No research has previously been conducted on the application of PET/CT in detecting radiation-induced kidney damage (RIKD).
18F-FDG is a structural analogue of 2-deoxyglucose and so is likely to be enriched in tissues upon a high glucose consumption. Activated inflammatory cells also show increased expression of glucose transporters, resulting in
18F-FDG accumulation [
13]. In our study, comparing PET values pre- and post-radiation exposure, the results showed that PET/CT, can be used as a diagnosis imaging method to detect RIKD in Tibet minipigs. In addition, the results of
18F-FDG PET/CT were consistent with other test results (especially the results of BUN concentrations). Further research is now needed to determine whether this method can be applied to humans, since in humans FDG accumulates to a significant degree in the urinary systems including the renal pelvis due to rapid urine excretion, and the anatomic structure of kidneys of Tibet minipigs is not totally identical to that of humans. Our findings also highlighted that the SUVs may be related to dosages and observed time intervals. Generally, uptake of
18F-FDG depends upon glucose transporters expressed in the cell membrane, the local cell density, and the metabolic activity of the surrounding tissue [
14]. Histological microscopy observations from earlier studies have shown that tubules are more susceptible to radiation than glomerular tissue [
15], and concentrative glucose transporters have been identified in the apical domain of the proximal tubules of the kidney. On the other hand, sugars molecules are mainly metabolized in the proximal tubules. Therefore, the uptake of
18F-FDG may be dependent on glucose transporters expressed in the proximal tubules. Moreover, activated inflammatory cells in renal interstitium increase the expression of glucose transporters resulting in
18F-FDG accumulation [
13]. The results were possibly caused by the increase of activated inflammatory cells in renal tubule and collecting duct. The expression levels of IL-10 and TNF-α protein were positively correlated with radiation doses up to 8 Gy.
The mechanism of radiation damage on the kidney has not yet been clarified. Compared with other structural elements of the kidney, some authors consider that tubules are the most susceptible to radiation [
8], whereas others hold a different opinion [
9]. Our findings are based on a single large dose of radiation and are consistent with the previous results. The proximal convoluted tubules showed degenerative changes in the cytoplasm that were visible under a light microscope as early as 6 h after 11 Gy irradiation. Damage evident in the 8 Gy groups under an electron microscope included chromatin condensation and aggregation, dilatation of the mitochondria, numerous lysosomal structures, lipid droplets and fusion of foot processes. These changes are similar to those occurred in case of mild nephrosis, except that the glomerular tissue showed no obvious damage. Over the past few decades the lowest dose needed to cause kidney damage has been fiercely debated by researchers. Sarin et al. reported that the tolerance dose of whole kidneys after TBI is 14 Gy in humans [
16], whereas, Safwat et al. stated that 11 Gy is the lowest dose to cause kidneys damage in a mouse model [
17]. Our findings showed that the lowest dose to cause damage visible under microscopy is between 8 and 11 Gy in the Tibet minipig model.