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Original Research |
1 Department of Radiology, Haga Teaching Hospital, Location Leyweg, Leyweg 275,
2545 CH, The Hague, The Netherlands.
2 Department of Radiology, Leiden University Medical Centre, Leiden, The
Netherlands.
3 Department of Surgery, Haga Teaching Hospital, Location Leyweg, The Hague, The
Netherlands.
4 Present address: Department of Surgery, Leiden University Medical Centre,
Leiden, The Netherlands.
5 Department of Pediatrics, Haga Teaching Hospital, Location Juliana Children's
Hospital, The Hague, The Netherlands.
6 Department of Radiology, Haga Teaching Hospital. Location Juliana Children's
Hospital, The Hague, The Netherlands.
Received May 21, 2007;
accepted after revision August 7, 2007.
Address correspondence to F. Wiersma
(fwiersma80{at}hotmail.com).
Abstract
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MATERIALS AND METHODS. Between January 2005 and February 2006, 189 consecutive patients (112 boys and 77 girls; mean age, 10 years) presenting with acute abdominal pain were examined with sonography. Patients with a known history of renal disease and those with acute urinary tract infection were excluded from the study. Echogenicity of the renal cortex in comparison with adjacent liver was recorded. Renal cortex echogenicity was divided into three groups; group 1, renal cortex echogenicity less than liver parenchyma echogenicity; group 2, renal cortex echogenicity similar to that of liver parenchyma; and group 3, renal cortex echogenicity greater than that of liver parenchyma. Patients with hyperechogenicity were reexamined with sonography after 2 weeks or more. The final sonographic diagnosis and clinical outcome were noted.
RESULTS. Renal cortex echogenicity was equal to or greater than that of the liver parenchyma in 18% (n = 34) of 189 patients. Increased echogenicity of the renal cortex returned to normal in 2 or more weeks in all patients. Three patients had no follow-up. Clinical diagnoses were idiopathic acute abdominal pain (n = 74), appendicitis (n = 83), mesenteric lymphadenitis (n = 15), ileocecitis (n = 7), gastroenteritis (n = 7), Crohn's disease (n = 1), intussusception (n = 1), and pneumonia (n = 1). No concurrent renal disease was diagnosed.
CONCLUSION. Increased echogenicity of renal parenchyma in children with acute illness is a transient feature and does not necessarily indicate renal disease.
Keywords: abdomen children kidney pediatric imaging renal echogenicity sonography
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The purpose of this study was to determine the frequency of hyperechogenicity of the renal cortex in children with acute abdominal illness but no history of renal abnormalities, and to assess the assumed transient feature of this finding.
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All patients with a history of renal disease (including recent acute pyelonephritis or glomerulonephritis, acute fungal infections, stasis nephropathy, hemolytic-uremic syndrome, and renal artery or renal vein thrombosis), renal neoplasms, kidney transplantation, solitary kidney or other renal anomalies, multicystic dysplastic kidney disease, urologic surgery, or vesicoureteral reflux were excluded from the study (n = 4). Patients with concurrent use of diuretics were excluded. All patients younger than 2 years were also excluded from the study (n = 8) because the renal cortex in normal neonates and infants can be hyperechoic [6, 7]. Of a total of 201 patients with acute abdominal illness who where referred for abdominal sonography, 189 patients with a mean age of 10 years (age range, 2-15 years) were included in our study. Final diagnoses after sonography and after additional sonography or CT if necessary as well as findings of clinical or pathologic evaluation were noted. Serum creatinine was tested and urine analysis was performed for 17 and 23 patients, respectively, with increased renal cortex echogenicity. After 1 year, records of patients with increased echogenicity of the renal parenchyma records were evaluated for renal disease.
Informed consent was obtained from each patient or his or her parents in conformance with the rules of our country. Institutional review board approval was obtained for our observational study.
Imaging Observations
All children underwent comprehensive abdominal sonography. The images were
obtained using an HDI 5000 scanner (ATL HDI 5000, Philips Medical Systems)
with a curved array (2-5 MHz) transducer. The sonographic examinations were
performed by a pediatric radiologist, a staff radiologist, or a resident in
radiology. The radiologists had 6-14 years of experience in pediatric
abdominal sonography. The residents were in the third or fourth year of their
medical training and had about 6 months of specific experience.
Transverse and longitudinal images of the kidneys were obtained. The renal parenchyma was analyzed for diffuse renal cortex echogenicity. Renal cortex echogenicity of the right kidney was compared with echogenicity of the liver parenchyma and classified into three groups: group 1, in which renal cortex echogenicity was less than liver echogenicity; group 2, in which renal cortex echogenicity was equal to liver echogenicity; and group 3, in which renal cortex echogenicity was greater than liver echogenicity. Renal cortex echogenicity was determined by the radiologist during the examination.
Almost all patients with increased renal cortex echogenicity (i.e., patients in groups 2 and 3) were reexamined after 2 weeks. At the time of reexamination, the acute abdominal complaints had resolved (range until reexamination, 1 day-1 year). Three patients were not reexamined.
Statistical Analysis
The chi-square test was used for the comparison of subgroups. A p
value of less than 0.05 was considered to indicate a statistical
difference.
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Imaging Findings
In 34 (18%) of the 189 patients, echogenicity of the renal cortex was
increased in comparison with that of the adjacent liver. In 15 (8%) patients,
the renal echogenicity was equal to the liver (group 2), and in 19 (10%)
patients, renal echogenicity was greater than the liver (group 3).
Figures 1 and 2A show the hyperechogenicity of the renal cortex in two patients with appendicitis. Renal cortex echogenicity was increased in patients with appendicitis, gastroenteritis, mesenteric lymphadenitis, ileocecitis, Crohn's disease, and pneumonia. Table 2 shows the type of recorded renal cortex echogenicity and the final clinical diagnosis of all patients. Clinical diagnosis was based on sonographic, clinical, and pathologic results.
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Renal cortex echogenicity returned to normal in all reexamined patients, as shown in Figure 2B. In one patient, the increased echogenicity returned to normal in 1 day, detected coincidentally during screening for persistent pain after surgical resection of an acutely inflamed appendix.
Statistical Analysis
Renal cortex echogenicity was not significantly (p = 0.66) greater
in patients with a perforated appendix or a periappendicular abscess than in
patients with uncomplicated appendicitis. However, renal cortex echogenicity
was statistically significantly (p = 0.000033) greater in children
with appendicitis (both uncomplicated and complicated) than in children with
abdominal pain not diagnosed as appendicitis.
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The cause of increased renal cortex echogenicity remains unclear. Manley and O'Neill [11], believed that renal cortex echogenicity can be influenced by the state of diuresis or hydration. Those authors reported that echogenicity is greater in well-hydrated healthy patients. Although we have no proof, we believe, contrary to Manley and O'Neill, that increased renal cortex echogenicity can be explained by a less hydrated state of the patients rather than a more hydrated state. In our study, patients tended to have decreased hydration as a consequence of their acute abdominal illness due to vomiting, diarrhea, and decreased intake. An explanation might be the increase of acoustic interfaces as a consequence of swelling of interstitial renal parenchyma. However, this is not evidence-based. Unfortunately, routine evaluation of blood values in the emergency department includes no electrolyte evaluation or serum creatinine, urea, or liver function parameters. However, serum creatinine was normal in all tested cases. This finding is in accordance with the findings of Kasap et al. [9], who found no significant difference in blood parameters (serum creatinine) in children with a renal cortex echogenicity equal to that of the liver or in those children with renal cortex echogenicity more than that of the liver parenchyma.
A limitation of this study was the subjectivity of the evaluation of the cortical echogenicity. Few reports have stated that densitometric measurement of echogenicity is more reliable than naked eye evaluations [10, 12, 13]. However, in our institute these measurements are not made in regular practice.
Another limitation was that the echogenicity of liver parenchyma was used as an internal standard in determining renal cortex echogenicity. Changes in the liver could influence the ratio of the renal cortex echogenicity in the absence of changes in the structure of the kidney. No studies are available that support a change in liver echotexture in acutely ill children. In a study on hepatic echogenicity, however, Samad et al. [14] detected no statistically significant difference in echogenicity of the liver in children with hepatic dysfunction and children in a control group. We think, therefore, that comparison with liver parenchyma can be used as a reliable method. According to most studies of echogenicity of the renal parenchyma, right kidney echogenicity is best compared with the echogenicity of the adjacent liver [3, 11, 13, 14].
Care should always been taken, however, in interpreting the estimates of renal cortex echogenicity [15]. According to Vehmas and Kaukiainen [16], the optimum method for evaluating renal cortex echogenicity in daily practice remains to be clarified.
This study was limited by lack of a control group. At the outset, we thought that a control group would be redundant because previous studies had already proven that renal cortex echogenicity in normal healthy patients is less than that of the adjacent liver parenchyma [3, 5].
In conclusion, the results of this study show that increased echogenicity of the renal cortex in children with acute abdominal illness is a nonspecific finding and does not necessarily indicate true renal disease. Increased echogenicity of the renal cortex is a transient phenomenon in this clinical setting. Hyperechogenicity of the renal cortex in children with acute abdominal illness should alert the radiologist to search the abdomen more thoroughly for a cause of the acute abdominal illness, such as appendicitis.
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