Renal angiomyolipoma (AML) is a relatively rare renal cortical neoplasm that has been identified in less than 0.2% of the general population. AMLs are composed of smooth muscle cells, dysmorphic blood vessels, and fatty tissue with a known benign nature. AML is usually asymptomatic and is often managed with active surveillance protocols (1). AMLs account for 24% of spontaneous renal hematomas and sudden-onset flank pain is the most common symptom (2). Conditions for intervention are suspicion of malignancy, size greater than 4 cm, spontaneous hemorrhage, and pain (3).

The classical appearance of an AML on a CT scan is a predominantly fatty inhomogeneous mass with varying amounts of tissue density interspersed within it. The fat seen in this lesion is similar in appearance to subcutaneous or retroperitoneal fat (4). On a CT, fat is characterized by its negative number of Hounsfield units (HUs). A tissue attenuation of -10 HU is typically a reliable indicator of fat. A well-circumscribed renal mass with intratumoral fat on CT scan is similar to the diagnostic finding of renal angiomyolipoma (5).

Currently, positron emission tomography (PET) forms part of the routine assessment of malignant diseases. The vast majority of PET scans are performed with fluorine-18 fluoro-2-deoxy-D-glucose (FDG), an analogue of glucose. Many cancers correlate with their metabolic activities, as indicated by the degree of FDG accumulation on PET imaging (6).

Angiomyolipoma is the most common benign tumor of the kidney (5). However, literature describing the FDG PET or PET/CT findings on renal AML is limited. This study reports FDG PET and PET/CT findings of 21 cases of renal AML.

Between January 2006 and December 2010, 473 patients were diagnosed with typical AMLs on CT scan with active surveillance for 6 months in our hospital. Researchers retrospectively extracted clinical and radiographic data from the complete medical records. Twenty-one cases had received FDG PET or PET/CT imaging for other oncologic surveys; these formed the basis of this study. The time gap between the diagnostic CT and the FDG PET (or PET/CT) was within one month. This study was approved by the hospital ethics committee (DMR-99-IRB-010-2).

Table 1 shows the profile of the renal AML patients, tumor size on CT scan, and SUV_max of tumor on FDG PET and PET/CT. Of the 21 patients, 15 were women and 6 were men. The mean age of the patients was 57.14 ± 9.67 years. The mean diameter of 21 renal AMLs on CT scan was 1.76 ± 1.00 cm. The minimum tumor diameter on CT scans was 0.6 cm and maximum diameter was 4.4 cm. The mean SUV_max was 1.25 ± 0.34. None of the 21 AML showed SUV_max greater than 1.98 (Figs. 1, 2). Generally, FDG uptake (expressed as SUV_max > 2.5) is interpreted as being "positive" or PET-avid. No positive FDG PET or PET/CT imaging was found in the renal AML of our study. There was no statistically significant correlation between SUV_max and tumor size (B = 0.045, p = 0.85).

Renal angiomyolipoma is a fairly common benign renal tumor that is often found incidentally. Renal AML is composed of mature adipose tissue, smooth muscle and blood vessels. AML is not always located in the kidney, but may also be found in the liver, spleen, uterus, and tubes (7).

Literature on the role of FDG PET or PET/CT in the diagnosis AMLs is limited. Lhommel et al. (8) reported a case where a liver AML did not have increased FDG uptake but had increased C11 acetate uptake. Ho et al. (9) reported increased C11 acetate uptake but no abnormal FDG uptake in a renal AML. Arnold and Myers (10) documented renal AML as metabolically active on FDG PET and falsely positive for renal cell carcinoma (RCC).

Diagnosis of renal AMLs relies on demonstrating macroscopic fat within a lesion on a CT scan. Some studies report that renal AML may be distinguished from RCC on images by identifying macroscopic fat (11). Davenport et al. reported that a threshold of -10 HU or lower enables accurate differentiation of renal AML from RCC on non-enhanced phase (12). Although demonstrable fat on a CT scan is highly suggestive of an AML, with differential diagnosis of a fat-containing tumor in the kidney, the possibility that it may be an RCC, lipoma, liposarcoma, and Wilms tumor needs to be considered. The most important differential is that of an RCC (5). The mean SUV_max value of pathologic confirmed primary RCC in Namura et al. (13) was 10.62 (range, 5.2 - 16.6), which was much higher than the SUV_max of renal AML in our study (mean, 1.25; range, 0.81 - 1.98).

Renal cell carcinoma accounts for 3.5% of all adult malignancies and 25% of patients with RCC will not survive (14). Bachor et al. (15) reported that the true positive rate of solid renal masses with confirmed RCC on PET is 77%. A pathologic confirmed RCC case with high SUV_max is shown in Figure 3. Kang et al. (16) found that on clinical use of PET in detection of RCC, FDG PET exhibited a sensitivity of 60% and specificity of 100% for primary RCC. Aide et al. (17) reported that high false negative rates of diagnosis of RCC on FDG PET resulted in a sensitivity, specificity, and accuracy of 47%, 80%, and 51%, respectively. A false negative case of pathologic confirmed RCC is shown in Figure 4. One meta-analysis study suggested that FDG PET can be useful in detecting recurrent or metastatic RCC, with 85.7% accuracy (18). The significant variability in the uptake of FDG by RCC is partly due to the excretion of FDG via the urinary tract.

Determinants of FDG accumulation include tumor blood flow, glucose transport, and glycolytic rate. All renal AMLs in this study demonstrated very low to low uptake on FDG PET and PET/CT imaging, suggesting that these tumors were not FDG-avid. AMLs are known to be hyper-vascular with an associated risk of spontaneous hemorrhage; however, there was no significant correlation between tumor size and SUV_max in this study. Neither tumor size nor blood flow explains the relative paucity of FDG activity in renal AML. Studies report glycolytic enzyme expression to be under the influence of mammalian target of rapamycin (mTRO), and that treatment with rapamycin suppressed the rate of glycolysis (19). Jiang et al. (20) reported that mammalian rapamycin complex (mTROC1) is insufficient for increased glycolysis in tumors and that constitutive mTROC1 activity with negatively regulated glucose transporter trafficking. Their in vivo data indicated that constitutive activation of mTORC1 negatively regulates hexose transporter trafficking and glucose uptake. Their study's 3 renal AML cases confirm the relevance of their findings in humans (20). The minimal FDG uptake in 21 renal AML patients in the present study may be explained by mTROC1 activity with negatively regulated glucose transporter trafficking and resulting in a reduction in glucose uptake in our 21 renal AMLs.