Elevated Renal Rind - Journal of Ultrasound in Medicine

Elevated Renal Rind
Anne Paterson, MRCP, FRCR, Donald P. Frush, MD,
Louise E. Sweeney, FFR RCSI, FRCR, Paul S. Thomas, FRCR
We describe the findings from a group of five
infants ranging in age from 3 weeks to 13 months
who had shock of differing causes. In each case,
sonographic evaluation of the abdomen revealed
bilateral perirenal hyperechoic bands several millimeters
thick, surrounding a thin, hypoechoic rim of
fluid. The findings were identified during the acute
phase of each child’s illness and persisted after the
patient’s condition had clinically improved, eventually
resolving in the three surviving children. We
have dubbed this sign the “elevated renal rind.” We
believe that the changes are likely secondary to systemic
inflammatory mediators and do not reflect
localized intraabdominal disease. KEY WORDS:
Fascia, renal; Shock, pediatric; Kidney; Renal rind
sign.
Abdominal sonography is commonly
requested as a screening examination in
cases of shock, in an attempt to determine
the underlying cause for a patient’s symptoms. We
ABBREVIATIONS
ICU, Intensive care unit; PUV, Posterior urethral valves; CT,
Computed tomography
describe a group of five children who were examined
at our hospital over a period of 8 years. The sonographic
abnormalities were all detected in severely
ill children in the ICU. The studies were reviewed
retrospectively by two experienced pediatric radiologists
(L.E.S., P.S.T.). In all cases, characteristic
changes were seen in the perirenal tissues, which we
termed the “elevated renal rind.”
CASE REPORTS
See Table 1 (Figs. 1, 2).
Received November 29, 1999, from the Radiology Department,
Royal Belfast Hospital for Sick Children (A.P., L.E.S., P.S.T.), Belfast,
Northern Ireland; and Division of Pediatric Radiology, Department
of Pediatric Radiology, Duke University Medical Center (D.P.F.),
Durham, North Carolina. Revised manuscript accepted for publication
March 22, 2000.
Address correspondence and reprint requests to Anne Paterson,
MRCP, FRCR, Radiology Department, Royal Belfast Hospital for Sick
Children, 180, Falls Road, Belfast BT12 6BE, Northern Ireland.
DISCUSSION
The kidney and adrenal gland are encased in the
anterior (Zuckerkandl) and posterior (Gerota) perirenal
fasciae (Fig. 3). The lateroconal fascia lies laterally
and blends anteriorly with the parietal peritoneum.
© 2000 by the American Institute of Ultrasound in Medicine • J Ultrasound Med 19:459–463, 2000 • 0278-4297/00/$3.50

460 ELEVATED RENAL RIND J Ultrasound Med 19:459–463, 2000
Table 1: Data and Outcome of Five Cases of Elevated Renal Rind
Underlying Maximum
Sex/ Cause of Organisms Associated Creatinine Sonographic
Age Shock Cultured Clinical Problems Level Findings Outcome
Case 1 M, 17 days Necrotizing Staphylococcus, Prematurity, symmetrical 152 m mol/l Bilateral pelviectasis, Death at 23 days due to
(born at enterocolitis enterococcus intrauterine growth elevated renal rind cardiac failure
33 weeks’ retardation, unbalanced
gestation) atrioventricular canal defect
Case 2 M, 28 days Meningitis and Escherichia coli Posterior urethral valves 194 m mol/l Bilateral pelviectasis, Survival with chronic
urinary tract elevated renal rind renal impairment;
infection sonogram after 8 days
was unchanged; long-term
sonographic follow-up shows
hyperechoic kidneys with
normal perirenal tissues
Case 3 M, 12 weeks Pneumonia None Apneic episode 98 m mol/l Minimal pelviectasis Survival with profound
(presumed with pelvic urothelial motor and developmental
aspiration) thickening, elevated deficit; sonogram at 1 year
renal rind (Fig. 1) of age showed normal kidneys
Case 4 F, 13 months Infection with Group A None 37 m mol/l Minimal pelviectasis, Survived; sonography at
erythematous, streptococci elevated renal rind follow-up evaluation showed
maculopapular (Fig. 2) normal kidneys
rash
Case 5 M, 12 weeks Pneumonia Escherichia coli Prematurity, trisomy 21, 122 m mol/l Enlarged kidneys Renal function recovered
(born at unbalanced atrioventricular with loss of cortico- after 4 weeks; sonography
27 weeks’ canal defect, necrotizing medullary differentiation, unchanged at that time,
gestation) enterocolitis with bowel elevated renal rind but infant died aged
resection and ileostomy at 17 weeks due to cardiac
4 weeks, bronchopulmonary failure and chronic lung
dysplasia disease

J Ultrasound Med 19:459–463, 2000
PATERSON ET AL
461
The perirenal space contains fat and is bounded by the
perirenal fasciae. The anterior pararenal space separates
the posterior aspect of the parietal peritoneum
from the anterior perirenal fascia. It is continuous
across the midline and contains the pancreas, duodenum,
and ascending and descending colons. The posterior
pararenal space is formed anteriorly by the
posterior perirenal fascia and posteriorly by the transverse
fascia; it contains no organs.
Using CT, thickening of the perirenal fascia has
been described in adults as a nonspecific indicator of
intraabdominal sepsis or neoplasia. 1,2 The normal
perirenal fascia cannot be visualized at sonography,
but two studies have measured the “anterior
extrarenal space” (the sum of the anterior perirenal
plus pararenal spaces) in adults, and the authors have
concluded that this space increases in width and
echogenicity in association with acute, localized
abdominal inflammation, trauma, and malignancy. 3,4
Belli and Joseph 3 coined the term “renal rind sign”as
a descriptor for this sonographic finding. In addition,
an increase in the width but not the echogenicity of
the so-called anterior extrarenal space was noted with
chronic, local inflammatory disease and in cushingoid
patients. 4 In both of these studies, 3,4 the authors
concluded that a careful search for intraabdominal
pathologic lesions should be conducted if the renal
rind sign was present.
Figure 1 Case 3. A,B, Longitudinal and transverse sonograms of the right kidney during the acute phase of the illness. A perinephric
hypoechoic rim with surrounding hyperechoic band is evident. C, Longitudinal sonogram of the left kidney during the
acute illness. D, Longitudinal sonogram of the right kidney at 10 months of age shows normal perirenal tissues.
A
B
C
D

462 ELEVATED RENAL RIND J Ultrasound Med 19:459–463, 2000
A
B
Figure 2 Case 4. Longitudinal (A) and transverse (B) sonograms of the right kidney during the acute febrile illness. The perirenal
hypoechoic rim and hyperechoic band are again present.
Review of the literature reveals one additional case
report describing an increase in the thickness and
echogenicity of the right-sided perirenal fascia at
sonography. 5 The findings were observed in an
elderly man with global infarction of the right kidney
associated with aortic dissection. Again, the
authors believed that such findings were specific and
would serve as a useful indicator of renal infarction
in the absence of any other sonographic abnormalities.
They documented resolution of the perirenal
changes on a follow-up sonogram 5 months later.
Sonographic descriptions of perirenal changes are
scarce in the pediatric literature. A solitary case
report by Swischuk and Hayden 6 described an
increase in the width and echogenicity of the right
pararenal space in two children with pancreatitis. In
this instance, the authors concluded that the appearance
should serve “as a strongly positive, ancillary
finding of pancreatitis.”
The five patients described in this paper were in
shock and required ionotropic support. The underlying
cause for the shock was different in each of the
children, although four of them had septicemia.
Clinically, none of the patients had primary renal disease,
but four of the children developed acute renal
failure during the course of their illness. Regardless
of the underlying cause of sepsis, the perirenal sonographic
changes were identical. In all of the documented
cases, a thin hypoechoic rim (presumed to be
fluid) distended the perirenal space. The thickened,
hyperechoic perirenal fascia was clearly demarcated
adjacent to the hypoechoic perirenal fluid. The
changes were bilateral in all cases. One patient with
acute renal failure had associated swollen kidneys
with loss of corticomedullary differentiation (case 5).
The remaining four infants had mild pelviectasis but
otherwise had a normal renal echotexture. No sonographic
abnormalities were seen in the remainder of
the abdomen or pelvis in any of the patients.
Specifically, none of the infants had associated ascites
or focal signs of intraabdominal sepsis. The changes
in the perirenal tissues were documented to resolve
in the three surviving children at follow-up examinations.
Autopsy was refused by the parents of the
two infants who died.
Figure 3 Cross-sectional diagram shows the retroperitoneal
fascial planes. APaS, Anterior pararenal space; Ao, aorta; DC,
descending colon; GF, Gerota fascia; IVC, inferior vena cava;
LF, lateroconal fascia; LK, left kidney; LV, lumbar vertebra;
PeS, perirenal space; PP, parietal peritoneum; PPaS, posterior
pararenal space; TF, transverse fascia; ZF, Zuckerkandl fascia.

J Ultrasound Med 19:459–463, 2000
PATERSON ET AL
463
The elevated renal rind differs therefore from the
descriptions in prior reports of sonographic perirenal
fascial changes. In the previously described cases, the
thickened perirenal fascia (the renal rind) could not
be seen as separate from, and appeared adherent to,
the renal capsule. In our patients, a hypoechoic
perirenal fluid collection was observed, which elevated
the hyperechoic perirenal fascia. In the children
described here, the changes were bilateral and could
not be attributed directly to localized intraabdominal
disease. In addition, resolution of the changes was
documented in all of the surviving children.
The cause of the visualized abnormalities is
unknown. With regard to the renal rind, the
authors 3,4,6 postulated that changes in the perirenal
fascia may be due to localized edema, fibrosis, hyperemia,
or lymphatic obstruction. These papers
described localized intraabdominal pathologic
changes associated with changes in the adjacent
perirenal tissues, and their individual authors each
believed they were describing a specific sonographic
sign of the disease entity presented. The common
denominator in the current patient population was
shock. In these patients, systemic inflammatory
mediators may well be responsible for the bilateral
sonographic changes observed, including the transudation
or exudation of fluid into the perirenal space.
A perinephric hematoma would also appear acutely
hypoechoic, but its echogenicity would increase over
time as the clot organized. Given that sonograms
obtained 8 days (case 2) and 4 weeks (case 5) apart
did not document a change in the appearance of the
hypoechoic perirenal rim, this mechanism is believed
to be unlikely to explain the presented findings, especially
given their bilaterality. In addition, none of the
patients developed a coagulopathy that would predispose
them to hematoma formation. Similarly, a
perinephric abscess would cause a hypoechoic rim
surrounding the kidney, but this is usually secondary
to focal, acute pyelonephritis. Bilateral abscesses
would be extremely unusual. Primary renal disease
was not documented as the underlying cause of sepsis
in any of the patients reported, although one
patient (case 2) later developed a urinary tract infection
secondary to distal obstruction from PUV. Both
perinephric hematomas and abscesses might reasonably
be expected to cause secondary, local inflammatory
changes in the adjacent perirenal fascia, thus
making it appear thickened and hyperechoic at
sonography.
In summary, we present five children who demonstrate
a sonographic sign we have called the elevated
renal rind. We believe that it may occur secondary to
systemic inflammatory mediators with fluid leakage
into the perirenal tissues, although we have not been
able to confirm this pathologically. Importantly, the
elevated renal rind is not an indicator of intrinsic
renal disease or of a localized intraabdominal pathologic
condition. Rather, it is seen in constitutionally
ill patients with shock, and further imaging evaluation
is not required when it is demonstrated. The
patient’s prognosis depends ultimately on the treatment
of the underlying condition; the perirenal
changes will resolve with time in those patients who
survive.
REFERENCES
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