British Journal of Radiology (2007) 80, e287-e289
© 2007 British Institute of Radiology
doi: 10.1259/bjr/86054374
Replacement lipomatosis: CT and MRI findings of a rare renal mass
M Kocaoglu, MD
U Bozlar, MD
H T Sanal, MD
and
I Guvenc, MD
Gulhane Military Medical School, Department of Radiology, Ankara, Turkey
Correspondence: Murat Kocaoglu, MD, Gulhane Military Medical School, Department of Radiology, 06018 Etlik, Ankara, Turkey. E-mail: kocaoglumurat{at}yahoo.com; kocaoglumurat{at}gata.edu.tr
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Abstract
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Replacement lipomatosis of the kidney (RLK) is an advanced form of renal sinus lipomatosis, in which infection, renal calculi and long-standing hydronephrosis are accompanied by renal parenchymal atrophy. The kidneys are usually poor or non-functioning. We present CT and MRI findings of an unusual focal RLK of a 52-year-old male, who was examined with the suspicion of renal malignancy.
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Introduction
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Replacement lipomatosis of the kidney (RLK) is a rare disorder in which a massive fatty tissue proliferation occurs within the renal sinus, hilum and perirenal region [1–4]. This condition, also referred to as replacement fibrolipomatosis, is the extreme form of renal sinus lipomatosis and generally occurs unilaterally [5, 6]. RLK is the result of significant atrophy of the renal parenchyma and fatty proliferation, which is usually accompanied by renal stone disease and inflammatory changes in about 70% of cases [3, 6]. Frequently, renal function is poor or the kidney is non-functioning. RLK can simulate renal malignancies; therefore, its differential diagnosis is important. Imaging methods including intravenous urography (IVU), ultrasonography, CT and MRI have been used to describe this entity. We present contrast-enhanced CT, as well as MRI with MR urography, findings of a patient with RLK.
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Case report
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A 52-year-old man was evaluated who had left flank pain and haematuria. A urine sample confirmed haematuria without urinary tract infection. His other clinical and laboratory findings were unremarkable.
An abdominal ultrasonograph obtained at an outside hospital showed a lobulated and hyperechoic solid renal mass with pelvicaliceal and proximal ureteral dilatation. Contrast-enhanced CT was performed to document the left kidney and the perirenal area, with the suspicion of renal neoplasia. CT confirmed the presence of a left renal mass occupying the renal hilum and extending to the perirenal space with loss of renal parenchyma. CT also demonstrated a left proximal ureteral stone associated with caliceal and proximal ureteral dilatation and delayed intravenous contrast excretion. Density measurement of several regions within the mass revealed values between –77 Hounsfield units (HU) and –102 HU, implicating fat predominance (Figure 1
). RLK was suspected, and therefore MRI with MR urography sequences were performed to demonstrate renal function, which would be important in the management of the disease.
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Figure 1. Axial excretory phase contrast-enhanced CT scan at level of renal hilum demonstrates a fat density mass, paranchymal atrophy and non-functioning of the left kidney.
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MRI was performed with a 1.5 Tesla superconducting MR scanner (The New lntera Nova; Philips Medical Systems, Best, The Netherlands). A non-contrast axial T1 weighted fast field echo (FFE) (repetition time (TR), 195 ms; echo time (TE), 4.6 ms; flip angle (FA), 80°) sequence with and without fat saturation and coronal T2 weighted turbo spin echo sequences (TR, 1600 ms; TE, 100 ms) were obtained. Later, intravenous (iv) gadopentetic acid (Gd-DTPA)-enhanced sequences at a dose of 0.1 mmol kg–1 using three-dimensional (3D) T1 weighted FFE sequences (TR, 4.0 ms; TE, 1.2 ms; FA, 40°) were performed. The post-contrast sequence was repeated 30 s, 1 min, 3 min, 5 min, 10 min and 30 min after iv contrast injection. With a maximum intensity projection technique, 3D urogram-like images were obtained. MR scans demonstrated a left hilum mass with fat signal intensity, traversing the kidney and extending to the left pararenal space. In addition, MRI revealed delayed renal function on the left side (Figure 2). Based on these imaging findings, the diagnosis of focal RLK was reached. After the passage of the stone down the distal ureter, it was cleared by ureteroscopy. On 12 month follow-up with ultrasonography, no change in the dimensions of the renal mass was seen. In addition, renal function was seen to be preserved on IVU.
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Figure 2. An axialT1 weighted fast field echo scan (a) without and (b) with fat saturation. (c) Axial T2 weighted turbo spin echo images confirm the fatty origin of the left renal mass, and renal parenchymal atrophy. Mild caliceal dilatation and stretching were also noted.
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Discussion
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There is a varying amount of fat within the renal sinus that covers major branches of the renal artery and vein along with the major and minor calices of the collecting system. The amount of fat in the renal sinus, hilum and perirenal region normally increases with both age and obesity, with a preserved volume of renal parenchymal tissue [7, 8]. Increased proliferation of the sinus adipose tissue and renal sinus lipomatosis exerts a mass effect on the intrarenal collecting structures; however, it infrequently produces symptoms because of the absence of caliceal obstruction [7, 8]. RLK is an aggressive variety of renal sinus lipomatosis that develops secondary to chronic obstructive renal stone disease with inflammation and renal parenchymal atrophy. These continuum fatty changes can be confused with neoplasms and sometimes cause diagnostic challenges on imaging. Two theories have been proposed in the pathogenesis of RLK. Some suggest a compensation mechanism in which proliferated fatty tissue occupies the space that is produced by the atrophied or destroyed kidney (it is noteworthy that this proliferated adipose tissue does not infiltrate the parenchyma). Occasionally, the huge amount of fat seen in replacement lipomatosis gives the impression of overcompensation, owing to loss of renal tissue. Therefore, others suggest that the inflammatory induction of fatty proliferation compensates renal tissue loss [4].
Different imaging methods including IVU, ultrasonography, CT and MRI have been used for cases of RLK. Abdominal radiography may reveal calculi, whereas IVU can demonstrate a poorly or non-functioning kidney with stretched infundibula. Ultrasonography may suggest the diagnosis of RLK by demonstrating parenchymal atrophy or a hyperechoic renal sinus mass with a stone; however, it cannot depict confidently the perirenal changes. CT appears to be an accurate method for demonstrating the different features of RLK, i.e. parenchymal atrophy, calculi and the characteristic distribution of adipose mass within the renal sinus and perirenal space, with negative attenuation values similar to those of adipose tissue that help to make a differential diagnosis. As a relatively new, multiplanar and non-irradiating method, MRI with new and fast sequences allows us to illustrate all of the urinary tract, even with non-dilated ureters [9]. MRI can suppress the fat homogeneously and provides useful information to aid in the differential diagnosis between fatty tumors arising in, or adjacent to, the kidneys. Additionally, MRI provides IVU-like images.
Xanthogranulomatous pyelonephritis and fat-containing neoplasms including lipoma, liposarcoma and angiomyolipoma should be considered in the differential diagnosis of RLK. Xanthogranulomatous pyelonephritis is a chronic renal inflammation condition associated with stone obstruction, in which lipid-laden macrophages infiltrate the renal parenchyma; however, in RLK, fat cells remain outside the renal parenchyma [1]. CT examination reveals the presence of renal stone, hydronephrosis/pyonephrosis and the atrophied parenchyma with parenchymal round low densities consistent with abscesses. Because of the accompanying pyonephrosis and abscesses, this condition has attenuation values between –15 HU and +15 HU. Xanthogranulomatous pyelonephritis and RLK can also coexist [10]. The key distinct features of angiomyolipoma are the existence of areas of fat attenuation within the tumour, a varying amount of iv contrast-enhancing soft tissue and possible saccular aneurysms. Conversely, fat-containing neoplasms are usually located intrarenally and/or extrarenally outside the renal sinus. They usually cause a mass effect on the intrarenal collecting system. Renal liposarcoma is usually located peripherally, between the kidney and the renal capsule, and therefore does not cause a defect in the renal parenchyma; as a result, the interface of the lesion with the kidney is smooth. A liposarcoma originating within the renal sinus fat would splay the parenchyma and a parenchymal defect is not seen. Lipoma found within the parenchyma is distinct from that seen with RLK. In RLK, excessive adipose tissue in the renal sinus and hilum extends to the intrarenal and extrarenal areas [1]. Additionally, absence of renal parenchymal atrophy, preserved function of the kidney and absence of a stone in those neoplasms help to make a differential diagnosis [1, 10].
Histopathological proof was lacking in our case. Apart from the unusual focal nature of the present case, the imaging findings and the lack of change after 12 months' follow-up helped us to reach diagnosis. This is an unusual case in that there was no history of chronic calculi. However, this patient was evaluated following acute flank pain and there was no history of renal calculi or infection. Because of the unusual focal nature of the replacement lipomatosis, we postulated that a chronic caliceal calculus may have caused focal fatty proliferation and that the patient came to our attention following the passage of the stone down to the ureter.
In conclusion, the important aspects of this case are: (1) RLK is a relatively uncommon disorder; (2) RLK may be confused with renal neoplasms that need differential diagnosis; and (3) RLK is usually associated with a poorly or non-functioning kidney and needs contrast-enhanced study with CT or MRI. Multiplanar MRI with MR urography sequences is a helpful diagnostic tool in the assessment of renal function and demonstration of the disease extension.
Received for publication June 16, 2006.
Revision received August 15, 2006.
Accepted for publication August 24, 2006.
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Abstract
Introduction
