|
|
|
| Evaluation of early renal injury development in diabetic rats using BOLD MRI |
| GUO Chuan-gen1, ZHANG Lan2, WANG Qi-dong1, WANG Zhao-ming1, XU Ying1, XIAO Wen-bo1 |
1. The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China;
2. The Fourth Affiliated Hospital, School of Medicine, Zhejiang University, Yiwu Zhejiang 322000, China |
|
|
|
|
Abstract Objective: To observe changes in renal oxygenation levels using BOLD MRI, and to evaluate the usefulness of BOLD MRI in development of early diabetic renal injury. Methods: A total of 62 diabetic rats with successful modeling were used as the experimental group(DN group, n=62), and 10 normal rats served as the normal control group(NC group, n=10). The NC group was used as the baseline for the BOLD MRI scan, and the rats in the DN group underwent MR imaging at 3, 7, 14, 21, 28, 35, 42, 49, 56, 63, and 70 days after modeling. Renal cortical and medullary R2*(CR2*, MR2*) values were measured and R2* ratio between medulla and cortex(MCR) was calculated. The urine albumin concentration and histopathological examination(GSI, Vvmes, Svcap) were evaluated at different time points. Results: CR2* and MR2* values of DN group were significantly higher than those of NC group. Those R2* values raised gradually and reached the peak at 35 days(CR2*=(33.95±0.34) s-1, MR2*=(43.79±1.46) s-1, then dropped gradually at 70 days(CR2*=(33.17±0.69) s-1, MR2*=(41.61±0.95) s-1), MCR in DN group gradually increased to the peak of 1.32 at 42 days and then decreased to 1.25 at 70 days. UAE of DN group increased gradually, it was significantly higher than that of NC group at 7 days(P<0.01). The GSI and Vvmes and Svcap were higher in DN group compared to NC group(P<0.01). Conclusions: BOLD MRI can noninvasively evaluate the renal hypoxia in diabetes and detect diabetic renal injury earlier than UAE. The dynamic changes of MCR in our study may suggest that renal injury may be from functional hypertonic compensation into organic lesions such as mesangial proliferation and glomerulosclerosis.
|
|
Received: 11 July 2017
|
|
|
|
|
|
[1]Miyata T, Takizawa S, van Ypersele de Strihou C. Hypoxia. 1. Intracellular sensors for oxygen and oxidative stress: novel therapeutic targets[J]. Am J Physiol Cell Physiol, 2011, 300(2): C226-231.
[2]Ogawa S, Lee TM, Kay AR, et al． Brain magnetic resonance imaging with contrast dependent on blood oxygenation[J]． Proc Natl Acad Sci USA, 1990, 87(24): 9868-9872．
[3]Thulbom KR, Watertom JC, Matitiews PM, et al． Oxygenation dependence of the transverse relaxation time of water protons in whole blood at thish field[J]． Bioehim Biophys Acta, 1982, 714(2): 265-270．
[4]Ries M, Basseau F, Tyndal B, et al. Renal diffusion and BOLD MRI in experimental diabetic nephropathy[J]. J Magn Reson Imaging, 2003, 17(1): 104-113.
[5]Dos Santos EA, Li LP, Ji L, et al. Early changes with diabetes in renal medullary hemodynamics as evaluated by fiberoptic probes and BOLD magnetic resonance imaging[J]. Invest Radiol, 2007, 42(3): 157-162.
[6]Yin WJ, Liu F, Li XM, et al. Noninvasive evaluation of renal oxygenation in diabetic nephropathy by BOLD-MRI[J]. Eur J Radiol, 2012, 81(7): 1426-1431.
[7]Inoue T, Kozawa E, Okada H, et al． Noninvasive evaluation of kidney hypoxia and fibrosis using magnetic resonance imaging[J]. J Am Soc Nephrol, 2011, 22(8): 1429-1434.
[8]Zhen JZ, Kumar R, Banerjee S, et al． Blood Oxygen Level-Dependent(BOLD) MRI of Diabetic Nephropathy: Preliminary Experience[J]. J Magn Reson Imaging, 2011, 33(3): 655-660.
[9]Lopes GS, Lemos CCS, Mandarim-De-Lacerda CA, et al. Effect of unilateral nephrectomy on renal function of diabetic rats[J]. Histol Histopathol, 2004, 19(4): 1085-1088.
[10]Szkudelski T. The mechanism of alloxan and streptozotocin action in B cells of the rat pancreas[J]. Physiol Res, 2001, 50(6): 537-546.
[11]Alhaider AA, Korashy HM, Sayed-Ahmed MM, et al. Metformin attenuates streptozotocin-induced diabetic nephropathy in rats through modulation of oxidative stress genes expression[J]. Chem Biol Interact, 2011, 192(3): 233-242.
[12]Pottumarthi VP, Robert RE, Franklin HE. Noninvasive Evaluation of Intrarenal Oxygenation With BOLD MRI[J]. Circulation, 1996, 94(12): 3271-3275.
[13]Thoeny HC, Zumstein D, Simon-Zoula S, et al. Functional Evaluation of Transplanted Kidneys with Diffusion-weighted and BOLD MR Imaging: Initial Experience[J]. Radiology, 2006, 241(3): 812-821.
[14]Pedersen M, Dissing TH, Morkenborg J, et al. Validation of quantitative BOLD MRI measurements in kidney: application to unilateral ureteral obstruction[J]. Kidney Int, 2005, 67(6): 2305-2312.
[15]Baines A, Ho P. Glucose stimulates O2 consumption, NOS, and Na/H exchange in diabetic rat proximal tubules[J]. Am J Physiol Renal Physiol, 2002, 283(2): F286-293.
[16]Palm F, Teerlink T, Hansell P. Nitric oxide and kidney oxygenation[J]. Curr Opin Nephrol Hypertens, 2009, 18(1): 68-73.
[17]Mogensen CE, Schmitz A, Christensen CK． Comparativei renal pathysiology relevant to IDDM and NIDDM patients[J]． Diabetes Meatball Rev, 1988, 4(5): 453-483.
[18]Yan SF, Ramasamy R, Schmidt AM. Receptor for AGE(RAGE)and its ligandscast into leading roles in diabetes and the inflammatory response[J]. J Mol Med(Berl), 2009, 87(3): 235-247.
[19]Ehlermann P, Eggers K, Bierhaus A, et al. Increased proinflammatory endothelial response to S100A8/A9 after preactivation through advanced glycation end products[J]. Cardiovascular Diabetology, 2006, 5: 6.
[20]Li LP, Li BS, Storey P, et al. Effect of free radical scavenger (tempol) on intrarenal oxygenation in hypertensive rats as evaluated by BOLD MRI[J]. J Magn Reson Imaging, 2005, 21(3): 245-248. |
|
|
|
