To assess if intravoxel incoherent motion (IVIM) and diffusion tensor imaging (DTI) can be used to evaluate renal fibrosis in a mouse model of diabetic nephropathy.Thirty-eight male CD1 mice (8 weeks old, 20-30g) formed the population of this study. Streptozotocin induced diabetes was created in twenty mice via a single intraperitoneal injection of streptozotocin at 150 mg/kg², while eighteen mice served as control group. The mice were scanned using a 7T microMRI scanner at 0, 12 and 24 weeks after injection of streptozotocin. Diffusion-weighted images were acquired using a multi-shot spin-echo echo-planar imaging sequence with the following parameters: TR/TE = 3000/41 ms, and b values of 0, 50, 100, 200, 400, 800, 1200 s/mm². DTI images were obtained using 12 diffusion directions and lower b values of 0, 100 and 400 s/mm². Fractional anisotropy (FA) and apparent diffusion coefficient (ADC) of DTI and IVIM parameters (D-tissue diffusivity, D*-blood flow, f-perfusion fraction) were obtained using region of interests drawn over the right renal cortex and medulla. Histopathological analysis of the right kidney was performed in all mice including Sirius Red staining for fibrosis. Results were analysed using an unpaired t-test with P<0.05 considered statistically significant.Renal cortex ADC was significantly higher and FA was significantly lower in the diabetes group at week 12 compared with the control group (P< 0.05). Renal cortex ADC and FA showed the same trends at week 24 with P values approaching significance (P= 0.05 and 0.07 respectively) (Fig. 2(A), (C)). The ADC and FA values of the medulla at 12 and 24 weeks did not show any significant difference (Fig. 2(A), (C)). Renal cortex D was also significantly higher in the diabetes group at week 12 with a trend towards significance at week 24 (Fig. 2(B)). D* was significantly decreased at the renal medulla at 24 weeks. There was no significant change for f. Histopathological analysis confirmed fibrosis in the diabetes group at 24 weeks (Fig. 3).Previous studies on diabetic nephropathy showed that FA was significantly lower in the medulla and cortex of the diabetic kidneys and may be attributed to renal pathologies such as glomerulosclerosis, tubulointerstitial fibrosis, and tubular damage.^1,2 Our study showed decrease in cortical FA in early renal fibrosis in diabetic nephropathy and provides evidence for this hypothesis. Previous studies have also shown that the ADC decreases with development of renal fibrosis.^3,4 In contrary, our study showed that ADC was elevated in the cortex at 12 weeks after induction of diabetes, which was similar to the findings by Hueper et al.¹ It is known that ADC reflects combination of diffusion (D) and perfusion (D*). In our study, D was significantly higher in the cortex of the diabetic group as compared to the control group at 12 weeks. Thus, the elevated ADC may be attributed to an increase in diffusivity. We hypothesize that the increase in diffusivity reflects increased tubule volume within the measured ROI, which are contributed by diabetic animals have a more than 5-fold higher urinary output and hyperfiltration. Hence, those effects far outweigh the effects of fibrosis at 12 weeks, a period of early diabetic nephropathy in which little tubulointerstitial fibrosis exists⁵ and nephromegaly and hyperfiltration predominate, to increase the global amount of diffusivity. At 24 weeks, the effects of the amount of fibrosis is relatively greater, accounting for no significant difference in the ADC when compared with the control group. Our results are also in agreement with those of Sigmund et al.⁶ who attributed the raised ADC in the renal cortex and medulla to increased tubule volume. Although the area of fibrosis stained by Sirius Red in the diabetes group at 12 and 24 weeks is increased, the difference is not statistically significant (Fig. 3). We feel that this reflects early fibrosis in early diabetic nephropathy. This is supported by the significant increase in glomerular volume (Fig. 4) and lack of significantly elevated serum creatinine, which are features seen in early diabetic nephropathy.FA allowed evaluation of the development of renal fibrosis and may be used in the detection and therapy monitoring of early diabetic nephropathy.