Renal diffusion and BOLD MRI in experimental diabetic nephropathy

Ries, Mario; Basseau, F; Tyndal, Benoît; Jones, Richard A.; Déminière, C.; Catargi, Bogdan; Combe, Christian; Moonen, C.; Grenier, N.

doi:10.1002/jmri.10224

Cited by 209 publications

(196 citation statements)

References 36 publications

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“…It is also important to point out that the inner medulla on the map is relatively dark even though it has been shown previously based on microelectrode measurements that the tissue pO 2 may be the lowest in this region. 15,45 This has been a consistent finding to date, 20,21,23,26,27 and we do not yet know the exact cause. It might result from high fluid content in inner medulla.…”

Section: Discussionmentioning

confidence: 58%

“…These are consistent with recent reports. 15,27 Diabetes was induced by a single dose of STZ, which causes hyperglycemia by destroying the β cells in the pancreas 38,39 and is widely used as an experimental model of type I diabetes in different species, such as cats, rats, and mice. Although potential nondiabetic effects of STZ cannot be completely ruled out, other studies have shown that type 1 diabetes is the predominant feature of rats treated with STZ at the dose used in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…Data from the literature reveal that hyperfiltration phenomenon can be seen as early as 2 days after induction of diabetes. 50 Ries et al 27 suggested that changes in medullary oxygenation observed by BOLD MRI at 5 days post induction were related to hyperfiltration.…”

Section: Discussionmentioning

confidence: 99%

“…Blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) has been shown to be very useful in monitoring intrarenal oxygenation. [16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31][32] A major advantage of the noninvasive BOLD MRI is the ability to perform similar measurement in humans.…”

mentioning

confidence: 99%

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Early Changes With Diabetes in Renal Medullary Hemodynamics as Evaluated by Fiberoptic Probes and BOLD Magnetic Resonance Imaging

Santos

et al. 2007

Investigative Radiology

114

107

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Objective-We sought to evaluate the influence of streptozotocin (STZ)-induced diabetes on renal outer medullary pO 2 and blood flow by invasive microprobes and to demonstrate feasibility that blood oxygenation level-dependent (BOLD) magnetic resonance imaging (MRI) can monitor these changes.Materials and Methods-A total of 60 Wistar-Furth rats were used. Diabetes was induced by STZ in 48. Animals were divided into OxyLite group (n = 30) and BOLD MRI groups (n = 30) each with a 5 subgroups of 6 animals: control and 2, 5, 14, and 28 days after induction of diabetes. Outer renal medullary oxygen tension and blood flow were measured by the combined OxyLite/OxyFlo probes. Results-BothOxyLite and BOLD MRI showed a significant increase in the renal hypoxia levels after STZ at all time points. However, no changes were observed in the outer renal medullary oxygen tension and blood flow between diabetic and control groups.Conclusions-These preliminary results suggest that hypoxic changes can be detected as early as 2 days in rat kidneys with diabetes by BOLD MRI and that these early changes are not dependent on blood flow.

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Section: Discussionmentioning

confidence: 58%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Early Changes With Diabetes in Renal Medullary Hemodynamics as Evaluated by Fiberoptic Probes and BOLD Magnetic Resonance Imaging

Santos

et al. 2007

Investigative Radiology

114

107

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“…Chronic hypoxia of the diabetic kidney was demonstrated by pimonidazole [33], measurement with a microelectrode [34], and blood-oxygen level-dependent magnetic resonance imaging [35]. We established the hypoxia-sensing transgenic rats expressing the HRE-driven luciferase vector tagged with FLAG.…”

Section: Chronic Kidney Diseasementioning

confidence: 99%

Hypoxia and the HIF system in kidney disease

2007

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The kidney is sensitive to changes in oxygen delivery. This sensitivity has the merit of facilitating the kidneys in their adjustment of erythropoietin (EPO) production to changes in oxygen supply. The main determinant of EPO synthesis is the transcriptional activity of its gene in kidneys, which is related to local oxygen tensions. Regulation of EPO production is mediated by hypoxia-inducible factor (HIF). When local oxygen tension decreases, accumulated HIF binds to the key sequence of the EPO gene, the hypoxia-responsive element (HRE), and activates transcription of EPO. HIF consists of a constitutive β-subunit and one of alternative oxygen-regulated HIF α-subunits (HIF-1α, HIF-2α, and HIF-3α), and HIF-2α is responsible for erythropoietin production. However, the high sensitivity to changes in oxygen tension also makes the kidney prone to hypoxic injury. Severe energy depletion and subsequent activation of a number of critical alterations in metabolism occurs under hypoxic conditions. Hypoxia is also a profibrogenic stimulus. In addition to ischemic acute renal failure, hypoxia can also play a crucial role in the development of nephrotoxic acute kidney injury, radiocontrast nephropathy, and acute glomerulonephritis. Furthermore, accumulating evidence suggests that chronic hypoxia is a final common pathway to end-stage kidney failure in chronic kidney disease. Given that renal hypoxia has pivotal roles on the development and progression of both acute and chronic kidney disease, hypoxia can be a valid therapeutic target for chronic kidney disease. Activation of HIF leads to expression of a variety of adaptive genes in a coordinated manner. Studies utilizing HIF-stimulating agents proved efficacy in various kidney disease models, suggesting that HIF activation is an ideal target of future therapeutic approaches.

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Pathophysiology of the Diabetic Kidney

Vallon

Komers

2011

Comprehensive Physiology

206

162

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Diabetes mellitus contributes greatly to morbidity, mortality, and overall health care costs. In major part, these outcomes derive from the high incidence of progressive kidney dysfunction in patients with diabetes making diabetic nephropathy a leading cause of end-stage renal disease. A better understanding of the molecular mechanism involved and of the early dysfunctions observed in the diabetic kidney may permit the development of new strategies to prevent diabetic nephropathy. Here we review the pathophysiological changes that occur in the kidney in response to hyperglycemia, including the cellular responses to high glucose and the responses in vascular, glomerular, podocyte, and tubular function. The molecular basis, characteristics, and consequences of the unique growth phenotypes observed in the diabetic kidney, including glomerular structures and tubular segments, are outlined. We delineate mechanisms of early diabetic glomerular hyperfiltration including primary vascular events as well as the primary role of tubular growth, hyperreabsorption, and tubuloglomerular communication as part of a “tubulocentric” concept of early diabetic kidney function. The latter also explains the “salt paradox” of the diabetic kidney, that is, a unique and inverse relationship between glomerular filtration rate and dietary salt intake. The mechanisms and consequences of the intrarenal activation of the renin-angiotensin system and of diabetes-induced tubular glycogen accumulation are discussed. Moreover, we aim to link the changes that occur early in the diabetic kidney including the growth phenotype, oxidative stress, hypoxia, and formation of advanced glycation end products to mechanisms involved in progressive kidney disease.

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Renal diffusion and BOLD MRI in experimental diabetic nephropathy

Cited by 209 publications

References 36 publications

Early Changes With Diabetes in Renal Medullary Hemodynamics as Evaluated by Fiberoptic Probes and BOLD Magnetic Resonance Imaging

Early Changes With Diabetes in Renal Medullary Hemodynamics as Evaluated by Fiberoptic Probes and BOLD Magnetic Resonance Imaging

Hypoxia and the HIF system in kidney disease

Pathophysiology of the Diabetic Kidney

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