C. Keith Hayden, Jr., M.D.

Frank R. Santa-Cruz, M.D.

Ultrasonographic Evaluation of the
Eugenio C. Amparo, M.D.
Ben Brouhard, M.D.
Renal Parenchyma in Infancy and
Leonard E. Swischuk, M.D.
Deborah K. Ahrendt, M.D. Childhood’

The authors evaluated 46 patients several S EVERAL retrospective studies have compared the sonognaphic and
hours to 10 years of age and found that in histological findings in various forms of adult renal parenchymal
neonates and young infants, the renal disease (1-6). However, these findings cannot be applied directly to
cortex is normally as echogenic as the he- the pediatric patient for two reasons. The types of renal panenchyma!
patic parenchyma. Within 2 to 3 months, disease encountered in infancy and childhood are very different from
the renal cortex becomes progressively those in adults; indeed, they differ even among newborns, infants,
less echogenic than the liver; however, in and olden children. Moreover, the sonographic appearance of the
patients with renal parenchymal disease, normal neonatal or infantile kidney is not the same as that of the adult
cortical echogenicity increases. Sonogra- kidney. In the normal adult kidney, the cortex is less echogenic than
phy is very sensitive to this condition, the hepatic panenchyma; however, cortical echogenicity increases
especially in older children; however, the following the development of rena! parenchymal disease. Similar
overall findings are nonspecific. The au- findings may be observed in older infants and children (7). Yet in
thors conclude that ultrasound is helpful normal neonates and young infants the renal cortex can be just as
in screening for renal parenchymal ab- echogenic as the liven (8-10), and it is not known when the pattern
normalities in the pediatric patient, since changes from “neonatal” to “adult.” Thus before one can categorize
(a) it is very sensitive in the detection of the sonognaphic patterns encountered in patients with renal paren-
parenchymal disease, particularly in the chymal disease, he must first be familiar with the normal sonographic
neonatal period, and (b) older patients appearance of the kidney in different age groups.
demonstrate a direct correlation between
parenchymal abnormality and increased
MATERIAL AND METHODS
cortical echogenicity; this is not possible
in the neonate because the renal cortex is Over a period of 20 months, 349 patients ranging from several hours to 10
normally as echogenic as the liver. How- years of age had renal ultrasound using a Technicare real-time sector scanner
ever, ultrasound is relatively nonspecific with either of two transducers: (a) 5 MHz, 13 mm, optimal focal depth 2-6cm
except for renal cystic disease. and/or (b) 7.5 MHz, 10 mm, optimal focal depth 2-5 cm. Patients were scanned
only in the supine position, using the liver as a window to study the right
kidney.
Index terms: Kidney, diseases Kidney,
#{149} ultrasound
studies, 81.1298 Nephritis,
#{149} 81.69 Ultrasound,
#{149} in
Of the 349 patients examined, 303 had no clinical and/or laboratory evi-
dence of liver or kidney disease: these included 90 newborn infants, 140
infants and children Ultrasound,
#{149} tissue characteri-
infants 2 weeks to 6 months of age, 28 infants 7-12 months of age, and 45
zation
children 13 months to 10 years of age. In the remaining 46 patients, clinical,
Radiology 1984; 152: 413-417 laboratory, and/or radiographic findings demonstrated renal parenchymal
disease. In 35 patients, the histological diagnosis was correlated with the
sonograms; in the other 1 1, the final diagnosis was based on clinical, labora-
tory, and/or radiographic findings. These patients were divided into neonates
or young infants (newborn to 3 mo.) and older infants or children (3 mo).
Most patients were children aged 15 months to 10 years (TABLE I), with the
remainder included in the neonatal group (TABLE II).
Laboratory tests included serum creatinine, blood urea nitrogen (BUN),
serum albumin, total serum protein, and urinary sediment analysis. The
histological examination included light, immunofluorescence, and electron
microscopy. Using light microscopy, we recorded the number of glomeruli,
I From the Departments of Radiology (C.K.H. and the presence and extent of global or segmental glomerulosclerosis, the pres-
E.C.A., Assistant Professors; F.R.S.-C., resident; L.E.S., ence and degree (mild, moderate, or severe) of tubular atrophy and interstitial
Professor; D.K.A., fellow) and Pediatrics (C.K.H., fibrosis and/or infiltration, and the presence or absence of an inheritable
Assistant Professor; B.B. and L.E.S., Professors), Uni-
abnormality such as cystic disease or dysplasia. Immunofluoroscence studies
versity of Texas Medical Branch, Galveston, Texas.
involved staining with antisera to IgG, 1gM, IgA, Clq, C3, C4, fibrin, albumin,
Presented at the Sixty-ninth Scientific Assembly and
and cr-2-macroglobulin.
Annual Meeting of the Radiological Society of North
America, Chicago, Ill., Nov. 13-18, 1983. Received Sonograms of the right kidney were evaluated with emphasis on the
Dec. 2, 1983; accepted and revision requested Dec. 30; prominence and hypoechoic nature of the renal pyramids, distinction of the
revision received Feb. 29, 1984. corticomedullary junction, and cortical echogenicity in relation to the renal
C RSNA, 1984 sjh sinus and liver parenchyma. In older patients, cortical echogenicity was

413
TABLE I: Renal Parenchymal Disease in Childhood Of the 36 patients with renal paren-
chymal disease who presented at be-
Sonographic Characteristics
Cortical Corticomedullary tween 15 months and 10 years of age
No. of Patients Echogenicityt Definitiont (TABLE I), there was no correlation be-
tween the sonognaphic appearance and
Focal segmental nephrosclerosis 8
1 tt + the specific type of renal disease;
1 however, we did observe a significant
6 +
7
correlation between the degree of
Mesangial 1gM nephropathy
4 + cortical echogenicity and the extent of
3 +
abnormality. Loss of corticomedullary
Minimal-change nephrotic syndrome 5
3 + definition did not prove to be reliable
2 + as a criterion of significant panenchy-
Acute glomerulonephritis ma! involvement. In the 10 patients
3 = +
2 + younger than 3 months of age (TABLE
Juvenile polycystic kidney disease 2
II), the sonogram did not permit a
2 (? cortical rim)
Alport disease 2 specific diagnosis except in the case of
+ polycystic kidney disease. While ul-
1 ‘1 +
2
trasound did appear to be very sensi-
Primary oxalosis with nephrocalcinosis
1 tive to even mild renal abnormality, it
+
was difficult to correlate the severity of
Henoch-Sch#{246}nlein syndrome 2 +
Idiopathic nephrocalcinosis + involvement with the sonographic
+ findings, since the limitations inherent
* = less than the liver in the base-line appearance of the
= = equal to the liver normal neonatal kidney do not allow
#{182}
greater
= than the liver but less than the renal sinus for gradation as is possible in older
I equal
= to the renal sinus
patients. Also as in olden patients, loss
t + = normal
± = indistinct of corticomedullary definition was not
- = absent helpful in establishing the presence of
parenchymal involvement.
TABLE II: Renal Parenchymal Disease in the Neonate and Young Infant

Sonographic Characteristics DISCUSSION

No. of Cortical Corticomedullary
Patients Echogenicity* Definitiont Not only is renal panenchymal dis-
ease very different in infants and
Cortical necrosis 2 t +
Nonspecific interstitial fibrosis 2 children than it is in adults, but the
manifestations vary even among
:1:
newborns, infants, and olden children.
Methicillin nephritis 1 ±
Finnish nephrosis 1 - In the adult, lupus nephritis, mem-
Cystic dysplasia 1 + branous glomerulosclenosis, focal gb-
Adult polycystic kidney disease presenting in infancy 1 -

1 +?
merulonephritis, and diabetic neph-
Infantile polycystic kidney disease
(? cortical rim) rosclerosis are common causes. In
Acute stem-cell leukemia 1 f (focal) +
contrast, renal parenchymal disease in
* = greater than the liver childhood is most frequently secon-
equal to the liver
= =
dary to acute gbomerulonephritis and
= less than the liver
t + = normal nephrotic syndrome (massive pro-
:1: = indistinct teinunia, hypoabbuminemia, hypenli-
- = absent pemia, and edema), which in turn can
have various causes. Juvenile glomer-
ulonephnitis frequently represents
an acute immune-complex-mediated
condition, with the acute post-strep-
graded using the system described by Hri- to 4 weeks, while nearly an equally tococcal form being by fan the most
cak ef a!. (6). However, the same system small number (10%) continued to ex- common (11). This condition is most
could not be used in neonates and young
hibit the “neonatal” pattern at 14-17 prevalent during the school-age years,
infants, in whom the renal cortex is nor-
weeks (Fig. 2). In establishing the age developing at an average of 6 to 7 years
mally just as echogenic as the liver and the
at which transition occurred, it did not of age (12). In contrast, nephnotic syn-
renal sinus is not as echogenic as in older
children or adults; thus we simply indicated
seem to matter whether the infant was drome usually presents at a younger
whether the renal cortex was isoechoic or full-term or premature, though more age and can be caused by a number of
hyperechoic compared to the liver. premature infants need to be examined primary renal (90%) or systemic con-
before a statistically valid observation ditions (10%) (13); in most cases, how-
can be made. Even in neonates and even, the histological diagnosis is
RESULTS
young infants the renal cortex was minimal-change nephrotic syndrome
Scans of the normal patients con- never more echogenic than the liver. on a variant thereof.
firmed that the renal cortex was as The corticomedullary junction was Nephritis, nephnosis, and nephnotic
echogenic as the liver in neonates and distinct in all patients, regardless of syndrome are uncommon in neonates
young infants (Fig. 1, a); however, be- age, but it was particularly prominent and young infants. In this country, the
tween 2 and 3 months this changed to in the neonates and young infants. Fi- few cases of nephnotic syndrome that
the “adult” pattern in most cases (Fig. na!!y, the renal sinus was not as echo- are encountered in this age group are
1, b). A few neonates (17.5%) already genic in the neonates and young in- most frequently due to syphilis (14, 15)
demonstrated the “adult” pattern by 2 fants as it was in the older patients. but can also be seen with other infec-

414 #{149}Radiology August 1984

tions such as rubella (16), toxop!asmo- Figure 1
sis (16, 17), and cytomegalic inclusion
disease. In Scandinavia, a familial form
of congenital nephrotic syndrome,
known as the Finnish type, is more
common (18). However, abnormalities
involving the renal parenchyma in this
age group are more frequently secon-
dary to renal vascular disease (renal
vein thrombosis, renal corticomedul-
lary necrosis, renal artery thrombosis)
or renal cystic disease. In the neonate,
renal vascular disease is most often
secondary to dehydration, sepsis,
massive blood loss, and severe hypoxia
(19-23). In infancy, renal cystic disease a. b.
is most commonly “infantile” poly-
a. Normal newborn kidney. The renal cortex exhibits the same echogenicity as the adjacent
cystic disease, an autosomal recessive liver. The renal pyramids are prominent and hypoechoic.
disorder classified by Osathanondh b. Normal 5-month-old infant. The renal cortex is less echogenic than the liver. The renal
and Potter (24) as type I, whereas pyramids are unchanged.
“adult” polycystic disease (Potter’s type
III) is inherited as an autosomal domi-
nant trait, usually not seen until after
Figure 2
the age of 30. Only recently has it be-
come apparent that neonates can ex-
hibit this form of renal cystic disease
(25-28).
Because of the wide spectrum of
renal parenchymal disease encoun-
tened in infancy and childhood, we had
hoped to be able to not only correlate
the ultrasound findings with specific
types of renal disease but also deter-
mine how changes in the sonographic
appearance might be related to seven- 24 $.S #{149}.I3 I4.I7 IS-il * 22.= 7.3

ty. However, in both infancy and PATiENTS’ AGES

childhood the sonognam proved to be
S dmonsirating nonatal.Iik.
nonspecific except in polycystic dis-
0 “ dult.Iike ptt.rn
ease. In the infant with “adult” po!y-
Sonographic appearance of the normal kidney in 303 pediatric
cystic disease, the kidneys were en-
patients.
larged and the renal pelvis was seen as
a central hypoechoic region sun-
rounded by markedly increased echo-
genicity with complete loss of the renal Figure 3
pyramids (Fig. 3, a) and several small
peripheral cysts. In contrast, the infant
with “infantile” polycystic kidney
disease also had large kidneys dem-
onstrating a central hypoechoic region
surrounded by increased echogenicity,
but what appeared to be the outer rim
of the cortex was quite hypoechoic (Fig.
3, b). Two of our olden patients (6 and
7 yr.) with “infantile” polycystic dis- ..-,
ease also exhibited these findings, so
that they may be more than just coin-
cidenta!. The hypoechoic “cortical” rim a.

could have considerable diagnostic a. “Adult” polycystic kidney disease in an infant. The renal cortex is hyperechoic and the renal
value, but more cases will be needed to pyramids are absent. Note the small peripheral cysts (arrows).
b. “Infantile” polycystic kidney disease. The medulla is hyperechoic and surrounded by what
confirm this.
appears to be a hypoechoic cortical rim.
In our olden patients, there was a
direct and significant correlation be-
tween cortical echogenicity and pa-
renchymal abnormality (Fig. 4). In
most of them, this abnormality nepre- and edematous kidney. Of the 1 1 pa- than the liven (Fig. 5). Similarly, in-
sented structural changes such as gb- tients with minimal-change nephrotic creased echogenicity is seen in acute
bal and/on segmental glomeru!osc!e- syndrome and mesangial 1gM ne- glomenulonephnitis (Fig. 6). All 11
rosis and/or interstitial fibrosis and phnopathy, the sonognam was normal demonstrated only minimal wrinkling
infiltration; however, in some cases it in 5 while in 6 cortical echogenicity and irregularity of the glomenulan
appeared to be secondary to a swollen was increased, though never greaten basement membrane, with little if any

Volume 152 Number 2 Radiology 415

#{149}
Figure 4 Figure 5

- .,,,-

4.

:‘

_,,,; c
,.,c’
a. b.

a. Severe focal segmental glomerulosclerosis. The renal cortex is more echogenic than the
liver and isoechoic with the renal sinus. The renal pyramids remain well defined and hy-
poechoic. Mesangial 1gM nephropathy. The renal pa-
b. Mild focal glomerulosclerosis. The renal cortex is isoechoic with the liver. renchyma is just as echogenic as the liver and
the corticomedullary junction remains well
defined. Note the pleural effusion (arrow).

Figure 6 tubulo-intenstitial abnormality. Sub-

sequent analysis showed that increased
cortical echogenicity was directly re-
bated to peripheral edema and/or low
serum albumin. Unfortunately, we
could not make a similar correlation
between severity of disease and sono-
graphic changes in our younger pa-
tients, for, as noted earlier and con-
firmed in the first part of our study, the
renal cortex in the neonate and young
infant can normally be just as echo-
genic as the liver (Fig. 1, a). If it is more
echogenic, abnormality should be
suspected, even though Erwin and
Carroll demonstrated that the renal
cortex was more echogenic than the
a. b.
liver in a significant number of normal
a. Acute post-streptococcal glomerulonephritis. On the initial scan, the renal cortex is as
premature infants (29). These data have
echogenic as the liver, while the corticomedullary junction remains well defined.
b. Nine weeks later, the renal cortex is much less echogenic than the liver.
not been duplicated by others as far as
we know, nor could we confirm them
in any of our 30 normal infants
weighing 800-2,000 g.
Hricak et al. (10) attributed increased
echogenicity of the normal neonatal

Figure 7

a. b. C.

a. Congenital nephrotic syndrome (Finnish type). Note the increased cortical echogenicity and loss of renal pyramids.
b. Hypersensitivity nephritis secondary to methicillin. The renal cortex is hyperechoic and the corticomedullary junction appears somewhat
blurred, although the renal pyramids remain hypoechoic.
C. Severe cortical necrosis. Note the increased echogenicity of the renal cortex, the preservation of the corticomedullary junction, and the
prominent, hypoechoic renal pyramids.

416 Radiology
#{149} August 1984
kidney to three facts: (a) the g!omeru!i appearance of acute pyelonephritis. Radi- lations and pathogenesis. Am J Dis Child
ology 1979; 132:683-685. 1979; 133:842-845.
occupy 18% of the neonatal renal con-
2. Kay CJ, Rosenfield AT, Taylor KJW, Rosen- 17. Shahin B, Papadopoulou ZL, Jenis EH.
tex, compared to 8.6% in the adult; (b) berg MA. Ultrasonic characteristics of Congenital nephrotic syndrome associated
the cellular component makes up a chronic atrophic pyelonephritis. AJR 1979; with congenital toxoplasmosis. J Pediatr
greater proportion of the gbomeruban 132:47-49. 1974; 85:366-370.
tuft; and (c) 20% of the loops of Henle 3. Rochester D, Aronson AJ, Bowie JD, 18. Anand 5K, Northway JD, Vernier RL.
Kunzmann A. Ultrasonic appearance of Congenital nephrotic syndrome: report of
are within the cortex rather than the
acute poststreptococcal glomerulonephritis. a patient with cystic tubular changes who
medulla. Presumably all of these fac- JCU 1978; 6:49-50. recovered. J Pediatr 1979; 95:265-268.
tons result in a greaten number of 4. Rosenfield AT, Taylor KJW, Jaffe CC. 19. Anand 5K, Northway JD, Smith JA. Neo-
acoustical interfaces, increasing the Clinical applications of ultrasound tissue natal renal papillary and cortical necrosis.
characterization. Radiol Clin North Am Am J Dis Child 1977; 131:773-777.
echogenicity of the renal cortex. Be-
1980; 18:31-58. 20. Chrispin AR, Lillie JC. [Acute kidney
cause of this, the examiner cannot use 5. Rosenfield AT, Siegel NJ. Renal paren- damage with tubular necrosis and papillary
the same gradation of rena! cortical chymal disease: histopathologic-sono- necrosis in young infants]. Ann Radiol 1971;
echogenicity as in an older patient. In graphic correlation. AJR 1981; 137:793- 14:199-204. [Fre]
798. 21. Husband P. Howlett KA. Renal papillary
addition, the neonatal renal sinus is not
6. Hricak H, Cruz C, Romanski R, et al. Renal necrosis in infancy. Arch Dis Child 1973;
as echogenic as in an olden child; thus parenchymal disease: sonographic-histo- 48:116-120.
any time the renal cortex becomes logic correlation. Radiology 1982; 144: 22. Kozlowski K, Brown RW. Renal medullary
more echogenic than the liver, it ex- 141-147. necrosis in infants and children. Pediatr
hibits the same echogenicity as the 7. Krensky AM, ReddishJM, Teele RL. Causes Radio! 1978; 7:85-89.
of increased renal echogenicity in pediatric 23. Kurnetz R, Bernstein J. Neonatal blood loss
renal sinus (Fig. 7). Although we could patients. Pediatrics 1983; 72:840-846. and hematuria. I Pediatr 1974; 84:452-455.
not correlate severity of panenchymal 8. Haller JO, Berdon WE, Friedman AP. In- 24. Osathanondh V, Potter EL. Pathogenesis
involvement with the ultrasound creased renal cortical echogenicity: a normal of polycystic kidneys. Historical survey.
findings in neonates, the sonogram did finding in neonates and infants. Radiology Arch Pathol 1964; 77:459-465.
1982; 142:173-174. 25. Ross DC, Travers H. Infantile presentation
appear to be very sensitive in identi-
9. Scheible W, Leopold CR. High-resolution of adult-type polycystic kidney disease in a
fying parenchyma! involvement; even real-time ultrasonography of neonatal kid- large kindred. J Pediatr 1975; 87:760-763.
with only mild tububo-intenstitial neys. J Ultrasound Med 1982; 1:133-138. 26. Fellows RA, LeonidasJC, Beatty EC Jr. Ra-
changes, the renal cortex became more 10. Hricak H, Slovis TL, Callen CW, Callen PW, diologic features of “adult type” polycystic
Romanski RN. Neonatal kidneys; sono- kidney disease in the neonate. Pediatr
echogenic than the liver (Fig. 7, b). graphic anatomic correlation. Radiology Radiol 1976; 4:87-92.
Finally, it should be noted that in 1983; 147:699-702. 27. Loh JP, Hailer JO, Kassner EC, Aloni A,
both age groups definition of the con- 11. Jordan SC, Lemire JM. Acute glomerulo- Glassberg K. Dominantly-inherited poly-
ticomedullary junction did not prove nephritis. Diagnosis and treatment. Pediatr cystic kidneys in infants: association with
Clin North Am 1982; 29:857-873. hypertrophic pyloric stenosis. Pediatr
to be reliable as a criterion of renal
12. Dodge WF, Spargo BH, Travis LB. et al. Radio! 1977; 6:27-31.
disease. When definition was lost, Poststreptococcal glomeru!onephritis. A 28. Proesmans W, Van Damme B, Casaer T,
significant panenchymal abnormality prospective study in children. N EnglJ Med Marcha! C. Autosomal dominant polycystic
was present (Fig. 7, a); however, in 1972; 286:273-278. kidney disease in the neonatal period:
13. McEnery PT, Strife CF. Nephrotic syn- association with a cerebral arteriovenous
many of our patients with severe pa-
drome in childhood. Management and malformation. Pediatrics 1982; 70:971-975.
renchymal abnormality, including 33 treatment in patients with minimal change 29. Erwin BC, Carroll BA. Renal cortical
of the 36 older patients and 4 of the 10 disease, mesangial proliferation, or focal echogenicity in the newborn period. Pre-
younger patients, definition was nei- glomerulosclerosis. Pediatr Clin North Am sented at the 28th annual convention of the
then lost nor altered (Fig. 7, c). 1982: 29:875-894. AlUM, New York, N.Y., Oct. 18-21, 1983.
14. Hill LL, Singer DB, Falletta J, Stasney R.
The nephrotic syndrome in congenital
Department of Radiology syphilis: an immunopathy. Pediatrics 1972;
Division of Pediatric Radiology 49:260-266.
University of Texas Medical Branch 15. McDonald R, Wiggelinkhuizen J, Kaschu!a
Galveston, Texas 77550 ROC. The nephrotic syndrome in very
young infants. Am J Dis Child 1971; 122:
507-512.
References 16. Beale MC, Strayer DS, Kissane JM, Robson
AM. Congenital glomerulosclerosis and
1. Edell SL, Bonavita JA. The sonographic nephrotic syndrome in two infants. Specu-

Volume 152 Number 2 Radiology 417

#{149}