less than
is a faith-based teaching hospital. The BUTH Research 10 mmol/L), persistent oligoanuria, un-affordability of
Ethics Review Committee provided ethical approval for HD, and other indications according to the Kidney Dis-
the study (ethical approval number: NHERC/12/04/2012). ease: Improving Global Outcomes (KDIGO) guidelines.
In addition, we obtained consent from the parents/care- The indicating preference for PD over HD included he-
givers and assent from older children. modynamically unstable patients, weight less than 10 kg
This was a prospective cohort study that involved 29 (only F-series dialyser cube; SA of 0.2 m2 was available for
pediatric patients who underwent acute PD out of 107 pediatric patients at the dialysis unit), and anticoagulant
with AKI managed at BUTH between December 2014 and intolerance.
January 2017. We included children aged 18 years and We carried out PD in a dedicated side room in the pedi-
younger and excluded children who were treated with atric ward. All children had a urethral catheter passed for
hemodialysis (HD) and conservative management for monitoring of urine output. Strict aseptic pre-conditions
470 www.krcp-ksn.org
Alao, et al. Survival after acute PD in children
were maintained throughout the procedure. The head cal state were monitored until discharge.
of the nephrology team, who is one of the authors, pre-
scribed PD and inserted the catheter at bedside. Trained Definitions
nurses carried out PD cycling manually with support of
the resident physicians. We administered intravenous 2 AKI was defined as an at least 0.3 mg/dL rise in baseline
mg/kg of intravenous ethamsylate 30 minutes before PD serum creatinine within 48 hours, 1.5 times increase in
catheter insertion. The anterior abdomen was cleaned baseline creatinine within seven days, or urine output ≤
with antiseptic (povidone-iodine), and the surgical site 0.5 mL/kg/hr within six hours based on the 2012 KDIGO
was infiltrated with 0.5% lidocaine at 4 mg/kg. A 0.5 cm criteria [19]. We obtained baseline creatinine values and
incision was made about 2.5 cm below the umbilicus estimated the eGFR at the first point of contact during ad-
with a size 15 surgical blade deep through to the fascia. mission. CKD was defined as eGFR less than 60 mL/min
If a sterile, reusable stylet was not available, an adapted, per 1.73 m2 at least three months after discharge [20,21].
sterile bicycle spoke was inserted into a fenestrated size Anuria was defined as urine < 1 mL/kg/d [22].
10 feeding tube for resilience through the skin nick with
sustained pressure until we felt some “give.” The adapted Follow-up
stylet was removed, and the tube was gently advanced
into the peritoneal cavity. A child was defined as “lost to follow-up” when he or
A deep subcutaneous purse-string suture was inserted she missed two consecutive clinic visits and attempts to
if the catheter ran loosely through the incision. The im- communicate with the parents by phone failed. Post-hos-
provised PD catheter was connected to a 3-way tap, with pitalization mortality was confirmed by follow-up calls
the second end connected to the PD fluid tubing, while to caregivers/parents following two consecutive clinic
the third drained the effluent into an improvised urinary defaults. Five children with nephrotic syndrome and AKI
bag. We used standard PD fluid (Fresenius SE & Co., Bad received angiotensin-converting enzyme inhibitor thera-
Homburg, Germany) with 1.5% glucose containing Na+ py as part of the management protocol during follow-up.
134 mmol/L, Ca2+ 1.75 mmol/L, Mg2+ 0.5 mmol/L, Cl-
103.5 mmol/L, pH 5.5, and caloric density of 60 kcal/L Outcomes
for PD. If a patient was edematous, 2.3% glucose was al-
ternated with 1.5% dextrose PD fluids. We spiked the PD The primary outcome was 18-month survival after
with 100 IU/L of heparin and 4 mg/L of gentamycin. We acute PD. The secondary outcomes were in-hospital
ran 5 to 10 mL/kg PD fluid for the first three cycles with- deaths, progression to CKD (defined as eGFR less than 60
out dwell time to ensure smooth operation. Subsequent- ml/min per 1.73 m2 at least three months after discharge)
ly, the PD fluid was increased to 20 to 40 mL/kg depend- [20], and factors associated with 18-month survival.
ing on tolerability and absence of respiratory distress.
Cycles of PD were performed until patients regained full Data and statistical analysis
consciousness, urinary output greater than 1.5 mL/kg/
hr, and were ambulating. However, in the event of recur- Data collected were analyzed using IBM SPSS ver-
rence of oliguric, anuric, or rising azotemia or worsening sion 23.0 for Windows (IBM Corp., Armonk, NY, USA).
encephalopathy, dialysis was re-commenced. If potas- Means and standard deviations were used to summarize
sium was less than 4 mmol/L, a potassium supplement of parametric continuous variables that were normally dis-
4 mmol/L was added to the PD fluid. Patients’ vital signs tributed (blood pressure). Age, weight, height, and body
were closely monitored throughout the procedures. The surface area were not normally distributed and were
presence of abdominal pain, tenderness, guarding, and summarized as median with interquartile range (IQR).
cloud effluent of PD fluid were suggestive of peritonitis. Discrete variables were summarized as frequency and
At the end of the procedure, the catheter tip and PD fluid percentage. The adjusted odds ratio (OR) was used to
were sent for microscopy culture and sensitivity when in- evaluate independent predictors of survival among pa-
dicated. Electrolyte urea and creatinine levels and clini- tients (14 survivors and 8 non-survivors) with complete
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Kidney Res Clin Pract Vol. 39, No. 4, December 2020
Deaths
(10.3%, 95% CI 2.2% to 27.3%) (n = 3)
Discharged (n = 26)
18 months follow-up
data at the end of follow-up. The variables were age, were community-acquired AKI, and 15 (51.7%) children
weight, height, body surface area, etiology, anuria, hy- had the non-oliguric form of AKI. The duration of PD
pertension, duration of hospitalization, and number of ranged from 1 to 8 days, as shown in Table 1.
dialysis sessions. The outcome of interest for the adjusted The most common cause of AKI was septicemia (n =
OR was survival at 18 months, which was plotted as a 11, 37.9%). Other causes of AKI included malaria (n = 3),
Kaplan-Meier curve. For plotting the curves, the primary obstructive uropathy (posterior urethral valve) (n = 4), ne-
event was 18-month survival of the cohort, and we cen- phrotic syndrome (n = 5, 17.2%), acute glomerulonephritis
sored those who were lost to follow-up and who survived (n = 3, 10.3%), and hemolytic uremic syndrome (n = 1,
beyond 18 months. The level of statistical significance 3.4%), as shown in Table 2. The etiology of AKI was compa-
was set at P < 0.05. rable among patients who underwent conservative man-
agement and those that received PD. Based on the index of
Results severity (KDIGO AKI classification), 63.0% (46/73) of chil-
dren in the conservative management group were stage 1,
A total of 107 children aged 4 months to 18 years expe- while 26.0% (19/73) and 11.0% (8/73) were stages 2 and 3,
rienced AKI over the study period, for a cumulative inci- respectively (Table 2). The children in the PD group were
dence of 8.43 per 100,000 person-years. Of 107 children all stage 3, as shown in Table 2. Mortality was significantly
who had AKI, 73 (68.2%) were conservatively managed, higher in children who underwent PD compared with
29 (27.1%) underwent PD, and 5 (4.7%) underwent HD, as children who were treated by conservative management
shown in Fig. 1. The median (IQR) age of 29 children with (P = 0.021). The indications for PD were azotemia (n = 15,
acute PD was 6 (3 to 11) years, and most were male (n = 51.7%), encephalopathy (n = 15, 51.7%), hyperkalemia (n =
20, 69.0%). Fever was the most common clinical feature 3, 10.3%), and anuria (n = 9, 31.0%), and eight children had
at presentation (n = 23, 79.3%), while six children (20.7%) multiple indications (Table 3).
had hypertension. We noted that 27 of 29 cases (93.1%) Of the 29 children who underwent acute PD, three died
472 www.krcp-ksn.org
Alao, et al. Survival after acute PD in children
during hospitalization, yielding a case fatality rate of organ dysfunction syndrome, as shown in Table 4. Five
10.3% (95% CI, 2.2% to 27.3%). The three patients who additional deaths were recorded during follow-up of the
died during hospitalization were lost due to multiple 26 survivors who had acute PD, yielding a cumulative
mortality rate of 27.6% (95% CI, 12.7% to 47.2%) as shown
Table 1. Clinical variables of children who were treated with in Fig. 1. During follow-up, two children died from febrile
peritoneal dialysis (n = 29) illness unrelated to kidney disease, one died from end
Clinical variable Value stage kidney disease, and we were unable to obtain the
Age (yr) 6 (3-11) details regarding cause of death in the remaining two
Male 20 (69.0) children (Table 4). The Kaplan-Meier curve showed that
Fever 23 (79.3) the 18-month survival during follow-up was 66.0% (95%
Diarrhea 5 (17.2)
CI, 45.0% to 86.5%) as shown in Fig. 2. The mean survival
Vomiting 17 (58.6)
was 18.6 months (95% CI, 14.8 to 22.4). Seven children
Jaundice 7 (24.1)
(26.9%) were lost to follow-up. Of the 14 who survived to
Cough 9 (31.0)
18 months post dialysis, six (42.9%) had fully recovered
Breathlessness 14 (48.3)
renal function, while eight (57.1%) progressed to CKD as
Dark brown urine 15 (51.7)
Weight (kg) 20 (13.5-28.5) shown in Fig. 1. At the end of 18 months, among those
Systolic blood pressure (mmHg) 110.9 ± 52.8 who had full recovery, the median (IQR) eGFR rose from
Diastolic blood pressure (mmHg) 68.6 ± 31.6 12.67 (7.05, 22.85) mL/min/1.73 m2 baseline at admission
Hypertension 6 (20.7) to 95.56 (64.50, 198.00) mL/min/1.73 m2, P = 0.031. There
Community-acquired AKI 27 (93.1)
Hospital-acquired AKI 2 (6.9)
Table 3. Indications for peritoneal dialysis (n = 29)
Non-oliguric AKI 15 (51.7)
Oliguric AKI 14 (48.3) Indication n (%)
PD cycles 20 (12-28) Azotemia 15 (51.7)
Duration of PD (day) 1-8 Uremic encephalopathy 15 (51.7)
Hyperkalemia 3 (10.3)
Data are presented as median (interquartile range), number (%), mean ±
standard deviation, or ranges only. Anuria 9 (31.0)
AKI, acute kidney injury; PD, peritoneal dialysis. Persistent hypertension 1 (3.4)
Table 2. Etiology, severity, and outcomes of AKI among the study children
Total AKIa Conservative and renal replacement therapy (n = 102)
Management Conservative (n = 73) Renal replacement therapy (PD) (n = 29) P value
KDIGO Stage 1 46
KDIGO Stage 2 19
KDIGO Stage 3 8 29
Median age (IQR), yr 7 (3 to 10.5) 6 (3 to 11) 0.853
Range (age) 3 mo to 17.5 yr 6 mo to 16 yr
Etiology
Septicemia 43 11 0.080
Post urethral valve 4 3 0.402
Malaria 5 4 0.269
Nephrotic syndrome 7 5 0.314
Diarrheal disease 6 2 0.050
Acute glomerulonephritis 5 3 0.685
Hemolytic uremic syndrome 3 1 1.000
Outcomes (survival/mortality) 73/0 26/3 0.021
AKI, acute kidney injury; IQR, interquartile range; KDIGO, Kidney Disease: Improving Global Outcomes; PD, peritoneal dialysis.
a
Included both conservative treatment and peritoneal dialysis.
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Kidney Res Clin Pract Vol. 39, No. 4, December 2020
Table 4. Clinical characteristics and causes of mortality among children who underwent acute peritoneal dialysis
AKI-related Duration of Remark including possible
Case Age and sex Etiology of AKI
complications hospitalization (d) cause of death
In-hospital mortality
Patient one 1 yr, male Sepsis Pulmonary edema, 1 MODS
encephalopathy
Patient two Six mo, male Post urethral valve Encephalopathy 20 MODS
with sepsis
Patient three 1 yr, male Sepsis Pulmonary edema, 13 MODS
encephalopathy
Post-hospitalization mortalitya
Patient four 11 yr, female Pelviureteric junction Uremic syndrome, 15 Died six months later from
obstruction anuria unknown cause of death
Patient five 3 yr, female Pelvic ureteric with Azotemia, anuria 10 Died 4 months later from
sepsis febrile illness
Patient six 2 yr, female Malaria Hyperkalemia, 12 Died 22 months later from
azotemia illness
Patient seven 16 yr, male Nephrotic syndrome Anuria, hypertension, 11 Died 36 months later from
azotemia ESKD
Patient eight 9 yr, male Nephrotic syndrome Encephalopathy 14 Died 10 months later from
unknown cause of death
AKI, acute kidney injury; ESKD, end stage kidney disease; MODS, multiple dysfunction syndrome.
a
Delayed deaths.
(eGFR) mL/min/1.73 m
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Alao, et al. Survival after acute PD in children
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Kidney Res Clin Pract Vol. 39, No. 4, December 2020
than the 37.8% described among a cohort of adults who diseases. A high index of suspicion should be placed on
underwent HD dialysis for AKI [24]. children with urinary tract infection, as 13% of children
In this study, presence of anuria during admission was who had PD for AKI in this present study had some form
not associated with increased mortality. This result dif- of obstructive uropathy as the underlying cause.
fers from some earlier studies of children with AKI [13,30]. Although our study appears to be the first to follow a
A retrospective study in India that found that the pres- cohort of children who underwent acute PD for an ex-
ence of anuria, septicemia, and severe infectious com- tended period of 18 months in sub-Saharan Africa, there
plications tend to be associated with increased mortality are some limitations. First, our sample size was relatively
[13]. Similarly, in Brazil, presence of oligoanuria was small, which may affect the statistical power of the study.
associated with poor outcomes in children with AKI and Secondly, one-quarter of the children (n = 7, 26.9%) were
sepsis [30]. lost to follow-up. Finally, no detailed autopsies were car-
Although we found no dissimilarities in baseline an- ried out to ascertain the cause of death for those who
thropometric indices of height, weight, and body surface died during follow-up. Rather, we relied on information
area between survivors and non-survivors of AKI post- provided by their parents.
acute PD, a study in Denmark observed such a contrast. In conclusion, we observed faster progression to CKD
In that study, patient weight lower than 5 kg was a risk among survivors of AKI who underwent acute PD than
factor for increased mortality in children who required among those who did not. Progression of post-PD AKI to
PD for AKI [29]. The inability to detect any differences CKD occurred in more than half of the survivors. Age less
in anthropometric indices between survivors and non- than five years was associated with greater survival.
survivors may be related to the small sample size of this
study. Malnutrition is associated with endothelial dys- Conflicts of interest
function, oxidative stress, high levels of proinflammatory
cytokines such as soluble intercellular adhesion mol- All authors have no conflicts of interest to declare.
ecule-1, and elevated c-reactive protein, which may con-
tribute to the higher mortality rate in children [31-33]. Authors’ contributions
This present study indicates that children younger than
five years have better odds of survival than children five Michael Abel Alao, Olayinka Rasheed Ibrahim, and
years and older. Although there is a paucity of compa- Adanze Onyenonachi Asinobi conceptualized, analysed,
rable studies, two studies in India examined factors asso- drafted the initial manuscript, and revised the manu-
ciated with mortality in children who underwent PD for script. Adanze Onyenonachi Asinobi and Akinwale Akin-
AKI. They found no relationships with age [13,34]. How- sola critically appraised and revised the manuscript. All
ever, a review of the long-term outcomes of chronic dial- authors read and approved the final manuscript.
ysis in children detected higher mortality in the younger
age group [35]. Our observation of better survival among References
children under five may be related to treatable infection-
related causes of AKI compared with the older patients [1] Bellomo R, Kellum JA, Ronco C. Acute kidney injury. Lan-
who may develop AKI on background CKD with further cet 2012;380:756-766.
risk of progression. [2] Cleto-Yamane TL, Gomes CLR, Suassuna JHR, Nogueira
The etiologies of AKI observed in this study are consis- PK. Acute kidney injury epidemiology in pediatrics. Braz J
tent with the results of other studies from LMIC, in which Nephrol 2019;41:275-283.
infectious and congenital anomalies of the kidney and [3] Susantitaphong P, Cruz DN, Cerda J, et al.; Acute Kidney
urinary tract (CAKUT) remain the leading causes of AKI Injury Advisory Group of the American Society of Nephrol-
[11,12]. The importance of this finding is that preven- ogy. World incidence of AKI: a meta-analysis. Clin J Am Soc
tive nephrology in developing countries should focus Nephrol 2013;8:1482-1493.
on antenatal screening for CAKUT and prompt and ap- [4] Sutherland SM, Ji J, Sheikhi FH, et al. AKI in hospitalized
propriate management of common childhood infectious children: epidemiology and clinical associations in a na-
476 www.krcp-ksn.org
Alao, et al. Survival after acute PD in children
tional cohort. Clin J Am Soc Nephrol 2013;8:1661-1669. [19] Kidney Disease: Improving Global Outcomes (KDIGO)
[5] Tanyildiz M, Ekim M, Kendirli T, et al. Acute kidney injury Acute Kidney Injury Work Group. KDIGO clinical practice
in congenital cardiac surgery: pediatric risk-injury-failure- guideline for acute kidney injury. Kidney Int Suppl 2012;2:
loss-end-stage renal disease and Acute Kidney Injury Net- 1-138.
work. Pediatr Int 2017;59:1252-1260. [20] Levey AS, Coresh J, Balk E, et al.; National Kidney Foun-
[6] Hoste EAJ, Kellum JA, Selby NM, et al. Global epidemiol- dation. National Kidney Foundation practice guidelines
ogy and outcomes of acute kidney injury. Nat Rev Nephrol for chronic kidney disease: evaluation, classification, and
2018;14:607-625. stratification. Ann Intern Med 2003;139:137-147.
[7] Lunyera J, Kilonzo K, Lewington A, Yeates K, Finkelstein [21] Long TE, Helgason D, Helgadottir S, et al. Mild Stage 1 post-
FO. Acute kidney injury in low-resource settings: barriers operative acute kidney injury: association with chronic kid-
to diagnosis, awareness, and treatment and strategies to ney disease and long-term survival. Clin Kidney J 2020 Feb
overcome these barriers. Am J Kidney Dis 2016;67:834-840. 10 [Epub]. Doi: 10.1093/ckj/sfz197.
[8] Macedo E, Cerdá J, Hingorani S, et al. Recognition and [22] Katibi OS, Adedoyin OT, Anoba S, et al. Current trends in
management of acute kidney injury in children: the ISN the management of acute kidney injury in children. Niger J
0by25 Global Snapshot study. PLoS One 2018;13:e0196586. Paediatr 2013;40:314-320.
[9] Mehta RL, Cerdá J, Burdmann EA, et al. International Soci- [23] Gullipalli P, Anjani A. Spectrum of paediatric acute kidney
ety of Nephrology's 0by25 initiative for acute kidney injury injury-a referral hospital experience in a developing na-
(zero preventable deaths by 2025): a human rights case for tion. IOSR J Dent Med Sci 2015;14:80-87.
nephrology. Lancet 2015;385:2616-2643. [24] Duran PA, Concepcion LA. Survival after acute kidney in-
[10] Olowu WA, Niang A, Osafo C, et al. Outcomes of acute kid- jury requiring dialysis: long-term follow up. Hemodial Int
ney injury in children and adults in sub-Saharan Africa: a 2014;18 Suppl 1:S1-S6.
systematic review. Lancet Glob Health 2016;4:e242-e250. [25] Moxey-Mims M. Kidney disease in African American chil-
[11] Esezobor CI, Ladapo TA, Lesi FE. Peritoneal dialysis for dren: biological and nonbiological disparities. Am J Kidney
children with acute kidney injury in Lagos, Nigeria: experi- Dis 2018;72(5 Suppl 1):S17-S21.
ence with adaptations. Perit Dial Int 2014;34:534-538. [26] Devarajan P, Jefferies JL. Progression of chronic kidney dis-
[12] Abdelraheem M, Ali el-T, Osman R, et al. Outcome of acute ease after acute kidney injury. Prog Pediatr Cardiol 2016;41:
kidney injury in Sudanese children - an experience from a 33-40.
sub-Saharan African unit. Perit Dial Int 2014;34:526-533. [27] Fiorentino M, Grandaliano G, Gesualdo L, Castellano G.
[13] Mishra OP, Gupta AK, Pooniya V, Prasad R, Tiwary NK, Acute kidney injury to chronic kidney disease transition.
Schaefer F. Peritoneal dialysis in children with acute kidney Contrib Nephrol 2018;193:45-54.
injury: a developing country experience. Perit Dial Int 2012; [28] Ademola AD, Asinobi AO, Ogunkunle OO, Yusuf BN, Ojo
32:431-436. OE. Peritoneal dialysis in childhood acute kidney injury:
[14] Abraham G, Varughese S, Mathew M, Vijayan M. A review experience in southwest Nigeria. Perit Dial Int 2012;32:267-
of acute and chronic peritoneal dialysis in developing 272.
countries. Clin Kidney J 2015;8:310-317. [29] Pedersen KR, Hjortdal VE, Christensen S, et al. Clinical out-
[15] Adedoyin OT, Ibrahim OR, Abdurrahman LO, et al. Perito- come in children with acute renal failure treated with peri-
neal dialysis in children with acute kidney injury: the Ilorin toneal dialysis after surgery for congenital heart disease.
experience. Afr J Paediatr Nephrol 2015;2:72-76. Kidney Int Suppl 2008;(108):S81-S86.
[16] Anochie IC, Eke FU. Paediatric acute peritoneal dialysis in [30] Gunnam S, Gullipalli P. Therapeutic efficacy of peritoneal
southern Nigeria. Postgrad Med J 2006;82:228-230. dialysis in pediatric acute kidney injury patients in a refer-
[17] Kilonzo KG, Ghosh S, Temu SA, et al. Outcome of acute ral hospital. IOSR J Dent Med Sci 2018;17:41-46.
peritoneal dialysis in northern Tanzania. Perit Dial Int [31] Choi HY, Lee JE, Han SH, et al. Association of inflammation
2012;32:261-266. and protein-energy wasting with endothelial dysfunction in
[18] Schwartz GJ, Work DF. Measurement and estimation of GFR peritoneal dialysis patients. Nephrol Dial Transplant 2010;
in children and adolescents. Clin J Am Soc Nephrol 2009;4: 25:1266-1271.
1832-1843. [32] Leinig CE, Moraes T, Ribeiro S, et al. Predictive value of
www.krcp-ksn.org 477
Kidney Res Clin Pract Vol. 39, No. 4, December 2020
malnutrition markers for mortality in peritoneal dialysis children with acute kidney injury: Dhaka Shishu (children)
patients. J Ren Nutr 2011;21:176-183. hospital experience. Anwer Khan Mod Med Coll J 2015;6:
[33] Al-Othman AM, Al-Naseeb AJM, Almajwal AM, et al. As- 11-14.
sociation of malnutrition in peritoneal dialysis patients of [35] Shroff R, Ledermann S. Long-term outcome of chronic di-
Saudi Arabia. Arab J Chem 2016;9 Suppl 2:S1059-S1062. alysis in children. Pediatr Nephrol 2009;24:463-474.
[34] Sarker NK, Hanif M, Rouf MA, et al. Peritoneal dialysis in
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