<i>N</i>-octanoyl dopamine treatment exerts renoprotective properties in acute kidney injury but not in renal allograft recipients

Klotz, Sarah; Pallavi, Prama; Tsagogiorgas, Charalambos; Zimmer, F.; Zöllner, Frank G.; Binzen, Uta; Greffrath, Wolfgang; Treede, Rolf‐Detlef; Walter, Jakob; Harmsen, Martin C.; Krämer, Bernhard K.; Hafner, Mathias; Yard, Benito A.; Hoeger, Simone

doi:10.1093/ndt/gfv363

Cited by 11 publications

(22 citation statements)

References 41 publications

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“…Recent data show that N‐octanoyl dopamine (NOD) treatment improves warm ischaemia‐induced acute AKI via TRPV1 in Lewis and Sprague Dawley rats, but not Trpv1 −/− Sprague Dawley rats (Klotz et al . ).…”

Section: Transient Receptor Potential Channelsmentioning

confidence: 97%

“…NOD treatment has been found to exert renoprotection through the activation of TRPV1 in AKI in wild‐type (WT) rats but not in animals deficient in TRPV1 ( Trpv1 −/− rats) (Klotz et al . ), with a possible role of TRPV1 channels in dorsal root ganglia (DRG) (Tsagogiorgas et al . ).…”

Section: Transient Receptor Potential Channelsmentioning

confidence: 99%

“…Interestingly, the observed improvement in renal function by NOD was not associated with putatively TRPV1 induced large increases in kidney perfusion as measured by magnetic resonance imaging (Klotz et al . ), which is unexpected as TRPV1 activation is a potent mechanism to produce vasodilation in the renal circulation (Chen et al . ).…”

Section: Transient Receptor Potential Channelsmentioning

confidence: 99%

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Renoprotection: focus on TRPV1, TRPV4, TRPC6 and TRPM2

et al. 2016

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Members of the transient receptor potential (TRP) cation channel receptor family have unique sites of regulatory function in the kidney which enables them to promote regional vasodilatation and controlled Ca influx into podocytes and tubular cells. Activated TRP vanilloid 1 receptor channels (TRPV1) have been found to elicit renoprotection in rodent models of acute kidney injury following ischaemia/reperfusion. Transient receptor potential cation channel, subfamily C, member 6 (TRPC6) in podocytes is involved in chronic proteinuric kidney disease, particularly in focal segmental glomerulosclerosis (FSGS). TRP vanilloid 4 receptor channels (TRPV4) are highly expressed in the kidney, where they induce Ca influx into endothelial and tubular cells. TRP melastatin (TRPM2) non-selective cation channels are expressed in the cytoplasm and intracellular organelles, where their inhibition ameliorates ischaemic renal pathology. Although some of their basic properties have been recently identified, the renovascular role of TRPV1, TRPV4, TRPC6 and TRPM2 channels in disease states such as obesity, hypertension and diabetes is largely unknown. In this review, we discuss recent evidence for TRPV1, TRPV4, TRPC6 and TRPM2 serving as potential targets for acute and chronic renoprotection in chronic vascular and metabolic disease.

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Section: Transient Receptor Potential Channelsmentioning

confidence: 97%

Section: Transient Receptor Potential Channelsmentioning

confidence: 99%

Section: Transient Receptor Potential Channelsmentioning

confidence: 99%

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Renoprotection: focus on TRPV1, TRPV4, TRPC6 and TRPM2

et al. 2016

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“…Functional MRI provides several approaches, 6 such as diffusionweighted imaging, 7 blood oxygen level dependent imaging, 8 arterial spin labelling, [9][10][11] longitudinal and transverse relaxation time measurements, 12,13 dynamic contrast enhanced imaging, 14 hyperpolarized MRS, 15 and sodium MRI, 16 to assess renal function and pathophysiology beside anatomical information. All these MRI-Abbreviations used: AKI, acute kidney injury; ATN, acute tubular necrosis; BUN, blood urea nitrogen; CEST, chemical exchange saturation transfer; KIRI, kidney ischemia reperfusion injury; ROI, region of interest; sCr, serum creatinine based methods may be useful to determine renal pathology by quantification of renal water diffusion, oxygenation, perfusion, tissue water content, and viability.…”

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confidence: 99%

Noninvasive evaluation of renal pH homeostasis after ischemia reperfusion injury by CEST‐MRI

et al. 2017

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Acute kidney injury (AKI) in mice caused by sustained ischemia followed by reperfusion is associated with acute tubular necrosis and renal dysfunctional blood flow. Although the principal role of the kidney is the maintenance of acid-base balance, current imaging approaches are unable to assess this important parameter, and clinical biomarkers are not robust enough in evaluating the severity of kidney damage. Therefore, novel noninvasive imaging approaches are needed to assess the acid-base homeostasis in vivo. This study investigates the usefulness of MRI-chemical exchange saturation transfer (CEST) pH imaging (through iopamidol injection) in characterizing moderate and severe AKI in mice following unilateral ischemia reperfusion injury. Moderate (20 min) and severe (40 min) ischemia were induced in Balb/C mice, which were imaged at several time points thereafter (Days 0, 1, 2, 7). A significant increase of renal pH values was observed as early as one day after the ischemia reperfusion damage for both moderate and severe ischemia. MRI-CEST pH imaging distinguished the evolution of moderate from severe AKI. A recovery of normal renal pH values was observed for moderate AKI, whereas a persisting renal pH increase was observed for severe AKI on Day 7. Renal filtration fraction was significantly lower for clamped kidneys (0.54-0.57) in comparison to contralateral kidneys (0.84-0.86) following impairment of glomerular filtration. The severe AKI group showed a reduced filtration fraction even after 7 days (0.38 for the clamped kidneys). Notably, renal pH values were significantly correlated with the histopathological score. In conclusion, MRI-CEST pH mapping is a valid tool for the noninvasive evaluation of both acid-base balance and renal filtration in patients with ischemia reperfusion injury.

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“…41–43 The BOLD effect allows for a measure of renal tissue oxygen tension which reveals initial and sustained hypoxic conditions in AKI. ASL allows for measurement of regional perfusion within the kidney.…”

Section: Discussionmentioning

confidence: 99%

Quantification of vascular damage in acute kidney injury with fluorine magnetic resonance imaging and spectroscopy

Moore

Chen

Pan

et al. 2017

Magnetic Resonance in Med

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Quantification of ischemia-reperfusion injury after acute kidney injury with fluorine MRI/MR spectroscopy of perfluorocarbon NPs objectively depicts the extent and severity of vascular injury and its linear relationship to renal dysfunction. The lack of kidney function improvement after early posttreatment thrombin inhibition confirms the rapid onset of ischemia-reperfusion injury as a consequence of vascular damage and non-reperfusion. The prolongation of medullary ischemia renders cortico-medullary tubular structures susceptible to continued necrosis despite restoration of large vessel flow, which suggests limitations to acute interventions after acute kidney injury, designed to interdict renal tubular damage. Magn Reson Med 79:3144-3153, 2018. © 2017 International Society for Magnetic Resonance in Medicine.

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N-octanoyl dopamine treatment exerts renoprotective properties in acute kidney injury but not in renal allograft recipients

Abstract: NOD treatment reduces renal injury in warm ischaemia, but is not effective in renal transplant in our experimental animal models. The salutary effect of NOD appears to be TPRV1-dependent, not involving large changes in renal perfusion.

Cited by 11 publications

References 41 publications

Renoprotection: focus on TRPV1, TRPV4, TRPC6 and TRPM2

Renoprotection: focus on TRPV1, TRPV4, TRPC6 and TRPM2

Noninvasive evaluation of renal pH homeostasis after ischemia reperfusion injury by CEST‐MRI

Quantification of vascular damage in acute kidney injury with fluorine magnetic resonance imaging and spectroscopy

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