Renal Failure During the First Year of Life

(1)

Renal

Failure

During

the

First

Year

of Life

Ekkehard W. Reimold, M.D., Tran Dinh Don, M.D., and Howard G. Worthen, M.D., Ph.D.

From the Department of Pediatrics, The University of Texas Health Science Center at Dallas, Southwestern Medical School

ABSTRACT. All cases of persistent renal failure in infants less than 1 year of age were reviewed to determine whether the prognosis has improved equally for infants as for adults. During a ten-year period, 52 infants were treated by applying uniform therapy; 28, more than half, were less than

4 weeks old. All cases were separated into two groups: 19

infants without and 33 infants with congenital renal or urinary tract anomalies. In 20 patients of the latter group, additional serious anomalies of other organs were present. The age distribution was strikingly different: in 18 of 21 infants, renal anomalies were present, as diagnosed on the first day of life. In contrast, only 3 of 1 1 infants, 4 to 12 months old, had urinary tract anomalies.

In infants without renal anomalies, renal failure was caused by hypotension or shock in 10 of 19 cases, by pyelonephritis or sepsis in 6 of 19. Of this group, eight infants (42%) recovered completely, nine (47%) died. Death occurred within one to two days of hospitalization in all but three cases, caused by shock or sepsis. In this group medical problems that are amenable to therapy have caused either renal failure or contributed to the infant’s death.

In infants with renal or urinary tract anomalies, renal

failure was caused by renal dysplasia or agenesis in 16 of 33 infants, by urinary tract obstruction in 12 of 33. Only three patients (9%) recovered, all older than 4 months, 20 (61%) died, and 10 are living with signs of chronic renal failure. Death usually occurred within one week of hospitalization and, in 16 of 20, it was caused by renal failure and multiple additional anomalies. The multiplicity and complexity of the congenital anomalies in most instances precluded effective, lifesaving therapy.

Renal failure in infants is still a serious disease accompanied by a high mortality rate in which therapeutic possibilities are limited. No improvement in prognosis can be expected in the near future. Pediatrics, 59:987-994, 1977,

RENAL FAILURE, CONGENITAL RENAL ANOMALIES, INFANT, ISCHEMIC RENAL DAMAGE.

prognosis for infants in renal failure, however,

still seems rather poor.

Only sporadic reports of a successful medical

treatment of renal failure in infants are found in

the literature’8 with the exception of a series of

100 cases from Mexico.9 The outcome of renal

failure in infants with present-day management

has not been examined systematically. The

prog-nosis seems as guarded as ever and many authors

still advise against dialysis and transplantation in

this age group.

This paper reviews all cases of advanced renal

failure occurring in the first year of life that we

have seen during a ten-year period. To evaluate

the prognosis of renal failure in this age group and

to define which patients were potentially

salvage-able, we reviewed the etiology, age of onset,

interval between diagnosis and death, prognosis,

and cause of death.

MATERIALS AND METHODS

All cases of azotemia or decreased urine output

in infants less than 1 year of age treated between

1964 and 1975 at our institution were reviewed. It

was decided to exclude from this study all cases

with transient, mild impairment of renal function.

Thus, all infants with temporarily elevated blood

urea nitrogen (BUN) accompanying diarrhea or

dehydration were excluded. Also excluded were

Recent diagnostic and therapeutic advances

have drastically changed the approach to renal

failure in adults and have had an impact on its

prognosis. After some delay, children benefited

from this development, and most techniques used

in adults are now also performed in children. The

(Received June 21, revision accepted for publication December 10, 1976.)

Presented in part at the annual meeting of the American Society of Pediatric Nephrology, April 27, 1976, St. Louis,

Missouri.

ADDRESS FOR REPRINTS: (E.W.R.) Department of

Pedi-atrics, The University of Texas Health Science Center at Dallas, Southwestern Medical School, 5323 Harry Hines Boulevard, Dallas, Texas 75235.

at Viet Nam:AAP Sponsored on September 8, 2020 www.aappublications.org/news

(2)

OLIGURIA

NO. OF CASES

LETHARGY

PALLOR (fflffluuiInlllliifflwtwlluhI

VOMITING

POOR FEEDING

CONVULSIONS .illflllllwnIllllfflllllffililihI

40 50

, I I I’

SIGNS ATTRIBUTABLE TO

GENERAL SIGNS

0 10 20 30 40 50

RENAL FAILURE IN INFANTS

RENAL SIGNS

C, 0 20 30

EDEMA

ENLARGED KIDNEY ‘flll!i’

HEMATURIA

HYPERTENSION

FIG. 1 Clinical signs attributable to renal failure in 52 infants observed when admitted to

hospital.

infants with postoperative renal failure in which

death occurred within one or two days and in

which renal failure was not a contributing factor

to the demise of the infant. Only cases with

unquestioned, severe, persistent renal failure that

did not resolve with initial therapy were included

in the study. The following criteria were applied:

oliguria for at least three days with a urine output

less than 200-250 ml/m2/24 hours; BUN > 30

mg% and rising; and creatinine > 1.5 mg% and

rising.

Additional studies routinely used in the workup

of our patients included voiding

cystourethro-gram, intravenous pyelogram, and more recently

abdominal sonography. In selected cases, a renal

arteriogram or a retrograde pyelogram was

performed. With these techniques it was always

possible to identify the size and position of the

kidneys and to visualize any congenital

anom-aly.

Blood and urine chemical determinations were

performed by standard micro-laboratory

tech-niques. Urine was tested with sulfosalicylic acid,

Labstix, and microscopic examination.

The therapeutic approach was uniform for all

infants. If renal failure was caused or

accom-panied by shock or dehydration, immediate

resto-ration of the circulating blood volume was

accomplished. When normal hydration was

pres-ent, a single dose of a sulfonamide diuretic

(

furosemide, hydrochlorothiazide) was given in an

attempt to increase the urine output. An osmotic

diuretic (mannitol) was given to two patients.

Infants with persistent unresponsive oliguria or

anuria were started on the “oliguria regimen”

with the appropriate restriction of fluid, protein,

and potassium intake. Peritoneal dialysis was used

in five patients. Hemodialysis was not used in any

of the infants.

In instances of pyelonephritis or sepsis, the

appropriate antibiotic dosage was based on

sensi-tivities and adjusted for the degree of renal

function. In some instances antibiotic blood levels

were available and were used to adjust the

dose.

RESULTS

Within the ten-year period, 52 patients with

renal failure during the first 12 months of life

were seen at our institutions. Although no

differ-ence was detectable in clinical signs and

symp-toms and in biochemical changes of blood and

urine, it SOOn became evident that these patients

were separated clinically and by other

character-istics into two groups: 33 patients with renal

failure caused or accompanied by a renal

anom-aly, and 19 patients in whom a congenital

abnor-mality of the urinary tract was not present.

Consequently, the subsequent discussion will

follow this logical division with the exception of

the diagnostic features.

Diagnostic Features

In the majority of cases the history revealed

only nonspecific complaints such as poor feeding,

vomiting, or failure to thrive. One child had

seizures before hospital admission. Findings

suggestive of renal disease were noted in 14 of the

52 infants: polyuria, hematuria, edema, swelling,

or a flank mass.

The physical examination and the observation

during the first stage of hospitalization revealed

the following general signs suggestive of systemic

disease (Fig. 1): lethargy and drowsiness, pallor,

vomiting, poor feeding, and convulsions. Of signs

directly suggestive of renal disease, oliguria was

by far the most common. Other findings were

generalized edema, enlarged palpable kidneys,

gross hematuria, and hypertension.

(3)

TABLE I

IMPORTANT LABORATORY DATA IN INFANTS WITH RENAL

FAILURE

Blood

TABLE II

following abnormal values in the majority of

patients (Table I): elevated BUN or creatinine or

both, decreased C09, decreased serum sodium,

elevated serum potassium, decreased serum

calcium, and increased serum phosphorus.

Decreased levels of hemoglobin and total protein

were also frequent. Urinalysis was performed for

41 patients and frequently showed proteinuria,

hematuria, and cylindruria. In almost half the

cases the urine tests showed positive results for

glucose and reducing substances.

Age: Thirty-six infants were less than 4 weeks

old, and 28 of these 36 were less than 1 week old

at the time of diagnosis; only 1 1 infants were

between 4 and 12 months of age. Expressed in a

different way, 69% of our cases were diagnosed in

the newborn period. As shown in Figure 2, renal

failure in the newborn period was predominantly

due to anomalies of the kidney or urinary tract;

86% of the infants were diagnosed on the first day

of life, and 78% of those diagnosed in the first

month had anomalies. However, renal failure was

caused by urinary tract anomalies in only 3 of 11

infants in the 4- to 12-month age group.

Diagnosis: In the infants without urinary tract

anomalies, renal failure characterized by oliguria

or anuria was the dominant feature. In addition to

vascular thrombosis the preceding events were in

most cases either hypotension and shock

follow-ing diarrhea (10 of 19 cases), or pyelonephritis and

sepsis (Table II). One infant had the clinical

features of the hemolytic uremic syndrome.

In infants with renal anomalies, however, the

presence of renal insufficiency was often not

obvious and required active investigation. The

underlying disorders were renal agenesis or

dysplasia (16 of 33 cases), urinary tract

obstruc-tion (12 patients), and cystic renal disease (Table

II). Additional anomalies were present in 73% as

listed in Table III, some of which (prune belly

BUN Range 34-172 > 30 mg% 46/52

Creatinine > 1.5 mg% 35/35

Na

K

< 135 mEq/l

> 145 mEq/I > 4.5 mEq/l

30/51

6/51

32/46

Ca < 8.6 mg% 28/31

P > 5.5 mg% 20/27

CO. < 16 InEq/I 34/38

Total protein < 5.5 gm%

5.5-7.Ogm%

9/18 8/18

Hgb < 11 gm%

> 13 gm%

Urine

28/49

15/49

Albumin > trace 36/4 1

Glucose > 1+ 16/34

Reducing substances > 1+ 16/22

Blood > 1+ 28/40

Sediment

WBC > 5/hpf 21/40

RBC > 10/hpf 27/40

Casts > 2/hpf 26/40

syndrome, imperforate anus, exstrophy) were of

obvious benefit in diagnosing urinary tract anom-alies.

Clinical course and outcome: Despite

imme-diate treatment, the recovery and survival rate

was poor. Only 1 1 infants recovered completely,

29 died, and 12 survived with signs of chronic

renal failure. Not unexpectedly, the outcome was

less favorable in the infants with congenital

anomalies (Table IV). Of this group, only 3 infants

who already were beyond the newborn period

recovered completely, 20 died (61%), and 10

survived with chronic renal failure. In contrast, in

infants with normal urinary tracts, eight

recov-DISEASE PRECEDING OR ACCOMPANYING RENAL FAILURE IN INFANTS

Normal Kidney and Urinary Tract Congenital Anomal ies of Kid neys and Urinary Tract

No. of Patients

Additional Anomalies

Shock, dehydration Sepsis, pyelonephritis Renal vein thrombosis Hemolytic-uremic syndrome

10 6 2 1

Renal dysplasia, agenesis Cystic renal disease Urinary tract obstruction

Posterior urethral valve Urethral stenosis Ureterovesical obstnlction Ureteropelvic obstruction Meatal stenosis

(7)

(4) (1)

16 5 12

13 4 7

Total 19 33 24

(4)

9

RENAL ANOMALIES

0

NORMAL KIDNEYS

16

14

C,) Lii U)

<12

0 LL.

0

io

a:

w

z

24 HR

DAYS WEEKS

TABLE III

FIG. 2 Age distribution in 52 infants less than 1-year-old treated for severe renal failure.

ered completely, nine died (47%), and two

survived with chronic renal failure (Table V). The

difference between the mortality rate of the two groups is statistically not significant.

The outcome was also related to the age of

onset. Figure 3 shows that, the earlier in life

symptoms began, the worse the prognosis. It is

not possible, however, to separate the effect of

age from the effect of the type of disease that

occurred in each age group.

Chronic renal failure: Following the acute

TABLE IV

OixrCo1E OF RENAL FAILURE IN INFANTS WITH

CONGENITAL RENAL ANOMALIES

Recovery CRF#{176} Dead

Renal dysplasia, hypoplasia, 1 5 10

agenesis

Cystic renal disease 1 3

Urinary tract obstruction

Posterior urethral valve, ur- 2 3 2

ethral stenosis

Ureteropelvic, ureterovesi- 1 4

cal obstruction

Meatal Stenosis 1

#{176}Chronic renal failure.

ADDITIONAL ANOMALIES OR SERIOUS COMPLICATIONS IN

24/33 INFANTS WITH RENAL OR URINARY TRACT

ANOMALIES

No. of Patients

Cardiovascular, pulmonary Congenital heart disease

Atresia, hypoplasia, cysts of lung Respiratory distress

8 6 3

Abdominal, gastrointestinal

Esophageal atresia, tracheo-esophageal fistula

3

Imperforate anus Intestinal anomalies

8 2 Cloaca, bladder exstrophy

Pnme belly Omphalocele

Diaphragmatic hernia Biliary obstniction

3 5 2 1 1

Genital

Undescended testes 10

Ambiguous genitalia Bifid uterus

2 2

Skeletal, CNS

Skeletal deformities 3

Hydrocephalus, meningocele 3

Prematurity 3

Diabetic mother 2

Sepsis 5

Pyelonephritis 4

Pneumonia 2

episode, renal failure persisted in 12 of the 23

surviving infants. Anomalies of the renal or

urinary tract and other organs were present in all

but two infants. Most of these children are still

alive with varying, but moderate degrees of renal

failure. The follow-up in these instances ranges

from 2#{189}to 1 1 years. All infants are receiving

conservative medical management. Three died

between one and three months after the acute

episode. Severe renal abnormalities complicated

by additional congenital anomalies (bladder

exstrophy, imperforate anus, omphalocele, etc)

were present in all three.

Peritoneal dialysis: Peritoneal dialysis was used

in a variety of clinical situations, applying

rela-tively strict criteria. We have denied the

indica-tion for dialysis, for instance, in patients with

multiple congenital anomalies, particularly those

that were not correctable. Table VI indicates that

the age of our patients ranged from 12 days to 11

months and that two infants died despite

imme-diate dialysis. The remaining three infants have

(5)

TABLE V

OUTC0SIE OF RENAL FAILURE IN INFANTS WITH NORMAL KIDNEYS AND URINARY TRACT

Recovery CRF’ Dead

Shock, hvpotension

Enteritis, dehydration 3 2

Enteritis, dehydration and microcephalus, congenital heart 2

disease, hyaline membrane

Congenital heart disease, mental retardation, pneunlonia 1 1

Neonatal hemorrhage 1

Infection

Pyelonephritis 2

Pelonephritis and sepsis 2

Pyelonephritis, sepsis and meningitis, imperforate anus, 2

Rh-isoimmunization

Other causes

Thrombosis renal vein, vena cava and congenital heart disease 2

I-Iemolvtic uremic syndrome 1

#{176}Chronic renal failure.

Cause of death: Of the total number of 52 cases,

29 infants died between one day and 3#{189}months

after the diagnosis of renal failure was made

(Table VII). The majority of deaths occurred

within three days of diagnosis. In every instance,

renal failure appeared to be a contributing factor,

although in the majority of cases death was

caused by multiple congenital anomalies or a

serious systemic disease. An autopsy was

performed in all but two cases. In these two

infants serious anomalies of the kidney and biliary

tract, respectively, were diagnosed by radiologic

and clinical techniques.

Six infants died from a combination of renal

failure and widespread ischemic damage caused

by prolonged hypotension and shock. Congenital

renal anomalies were not found in any of these

cases. In three of these six infants the disease

began with enteritis leading to severe

dehydra-tion and shock that was refractory to all

thera-peutic efforts including peritoneal dialysis in two

instances. Consequently, the autopsy results

described renal cortical necrosis in two cases and

extensive venous thrombosis in two others.

Exten-sive hemorrhagic infarcts were present in two

cases. Cardiac anomalies (transposition of the great vessels and severe coarctation of the aorta)

were observed in two cases.

In three infants, death was attributed to severe

systemic infection, complicated by renal failure.

The infection manifested itself by sepsis,

meningi-tis, pneumonia, and pvelonephritis in various

combinations. The following additional

compli-cating factors were observed: Rh

isoimmuniza-tion, microcephalus, hepatic necrosis,

imperfo-rate anus, renal tubular necrosis, and cardiac

arrest.

The great majority of infants who died had

congenital renal anomalies. These infants were

separated into those with and without

complicat-ing sepsis or thrombosis. Four infants did not

survive when the renal failure that was caused by

renal anomalies was complicated by extensive

thrombosis or septicemia. In one case thrombosis

of the renal artery had caused extensive infarcts in

a solitary kidney. Two infants died with

gram-negative sepsis complicating bilateral renal

dysplasia or severe hdronephrosis in a solitary

TABLE VI

PERITONEAL DIALYSIS IN INFANTS WITH RENAL FAILURE

Case Diagnosis Age Outcome

No.

15 Hypertonic dehydration 1 1 months Died after 20 hours

18 Shock, cortical necrosis, congenital

heart disease

3 months Died after 1 day

20 Cardiovascular collapse, congenital heart disease, mental retardation

7 weeks Chronic renal failure

21 Posterior urethral valve 5 weeks Chronic renal failure

35 Posterior urethral valve 12 days Chronic renal failure

(6)

RECOVERY

2

CHRONIC RENAL FAILURE

H

DEAD

OUTCOME OF INFANTS WITH RENAL FAILURE

C’)

Ui U) 0 LI 0 Ui

:D

z

f!Tfl RENAL LiiJ ANOMALIES

D NORMAL

KIDNEYS

FIG. 3. Outcome related to age at onset; the younger the

infant when symptoms began, the worse was the

progno-sis.

kidney. In this latter case intestinal obstruction

following surgery for imperforate anus was an

additional complicating factor. The fourth child

had been treated for chronic renal failure

secondary to a posterior urethral valve. In this

instance severe diarrhea had led to acute renal

shutdown, acidosis, and gram-negative

septi-cemia, and eventually hypoxic cerebral

degenera-tion that was refractory to all therapeutic

attempts including peritoneal dialysis.

In 16 cases renal anomalies (bilateral dysplasia

or agenesis; multicystic, polcystic, and

hypo-plastic kidneys; hydronephrosis) were

accompa-nied by serious systemic anomalies and were

major contributing factors in the cause of death.

These cases are classified as follows: eight infants

died with bilateral severe renal dysplasia or

agenesis that in three instances was part of a

prune belly syndrome with malrotation of the

bowel or sepsis. Two of these eight infants with

dysplastic kidneys had also imperforate anus and

esophageal atresia, one had a single cardiac

ventricle and lung hypoplasia, another had

Hirschsprung’s disease and pseudomonas sepsis.

In two infants, unilateral or bilateral multicystic

renal disease was a major cause of death and was

accompanied by biliary atresia in one instance

and a horseshoe kidney in the second instance.

The latter infant died at 4 months of age after

further therapy was refused. One infant died from

polycystic renal disease with lung hypoplasia and

hyaline membrane disease. Four infants had

severe hydronephrosis. In two of these four cases,

exstrophy of the bladder was present and was

further complicated by intestinal obstruction,

omphalocele, meningocele, and sepsis. In one

case hydronephrosis was caused by a severe

meatal stenosis present in a premature infant with

hyaline membrane disease. In one instance

hydronephrosis was caused by urethral stenosis

complicated by imperforate anus, a cardiac

anomaly, and pneumothorax in a premature

infant. One infant died with hypoplastic kidneys

accompanied by hypoplasia of the lungs and

chromosomal anomalies in a premature infant. In

only one case, the severe renal anomalies were the

only ones present and the cause of death.

Prognosis: To evaluate the prognosis of every

case and to find potentially salvageable cases, we

reviewed treatment, interval between diagnosis

and death, duration of hospital stay, and cause of

death.

In most cases, the renal failure was of short

duration. When it lead to death, it occurred

within 24 hours of hospitalization in 1 1 infants,

within three days in an additional five infants.

Shock, hypotension, overwhelming infection, or

multiple renal and other organ anomalies were

the cause of death in these instances.

A review of the six infants who died at a later

stage showed two infants who died because of

multiple, severe additional anomalies. Two

infants who had only mild renal failure died from

sepsis and intestinal obstruction. In the last two

infants, age and size of the child or poor follow-up

prevented aggressive treatment.

DISCUSSION

A review of our cases indicates that the

diag-nosis of renal failure was usually made without

(7)

TABLE VII

CAUSE OF DEATH IN INFANTS WITH RENAL FAILURE

delay, because the majority of patients had either

a disorder which is often accompanied by renal

shutdown such as shock or septicemia, or a

congenital anomaly which prompted the search

for renal disease.

In our cases, the commonly known signs and

symptoms of renal failure proved not very helpful

in establishing the diagnosis. Nonspecific signs

such as lethargy, pallor, or vomiting that

accompany so many other conditions

predomi-nate. Oliguria, however, although present in the

majority of infants, is easily overlooked,

particu-larly in the newborn period. Only generalized

edema, hematuria, or enlarged palpable kidneys

are convincing evidence for the presence of renal

disease. Because our patient material is so

different from that reported in the other two

larger series,29 a direct comparison of the clinical

presentation is not possible. The large number of

infants (19 of 52) who had convulsions, however,

is remarkable.

The distinct difference in prognosis between

our patients with anomalies and those without

make an overall estimate of outcome unreliable.

The initial mortality was only 25% higher in

infants with renal abnormalities, but of the

survi-vors, 77% of those with anomalies had chronic

renal disease, compared to 20% of those

with-out.

Most of the deaths in infants without anomalies

occurred within two days of diagnosis, making it

unlikely that renal failure was the immediate

cause of death. Autopsy results revealed

addi-tional diseases that might have caused death

(

pneumonia, extensive thrombosis, infarcts,

car-diac anomalies, meningitis) in all but one infant.

In this group, renal failure was caused in more

than half the cases by hypotension, generally

following dehydration or shock from other

reasons. Systemic infection and pyelonephritis

were the second most common causes for renal

shutdown. There was an even age distribution

over the first year of life and only half the infants

of this group (53%) survived.

Infants with urinary tract anomalies by

contrast, had not only a much less favorable

outcome, but death in most cases was at least

partly a result of the renal disease. Only 39% of

these infants survived, all but three with chronic

renal failure. It is further remarkable that in the

majority of cases, the anomaly was diagnosed in

the first week of life. Renal dysplasia was the most

commonly seen abnormality. A diagnosis of a

urinary tract anomaly made at an early age,

therefore, may be a significant predictive factor

when attempting to assess the outcome.

No. of Patients

Time After Diagnosis

Lschemic damage (systemic, 6 1-2 days

renal) and renal failure (shock, hypotension, cortical necrosis, renal vein thrombo-sis [no congenital renal anomalies])

Sepsis and renal failure (no 3 3,6 days, 4

congenital renal anomalies) weeks

Congenital renal anomalies 4 1 day, 1

and renal failure compli- week (x2)

cated by sepsis or extensive 3#{189}months thrombosis

Congenital renal anomalies 16 1 day-3

and renal failure and multi- weeks

pie additional anomalies, prematurity

It is difficult to compare our results with those

of other authors because in the published series

obstructive disease and renal anomalies are not

included as a cause of renal failure.129 When we

disregard these differences, the outcome in our

patients without renal anomalies is very similar to

those of the mentioned reports.29 Gordillo et al

observed 100 cases of renal failure in children

under the age of 2 years. In 94 cases, a serious

infection (enteritis, pyelonephritis, or

broncho-pneumonia) was the cause of the renal shutdown.

A renal anomaly was found in only one child.

Lieberman’ reviewed 32 cases of renal failure in

children up to 15 years of age, including seven

infants. Two infants had congenital heart disease,

but no infant with renal anomalies is included.

Similarly, Gianantonio et al.2 report 16 infants of

a total of 41 children with renal failure. In almost

all their cases (15 of 16) renal failure was caused

by hemolytic uremic syndrome. It is evident that

in every series the patient population has its own

characteristics, thus precluding a comparison of

results. The 47% mortality rate in our patients

who did not show a urinary tract anomaly is

similar, however, to the 53% mortality rate

reported by Gordillo9 and the 44% of Gianantonio

et al.2 But the series is too small to compare

mortality rate between the two different groups

of this report.

The question finally arises whether modern

therapeutic techniques have significantly

im-proved the prognosis of renal failure in infants.

For various reasons their impact was minimal.

Treatment of renal insufficiency in cases in which

it accompanied a serious underlying disease such

(8)

as septicemia or shock usually was unsuccessful.

In these instances the primary disease dominated

the clinical picture. The renal shutdown was

merely another indication for the profound

disturbance of vital functions. Treatment of renal

failure was clearly not the most pressing

thera-peutic step. Earlier institution of therapy to

prevent renal failure would have been lifesaving

in some instances.

In infants with urinary tract anomalies,

however, treatment of renal failure presents even

greater problems. Severe anomalies of other

organs were present in almost all infants. Where

therapy was possible, it was directed toward

establishing and maintaining vital functions. In

some cases the multitude of abnormalities was not

compatible with life. It is, therefore, not

surpris-ing that the majority of infants of this group who

died did so shortly after birth; none survived the

first four weeks of life.

A review of the literature shows that the use of

dialysis and renal transplantation in infants, in

most instances, meets with great difficulties.

According to the 1 ith report of the Human Renal

Transplant Registry’#{176} only 20% of children 0 to 5

years of age who receive a cadaver kidney

trans-plant have a functioning graft after two years. In

a series of 374 patients at one of the most

experienced transplant centers, four infants who

received cadaver kidney transplants died.” In

other reports a small number of infants is

included. 12. 13 Again, none of these infants

survived. The reluctance to perform dialysis and

renal transplantation in infants is further

demon-strated by the fact that in several reports of a

larger number of pediatric patients, children

under one year of age are not included.1418

It is clear, both from our cases and those

reported earlier, that renal failure early in life still

carries with it a grave prognosis and that the

advancements in diagnostics and therapy that

have changed this outcome in older persons have

had little impact on renal failure in the infant.

After reviewing the deaths in our patients, it

seems unlikely that hemodialysis or

transpianta-tion, the two most notable advances in recent

years, would have materially altered the outcome

in any of the patients. Death was caused in the

majority of cases either by overwhelming

systemic infection (and occurred shortly after

admission to the hospital) or by a combination of

multiple congenital anomalies, many of which

were not amenable to therapy. It is still possible

that dialysis and kidney transplantation may be

useful in the patients with chronic renal failure

following the acute episode. It is encouraging,

however, that most infants without urinary

anom-alies who survived the first few days of renal

failure recovered completely. More aggressive

therapy of the disorders leading to “medical”

renal failure in early life will almost certainly

improve the outlook even more.

REFERENCES

1. Lieberman E: Management of acute renal failure in infants and children. Nephron 1 1: 193-208, 1973.

2. Gianantonio CA, Vitacco M, Mendilaharzu J, Mandila-harzu F, Rutty A: Acute renal failure in infancy and childhood. J Pediatr 61:660-678, 1962.

3. Lugo C, Ceballos R, Brown W, Polhil R, Cassady G: Acute renal failure in the neonate managed by peritoneal dialysis. Am J Dis Child 118:655-659,

1969.

4. Leonidas JC, Berdon WE, Bribetz D: Bilateral renal cortical necrosis in the newborn infant: Roentgen-ographic diagnosis. J Pediatr 79:623-627, 1971. 5. Manley CL, Collipp PJ: Renal failure in the newborn.

Am J Dis Child 115:107-110, 1968.

6. Chrispin AR, Hull D, Lillie JG, Ridson RA: Renal tubular necrosis and papillary necrosis after gastroenteritis in infants. Br Med J 1:410-412,

1970.

7. Arneil CC, MacDonald AM, Murphy AV, Sweet EM: Renal venous thrombosis. Clin Nephrol 1:119-131,

1973.

8. Carre IJ, Squire JR: Anuria ascribed to acute tubular necrosis in infancy and early childhood. Arch Dis Child 31:512-522, 1956.

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Pediatrics

Ekkehard W. Reimold, Tran Dinh Don and Howard G. Worthen