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Acute Kidney Failure
A Pediatric Experience Over 20 Years
Debra M. Williams, MD;
Sue S. Sreedhar, MD;
John J. Mickell, MD;
James C. M. Chan, MD
Arch Pediatr Adolesc Med. 2002;156:893-900.
ABSTRACT
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Background Acute kidney failure in children is a catastrophic, life-threatening
event.
Objective To compare and contrast 2 decades of data, analyzing the underlying
causes, associated multiple organ system failures, outcome of dialysis procedures,
and other variables of interest.
Design Retrospective examination of clinical data collected between January
1, 1979, and December 31, 1998.
Setting Regional health care center in the mid-Atlantic area.
Participants Two hundred twenty-eight patients, aged from 1 day to 18 years, had
acute kidney failure and were referred to a pediatric nephrology service.
Main Outcome Measures Characteristics, percentage of mortality, intensive care unit admission,
procedures, and other variables and causes of acute renal failure.
Results The total number of cases analyzed represented 7% of all patients presented
to the pediatric nephrology service. Sex distribution, ethnicity, and survival
statistics were unchanged between both decades. The overall survival rate
was 73%. One hundred fifty-four patients (68%) were admitted to the pediatric
intensive care unit. The following 106 acute extracorporeal procedures were
performed on 93 patients (41%): 12 patients received extracorporeal membrane
oxygenation, 52 patients underwent peritoneal dialysis, 32 underwent hemodialysis,
3 patients received continuous venovenous hemofiltration, and 7 patients received
continuous arteriovenous hemofiltration. Sepsis and burns, other leading causes
of acute renal failure in the first decade, are replaced in the second decade
by hematologic-oncologic complications and pulmonary failure.
Conclusions Acute kidney failure following repair of cardiac lesions remains unchanged
as a leading risk factor of mortality in both decades. Three organ system
failures were associated with more than a 50% mortality rate. Predialysis
low serum albumin concentrations emerged as a significant copredictor of mortality.
INTRODUCTION
ACUTE KIDNEY failure is an abrupt cessation of kidney function, with
life-threatening consequences in children worldwide.1
Given the fact that acute kidney failure is sometimes associated with significant
multiple organ system failure (MOSF)2 and constitutes
an important population admitted to pediatric intensive care units (ICUs),3 it seems logical that the various risk factors of
this catastrophic event are issues of great importance in terms of tangible
and intangible costs to the well-being of patients and their families. We
share a 20-year experience at a single center with care provided by the same
attendings in critical care, nephrology, and neonatology. This study will
analyze the underlying diseases leading to acute kidney failure, the outcome
of MOSFs, and other variables associated with mortality in the first decade
compared with the second decade. Recently, hypoalbuminemia has been shown
to be a singular predictor of nutrition failure and presence of systemic disease
in children receiving chronic renal replacement therapy.4
We will examine whether it is also a co-mortality risk factor in acute kidney
failure.
This study has particular relevance in the light of advancing technology,
including the increase of extracorporeal membrane oxygenation in neonates,5 and the widespread and earlier use of acute renal
replacement therapy.6
PATIENTS AND METHODS
Between January 1979 and December 1998, 228 consecutive pediatric cases
of acute renal failure were diagnosed and treated at the Medical College of
Virginia Hospital, Richmond, a regional health care center in the mid-Atlantic
area. All medical data were entered prospectively each day on standard forms
("the yellow sheets" advocated by Frederic C. Bartter, MD*) under direction
of the same pediatric nephrologist (J.C.M.C.).
These forms remained unchanged in the 2 decades of the study and were
intended for future review as well as for clinical use as a flow sheet. We
obtained institutional review board approval for this study.
The diagnosis of acute kidney failure was made by the same attending
nephrologist (J.C.M.C.) using the following criteria: a sudden cessation of
kidney function characterized by oliguria, less than 0.5 mL/kg per hour, confirmed
by rising levels of serum urea nitrogen and creatinine to double that of normal
for age.1, 6 Patients with preexisting
chronic kidney diseases4 were excluded. The
criteria for admission to the ICU was determined by the same 2 attendings
(S.S.S. and J.J.M.), and were as follows: (1) the requirement of close monitoring
of critically ill patients, such as those who were recovering from postcardiac
surgery; (2) patients requiring invasive monitoring, that is, arterial lines,
ventriculostomies, and others; (3) those in congestive heart failure or respiratory
failure requiring intubation; and (4) patients with MOSFs7
requiring invasive monitoring. The established criteria for MOSF were adjusted
for age.7-8 The race, age, and
other clinical characteristics of the children are summarized in
Table 1.
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Table 1. Clinical Characteristics of 228 Cases of Pediatric Acute Renal
Failure
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In the patients described herein, univariant analysis was used on all
variables of interest in survivors and nonsurvivors. Fisher exact and  2 tests were used to compare data between the 2 decades (ie, decade
1, 1979-1988; decade 2, 1989-1998). A Kaplan-Meier survival plot for serum
albumin concentrations was used. All values were expressed as mean ±
SD. P<.05 denotes statistical significance.
RESULTS
The 228 patients with acute kidney failure represented 7% of all inpatient
and outpatient referrals made to the pediatric nephrology service over these
2 decades.9 The clinical characteristics were
as follows: slightly more male than female patients (60% vs 40% and 57% vs
43%, respectively). Comparing the first (1979-1988) and second (1989-1998)
decades, the ethnic distribution was, respectively, 53% and 54% white; 38%
and 33% black; and 9% and 13% others. No statistically significant differences
were noted between the first and the second decade in these patient characteristics
as given in Table 1.
Between the 2 decades, patient survival was 71% and 74%, respectively,
for an overall survival rate of 73%. The mortality rates between the 2 decades
were not significantly different as well, at 29% and 26%, respectively
(Table 1).
Table 2 lists the age of patients in relationship to mortality.
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Table 2. Mortality in Acute Renal Failure in Association With Age
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Among the survivors, the order of underlying causes for acute kidney
failure hardly change between the 2 decades. (Table 3) Hemolytic uremic syndrome (HUS)9
in the survivors was the leading cause of acute kidney failure in both decades,
38% and 22%, respectively. There was 1 death from HUS in the 2 decades, of
a total of 49 patients, making the mortality rate 2% for this condition. Twenty-one
percent and 57% of these patients required dialysis in their respective decades.
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Table 3. Underlying Cause and Outcome of Pediatric Acute Renal Failure
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Postcardiac surgery remained the leading cause of acute kidney failure
among the nonsurvivors in both decades. However, sepsis as a cause of acute
kidney failure dropped significantly from 23% (1979-1988) to 3% (1989-1998)
(P<.001). Figure
1 shows the organisms responsible for sepsis in each decade. Also,
extensive burns precipitating acute kidney failure accounted for 13% of acute
kidney failure in the first decade, but dropped significantly to 0% in the
second decade. Pulmonary causes of acute kidney failure among the nonsurvivors
increased between the 2 decades, 7% to 12%, but this did not reach statistical
significance. Hematologic-oncologic causes of acute kidney failure among the
nonsurvivors also increased from 10% in the first decade to 22% in the second
decade, in association with bone marrow transplant rejections, leukemia, tumor
lysis, hyperuricemia, and other complications (Figure 2). While tumor lysis was an important cause of death in
the first decade (Figure 2), it
was not so in the second, where the mortality rate from this cause was 0%.
"Anticipatory" intervention is prevalent and the improved results may be attributed
to this. The use of peritoneal dialysis (PD) dropped from 60% of all acute
renal replacement therapy in the first decade to 44% in the second decade
(Table 4). The use of hemodialysis,
continuous venovenous hemofiltration (CVVH), and continuous arteriovenous
hemofiltration (CAVH) increased to 43% of acute renal replacement therapy
in the second decade. Also, the interval between renal consultation for acute
kidney failure to the initiation of acute renal replacement therapy was 2.0
± 1.8 days vs 1.9 ± 1.4 days, respectively, between the 2 decades.
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Figure 1. Organisms responsible for sepsis
in acute renal failure.
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Figure 2. Hematologic-oncologic complications
associated with acute renal failure.
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Table 4. Need for ECMO, PD, HD, and CVVH*
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Figure 3 shows the data on
mortality in acute kidney failure in association with other organ failures.
In the first decade, 27% of the patients died with 2 MOSFs; 3 MOSFs, 57%;
and 4 MOSFs, 100%. However, in the second decade of this study, 2 MOSFs had
a mortality rate of 13%; 3 MOSFs, 68%; and 4 MOSFs, 88%.
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Figure 3. Mortality in association with
multiple organ system failure.
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Examination of all serum variables on the comprehensive metabolic profile,
for example, sodium, potassium, chloride, carbon dioxide, cholesterol, calcium,
glucose, and others, obtained immediately before acute kidney replacement
therapy did not show significant differences between survivors and nonsurvivors,
with the exception of the serum albumin concentrations (Figure 4). The serum albumin concentrations were 2.6 ± 0.7
g/dL in nonsurvivors vs 3.3 ± 0.9 g/dL in survivors (P<.05). Figure 5 shows
a survival distribution plot for serum albumin concentration. Hypoalbuminemia
was significantly associated with the nonsurvivors.
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Figure 4. Mean ± SD serum albumin
concentration obtained before acute renal replacement therapy.
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Figure 5. Hypoalbuminemia as a significant
risk factor of mortality. Kaplan-Meier survival curve for serum albumin concentration
shows that 20% of the patients with hypoalbuminemia died by day 5 and 40%
died by day 30.
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COMMENT
We reviewed all English-language published reports since 1977 of acute
kidney failure with 50 children or more (Table 5). It was surprising to find a persisting scarcity of published
data specifically addressing acute kidney failure and its risk factors and
morbidity and mortality in the pediatric population. In regard to our patient
data on morbidity and mortality and critical illness, our criteria for ICU
admission were (1) the requirement of close monitoring of critically ill patients,
such as those who were recovering from cardiac surgery; (2) patients requiring
invasive monitoring, that is, arterial lines, ventriculostomies, and others;
(3) those in congestive heart failure or respiratory failure requiring intubation;
and (4) patients with MOSFs, as established previously, requiring invasive
monitoring. Similar criteria for ICU admission were used by Moghal et al7 resulting in 48% of their 227 children (1984-1991)
with acute kidney failure admitted to their ICU compared with the 68% ICU
admission rate in our present series. If criteria for admission to the ICU
are to be taken as life-threateningly ill, our patients can be considered
at least as critical as those in the other series (Table 5). Also, the overall mortality rate of 27% in our study compares
favorably with the other published series, despite the persistent requirement
of ICU admissions for this disease.
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Table 5. Critically Ill Pediatric Patients With Acute Renal Failure*
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Smoyer et al17 and Zobel et al18 indicated that pediatric patients with acute kidney
failure with MOSF, even when treated with continuous kidney replacement therapy,
sustained a 60% to 100% mortality rate. In further review of the pediatric
literature (Table 5), we noted
that few studies examined the number of organ failures in relationship to
mortality rate in acute kidney failure.19-24
Our data (Figure 3) show that the
mortality rate between the 2 decades dropped, even with 4 organs failing.
The mortality rate fell from 100% to 88% in the second decade (1989-1998),
possibly related to advances in antibiotics, earlier therapy, and better volume
control in the recent decade. The examination by Shaw et al25
and Meeks and Sims26 examination of 831 children
with MOSFs did not provide specific data on the 5% of their patients who developed
kidney failure. However, our data of 57% to 68% mortality with 3 MOSFs are
lower than the 89% mortality reported by Shaw et al25
and Meeks and Sims,26 again verifying that
advances in technology appear to have allowed us to improve our management
of this particular risk factor.
Despite the tremendous advances in the last decade of both critical
care management and kidney replacement therapy, however, the significant finding
in our study was the persistently high mortality rate of critically ill patients
after cardiac surgery. Patients frequently developed acute kidney failure
as a result of poor perfusion and hypoxia secondary to prolonged pump time
during surgery for congenital heart disease, 27% in the first decade, 44%
in the second decade among the nonsurvivors. The younger the patient, the
poorer the prognosis, especially in patients younger than 1 year
(Table 2). It is also possible that the
difference is due to changes in the attending surgeons, increased complexity
of patients with heart disease in the second decade, and differences in techniques.
Although mortality from acute kidney failure secondary to an underlying
cardiac diagnosis did not appear to have changed significantly when data between
the 2 decades were compared, there was a shift in other underlying diagnoses.
In the first decade, acute kidney failure associated with cardiac surgery
was the major cause of mortality, followed by sepsis (Table 3), burns, pulmonary, and hematologic-oncologic complications.
Among nonsurvivors, sepsis-associated acute kidney failure dropped from 23%
in the first decade to 3% in the second decade (P<.001)
presumably, again, because of advances in antibiotic therapy and better management
of fluid volume control. Although the organisms causing sepsis did not change
in the 2 decades (Figure 1), there
was an increased emergence of methicillin-resistant Staphylococcus
aureus in the first decade and of penicillin-resistant Streptococcus pneumoniae in the second decade. Despite these changes
in sensitivity, we managed to have better outcomes in the second decade.
Also, in the second decade, the noncardiac causes of death shifted to
hematologic-oncologic complications, for example, leukemic-tumor lysis, hyperuricemia,
bone marrow transplantation (Figure 2),
and respiratory failure. The incidence of hematologic-oncologic complications
associated with death in acute kidney failure increased in the second decade
possibly because of the increase in aggressive chemotherapy, management, and
bone marrow transplantation availability. The latter procedure was unavailable
in the first decade of this study (Figure
2).
The significant drop in burns as a cause of acute kidney failure in
the second decade may be partly due to a change in burn care management, as
the care of pediatric burn patients was taken over by a newly developed burn
unit independent of the pediatric ICU in the second decade. It would also
appear that burn prevention and management have improved to a degree that
the hypovolemia of burns is successfully eliminated as a significant cause
of acute kidney failure in the second decade.
Another important and significant risk factor for mortality was age.
The youngest patients showed a higher mortality rate. Most published studies
of acute kidney failure in early life are small series19-26
of fewer than 25 patients, yet the mortality rate is high.19-26
In our study, neonates and infants, aged 1 day to 1 year, represented 57%
of the total nonsurvivor group (Table 2), and they composed a very large part of the postcardiac acute
kidney failure group. In addition, the 12 patients requiring extracorporeal
membrane oxygenation were all in the neonatal age group. Extracorporeal membrane
oxygenation, in turn, led to the choice of CVVH or CAVH over PD in all of
these infants because of the availability of dialysis access. These observations
in morbidity and mortality are in accord with the observations of Gong et
al16 that coma, hypovolemia, respiratory failure,
and acute tubular necrosis in infants younger than 1 year remain significant
mortality risk factors. Acute kidney failure in neonates and infants19-27
also represents a special clinical and technical challenge, because of the
tiny body size of the patients. Finally, the higher mortality rate in this
age group could possibly be due to other associated congenital anomalies.19-27
Our data indicated that in the more recent decade (1989-1998), the use
of acute PD had decreased significantly (Table 4). Acute hemodialysis, CVVH, CAVH, and renal replacement
procedures were used more frequently than before, with a corresponding decrease
in the use of PD. This trend of moving away from acute PD in favor of acute
hemodialysis, CVVH, or CAVH in renal replacement therapy in acute kidney failure
was first suggested by a questionnaire survey of pediatric nephrologists by
Warady and Bunchman.28 Our data over the span
of 20 years substantiated this trend. Acute PD, of course, will still be done
via Tenckhoff cannula, especially for our younger patients. However, CVVH
and CAVH will probably be preferred, especially whenever extracorporeal membrane
oxygenation is used with its need to limit the risk of infection from PD in
this particular group, as well as dialysis access availability.
In addition, acute kidney replacement therapy was initiated within 1.9
± 1.4 days in the more recent decade (1989-1998) compared with 2.0
± 1.8 days in the previous decade (1979-1988) between the renal consultation
and the start of acute kidney dialysis. Our data begin with our initial consultation,
which naturally affects our initiation of dialysis. Thus, together, our data
suggest more favorable outcomes with earlier, rather than later, time lags
of 4.2 to 4.8 days between the onset of kidney failure and the start of dialysis
as reported by Arora et al.1
An interesting finding in our analysis was that HUS29
represented the largest group of survivors, without differences between the
2 decades. There was only 1 death in our group of 49 patients with HUS, a
2 -year-old, resulting in a 2% mortality rate. This conforms to the
decrease in HUS mortality from 40% in the past to 5% in recent years.30 Although we used the same criteria for initiation
of dialysis in acute kidney failure throughout the 2 decades, we were more
aggressive in using dialysis in the recent decade. For example, we used dialysis
in 57% of the patients with HUS in the second decade compared with 21% in
the first decade. The improved survival in HUS in our study may be related
to our more aggressive dialysis therapy. These findings contrast with the
current 68% mortality rate in India. In this series of 25 patients with HUS
reported by Arora et al,1 late referral resulting
in more critically ill patients was the reason given for the higher mortality
rate. This is understandable with the persistence of significant differences
in availability of medical care and gross national income between the United
States and India. This continuing difference also has a greater significant
effect on both chronic and acute kidney diseases and the long-term survival
of children in India.
In long-term dialysis for end-stage kidney disease,4, 31-34
hypoalbuminemia is shown to be an index of malnutrition and a predictor of
mortality. Although Obialo et al35 showed that
hypoalbuminemia (<3.5 g/dL) can be a useful predictor of mortality in adults
with acute kidney failure, this had not been examined in children. Our data
(Figure 4) showed that there is
a significantly lower serum albumin predialysis level between nonsurvivors
(2.6 ± 0.7 g/dL) and survivors (3.3 ± 0.9 g/dL) (P<.05). In addition, the cumulative survival data (Figure 5) clearly established that hypoalbuminemia could discriminate
between the survivors and the nonsurvivors, with 40% dying by day 30. Thus,
our data ascertain the efficacy of using serum albumin concentration as a
copredictor of mortality in pediatric acute kidney failure. Obialo et al35 also suggested that low albumin concentrations in
adult patients may be correlated with the activation of inflammatory mediators.
Studies on a molecular basis of these observations may illuminate new avenues
to improve survival in these patients.
CONCLUSIONS
We have seen that postcardiac surgery36
associated with acute kidney failure remains the leading mortality risk factor.
Hematologic-oncologic complications have become a more frequent cause of acute
kidney failure in the recent decade because of advances in care management.
Sepsis as an associated cause of acute kidney failure dropped from 23% to
3% in the last 2 decades although the organisms responsible for the sepsis
did not change. Our data on acute dialysis indicated less PD being done in
the recent decade, a trend previously suggested in a questionnaire survey.28 Also, although mortality risks increase significantly
with MOSFs in association with acute kidney failure in adults,37
our data in this study suggest a slightly better prognosis in children.38-39 Another significant comorbid risk
factor is young age (ie, <1 year), combined with the need for extracorporeal
membrane oxygenation due to respiratory failure secondary to problems in fluid
management. Finally, our data suggest that hypoalbuminemia is a copredictor
of mortality in pediatric acute kidney failure.
AUTHOR INFORMATION
Accepted for publication April 4, 2002.
This study was supported by grants T32 DK07761 and R01 DK50419 from
the National Institutes of Health, Bethesda, Md (Dr Chan).
We thank Sung C. Choi, PhD, for statistical support; Karl S. Roth, MD,
and K. C. Lin, MSc, for review; and Betty Timozek for secretarial assistance.
This study was presented as a poster at the World Congress of Nephrology
American Society of Nephrology/International Society of Nephrology, San Francisco,
Calif, October 14-17, 2001.
*Frederic C. Bartter, possibly the longest serving branch chief of the
National Heart, Lung, and Blood Institute at the National Institutes of Health,
always advocated the use of the National Institutes of Health's data forms,
referred by generations of clinical associates as "the yellow sheets," to
keep patient data and to plan research studies.
What This Paper Adds
There is a scarcity of up-to-date published data specifically addressing
acute kidney failure in children. Studies involving large numbers of children
with this disorder are also rare. Because it can be such a catastrophic, life-threatening
event, it is important for community pediatricians to recognize the clinical
features of this disease with regard to morbidity and mortality. We report
a 20-year experience of 228 children at the same institution with the same
intensivists and nephrologist.
The results of our analysis suggest that although we have improved in
most areas of care and management, we still fared poorly with our patients
in infancy. The data also provided evidence that during the first decade,
burns and sepsis were major comorbid factors, but not so in the second decade.
In addition, more CVVH, CAVH, and less PD were done in the recent decade compared
with the earlier decade. We conclude that acute kidney failure in childhood
continues to carry significant mortality risks, especially in the presence
of other organ failures. Finally hypoalbuminemia, rather than elevated levels
of serum urea nitrogen or creatinine, at the start of dialysis is a significant
copredictor of mortality.
Corresponding author and reprints: James C. M. Chan, MD, The Barbara
Bush Children's Hospital, Maine Medical Center, 22 Bramhall St, Portland,
ME 04102-3175 (e-mail: chanj{at}mmc.org).
From the Departments of Pediatrics (Drs Williams, Sreedhar, Mickell,
and Chan) and Biochemistry Molecular Biophysics (Dr Chan), Virginia Commonwealth
University, Richmond. Dr Chan is now with The Barbara Bush Children's Hospital,
Maine Medical Center, Portland, and the Department of Pediatrics, University
of Vermont College of Medicine, Burlington.
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