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• W2019975627 abstract "The clinical detection of evolving acute tubular necrosis (ATN) and differentiating it from other causes of renal failure are currently limited. The maintenance of the corticomedullary sodium gradient, an indicator of normal kidney function, is presumably lost early in the course of ATN. Herein, sodium magnetic resonance imaging (23Na MRI) was applied to study the early alteration in renal sodium distribution in rat kidneys 6 h after the induction of ATN. Three-dimensional gradient echo sodium images were recorded at 4.7 T with high spatial resolution. ATN was produced by the administration of radiologic contrast medium, combined with inhibition of nitric oxide and prostaglandin synthesis. The sodium images revealed that the sham-controlled kidney exhibited a linear increase in sodium concentration along the corticomedullary axis of 30±2 mmol/l/mm, resulting in an inner medulla to cortex sodium ratio of 4.3±0.3 (n=5). In the ATN kidney, however, the cortico-outer medullary sodium gradient was reduced by 21% (P<0.01, n=7) and the inner medulla to cortex sodium ratio was decreased by 40% (P<0.001, n=7). Small, though significant, increments in plasma creatinine at this time inversely correlated with the decline in the corticomedullary sodium gradient. Histological findings demonstrated outer medullary ATN involving 4% of medullary thick ascending limbs. Hence, 23Na MRI non-invasively quantified changes in the corticomedullary sodium gradient in the ATN kidney when morphologic tubular injury was still focal and very limited. MRI detection of corticomedullary sodium gradient abnormalities may serve to identify evolving ATN at its early phases. The clinical detection of evolving acute tubular necrosis (ATN) and differentiating it from other causes of renal failure are currently limited. The maintenance of the corticomedullary sodium gradient, an indicator of normal kidney function, is presumably lost early in the course of ATN. Herein, sodium magnetic resonance imaging (23Na MRI) was applied to study the early alteration in renal sodium distribution in rat kidneys 6 h after the induction of ATN. Three-dimensional gradient echo sodium images were recorded at 4.7 T with high spatial resolution. ATN was produced by the administration of radiologic contrast medium, combined with inhibition of nitric oxide and prostaglandin synthesis. The sodium images revealed that the sham-controlled kidney exhibited a linear increase in sodium concentration along the corticomedullary axis of 30±2 mmol/l/mm, resulting in an inner medulla to cortex sodium ratio of 4.3±0.3 (n=5). In the ATN kidney, however, the cortico-outer medullary sodium gradient was reduced by 21% (P<0.01, n=7) and the inner medulla to cortex sodium ratio was decreased by 40% (P<0.001, n=7). Small, though significant, increments in plasma creatinine at this time inversely correlated with the decline in the corticomedullary sodium gradient. Histological findings demonstrated outer medullary ATN involving 4% of medullary thick ascending limbs. Hence, 23Na MRI non-invasively quantified changes in the corticomedullary sodium gradient in the ATN kidney when morphologic tubular injury was still focal and very limited. MRI detection of corticomedullary sodium gradient abnormalities may serve to identify evolving ATN at its early phases. The maintenance of the corticomedullary sodium gradient is a basic renal function, required for urine concentration. This gradient, produced by the countercurrent system, depends on the active reabsorption of sodium by ion pumps in the medullary thick ascending limb (mTAL), the difference in the permeability characters of the descending and the ascending limbs, and the unique paralleled structure of the nephron segments and vasculature in the medulla.1.Jamison R. Kriz W. Urinary Concentration Mechanism. Oxford University Press, Inc., New York, Oxford1982Google Scholar, 2.Zhang W. Edwards A. Oxygen transport across vasa recta in the renal medulla.Am J Physiol Heart Circ Physiol. 2002; 283: H1042-H1055Crossref PubMed Scopus (38) Google Scholar The outer medulla normally functions at very low oxygen tension, in part due to high oxygen consumption by those ion pumps.3.Brezis M. Rosen S. Hypoxia of the renal medulla – its implications for disease.N Engl J Med. 1995; 332: 647-655Crossref PubMed Scopus (959) Google Scholar This region is, therefore, vulnerable to injury, which plays an important role in the evolution of hypoxic acute tubular necrosis (ATN). Indeed, a declining urinary osmolarity, a hallmark of a disrupted concentrating system, is considered a very early sign of evolving ATN.4.Baek S. Brownm R. Shoemaker W. Early prediction of acute renal pailure and recovery. I. Sequential measurements of free water clearance.Ann Surg. 1973; 177: 253-258Crossref PubMed Scopus (37) Google Scholar, 5.Heimann T. Brau S. Sakurai H. et al.Urinary osmolal changes in renal dysfunction following open-heart operations.Ann Thorac Surg. 1976; 22: 44-49Abstract Full Text PDF PubMed Scopus (13) Google Scholar, 6.Landes R.G. Lillehei R.C. Lindsay W.G. et al.Free-water clearance and the early recognition of acute renal insufficiency after cardiopulmonary bypass.Ann Thorac Surg. 1976; 22: 41-43Abstract Full Text PDF PubMed Scopus (18) Google Scholar, 7.Holper K. Struck E. Sebening F. The diagnosis of acute renal failure (ARF) following cardiac surgery with cardio-pulmonary bypass.Thorac Cardiovasc Surg. 1979; 27: 231-237Crossref PubMed Scopus (9) Google Scholar, 8.Diamond J.R. Yoburn D.C. Nonoliguric acute renal failure associated with a low fractional excretion of sodium.Ann Intern Med. 1982; 96: 597-600Crossref PubMed Scopus (69) Google Scholar Clinical identification of early-stage ATN and its differentiation from other causes of acute renal failure are currently limited. The diagnosis of ATN is often done at an advanced, established phase, beyond the time-point of potential preventive intervention. Therefore, non-invasive real-time detection of the altered corticomedullary sodium gradient could serve for early detection of evolving ATN. Sodium magnetic resonance imaging (23Na MRI) provides the unique ability to directly measure and determine the tissue sodium concentration (TSC) non-invasively.9.Bansal N. Szczepaniak L. Ternullo D. et al.Effect of exercise on (23)Na MRI and relaxation characteristics of the human calf muscle.J Magn Reson Imaging. 2000; 11: 532-538Crossref PubMed Google Scholar, 10.Boada F.E. Christensen J.D. Huang-Hellinger F.R. et al.Quantitative in vivo tissue sodium concentration maps: the effects of biexponential relaxation.Magn Reson Med. 1994; 32: 219-223Crossref PubMed Scopus (59) Google Scholar, 11.Christensen J.D. Barrere B.J. Boada F.E. et al.Quantitative tissue sodium concentration mapping of normal rat brain.Magn Reson Med. 1996; 36: 83-89Crossref PubMed Scopus (77) Google Scholar, 12.Constantinides C.D. Gillen J.S. Boada F.E. et al.Human skeletal muscle: sodium MR imaging and quantification-potential applications in exercise and disease.Radiology. 2000; 216: 559-568Crossref PubMed Scopus (121) Google Scholar, 13.Constantinides C.D. Kraitchman D.L. O’Brien K.O. et al.Noninvasive quantification of total sodium concentrations in acute reperfused myocardial infarction using 23Na MRI.Magn Reson Med. 2001; 46: 1144-1151Crossref PubMed Scopus (62) Google Scholar, 14.Shapiro E.M. Borthakur A. Gougoutas A. et al.23Na MRI accurately measures fixed charge density in articular cartilage.Magn Reson Med. 2002; 47: 284-291Crossref PubMed Scopus (230) Google Scholar, 15.Thulborn K.R. Davis D. Adams H. et al.Quantitative tissue sodium concentration mapping of the growth of focal cerebral tumors with sodium magnetic resonance imaging.Magn Reson Med. 1999; 41: 351-359Crossref PubMed Scopus (106) Google Scholar Early studies showed the ability of 23Na MRI to detect the corticomedullary sodium gradient in exposed kidneys.16.Wolff S.D. Eng C. Balaban R.S. NMR studies of renal phosphate metabolites in vivo: effects of hydration and dehydration.Am J Physiol. 1988; 255: F581-F589PubMed Google Scholar, 17.Wolff S.D. Eng J. Berkowitz B.A. et al.Sodium-23 nuclear magnetic resonance imaging of the rabbit kidney in vivo.Am J Physiol. 1990; 258: F1125-F1131PubMed Google Scholar, 18.Bansal N. Seshan V. Three-dimensional triple quantum-filtered 23Na imaging of rabbit kidney with weighted signal averaging.J Magn Reson Imaging. 1995; 5: 761-767Crossref PubMed Scopus (27) Google Scholar We have recently demonstrated the use of sodium MRI to non-invasively quantify the corticomedullary TSC gradient in the intact rat kidney, and followed its modulation in hydronephrosis.19.Maril N. Margalit R. Mispelter J. et al.Functional sodium magnetic resonance imaging of the intact rat kidney.Kidney Int. 2004; 65: 927-935Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar Moreover, changes in outer medullary sodium content were specific and served to identify functional differences during mannitol- and furosemide-induced diuresis.20.Maril N. Margalit R. Mispelter J. et al.Sodium magnetic resonance imaging of diuresis: spatial and kinetic response.Magn Reson Med. 2005; 53: 545-552Crossref PubMed Scopus (37) Google Scholar We hypothesized that the early evolution of hypoxic ATN may manifest with the development of altered corticomedullary sodium gradient, detected non-invasively by sodium MRI. At 6 h after the insult, plasma creatinine rose to 0.59±0.02 mg/dl (n=7) in the ATN group, as compared with sham-injected control rats (0.38±0.03 mg/dl, P<0005, n=5). Morphologic evaluation revealed limited tubular injury, involving 4.2±1.9% of mTALs in the mid-inner strip (Figure 1), particularly in the mid-interbundle zone, most remote from the vasa recta. The sodium distribution in the kidneys of control rats was similar to that observed previously in normal rat kidneys (n=20).19.Maril N. Margalit R. Mispelter J. et al.Functional sodium magnetic resonance imaging of the intact rat kidney.Kidney Int. 2004; 65: 927-935Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar The images revealed a gradual increase of the sodium signal intensity from the cortex along the corticomedullary axis, reaching its highest value in the inner medulla (Figure 2a). Conversion of the units from signal intensity to concentration yielded a TSC gradient along the corticomedullary axis of 30±2 mmol/l/mm. Renal sodium images, recorded 6 h after inducing ATN, were clearly different from those of the sham-injected rats (Figure 2b). The strongest deviation was observed in the inner medulla, where the TSC declined by 42±6% compared to that in the sham-controlled kidney. Consequently, the inner medulla to cortex sodium ratio was reduced from 4.3±0.3 in sham control to 2.6±0.2 (P<0.001) in ATN kidneys. Analysis at pixel resolution revealed a marked change in the profile of TSC along the corticomedullary axis (Figure 2c and d). In contrast to the linear profile observed in the control kidneys throughout the corticomedullary axis, its contour in the ATN kidneys contained a positive linear slope (average linear correlation factor R=0.96±0.04) from the cortex to the outer medulla, and a negative slope from the outer to the inner medulla. Furthermore, the positive slope decreased significantly (P<0.01) by 21±2% to 23.7±1.5 mmol/l/mm in reference to that in the sham control kidney (30±1 mmol/l/mm). Interestingly, even at this early stage of ATN, the reduction of cortico-outer medullary sodium gradient correlated with the small increments in plasma creatinine (Figure 3; R=0.84). Early detection of evolving ATN and its differentiation from pre-renal causes of kidney dysfunction have major potential implications regarding the patient's management. However, clinically applicable diagnostic tools of ATN are currently insufficient. Functional indicators of urinary concentration and urinary sodium are useful diagnostic tools, but require freshly generated urine, and may be influenced to a great extent by therapeutic interventions. A loss of urinary concentrating capacity is an early indicator of ATN, reflecting altered countercurrent system and urine concentration capacity.4.Baek S. Brownm R. Shoemaker W. Early prediction of acute renal pailure and recovery. I. Sequential measurements of free water clearance.Ann Surg. 1973; 177: 253-258Crossref PubMed Scopus (37) Google Scholar, 5.Heimann T. Brau S. Sakurai H. et al.Urinary osmolal changes in renal dysfunction following open-heart operations.Ann Thorac Surg. 1976; 22: 44-49Abstract Full Text PDF PubMed Scopus (13) Google Scholar, 6.Landes R.G. Lillehei R.C. Lindsay W.G. et al.Free-water clearance and the early recognition of acute renal insufficiency after cardiopulmonary bypass.Ann Thorac Surg. 1976; 22: 41-43Abstract Full Text PDF PubMed Scopus (18) Google Scholar, 7.Holper K. Struck E. Sebening F. The diagnosis of acute renal failure (ARF) following cardiac surgery with cardio-pulmonary bypass.Thorac Cardiovasc Surg. 1979; 27: 231-237Crossref PubMed Scopus (9) Google Scholar, 8.Diamond J.R. Yoburn D.C. Nonoliguric acute renal failure associated with a low fractional excretion of sodium.Ann Intern Med. 1982; 96: 597-600Crossref PubMed Scopus (69) Google Scholar Non-invasive detection of the corticomedullary sodium gradient may, therefore, serve as an early real-time indicator of evolving ATN. Herein we show that the renal sodium MR images revealed a marked change in the corticomedullary sodium signal intensity profile during the early evolution of ATN. In general, the sodium signal intensity is determined by the TSC, as well as by the sodium longitude and transverse relaxation rates. In living tissue, the relaxation mechanisms of sodium are determined by the interaction of the sodium ions with macromolecules.21.Boulanger Y. Vinay P. Nuclear magnetic resonance monitoring of sodium in biological tissues.Can J Physiol Pharmacol. 1989; 67: 820-828Crossref PubMed Scopus (24) Google Scholar These relaxation rates were measured previously in the intact rat kidney and found to be similar in the cortex and the medulla.19.Maril N. Margalit R. Mispelter J. et al.Functional sodium magnetic resonance imaging of the intact rat kidney.Kidney Int. 2004; 65: 927-935Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar Moreover, extreme changes in tissue composition that resulted from diuresis did not affect these rates.20.Maril N. Margalit R. Mispelter J. et al.Sodium magnetic resonance imaging of diuresis: spatial and kinetic response.Magn Reson Med. 2005; 53: 545-552Crossref PubMed Scopus (37) Google Scholar Since the observed histological damage in the ATN kidneys was minimal, it is reasonable to assume that the sodium relaxation rates remained similar to those in the normal kidney. Therefore, the observed changes in the sodium signal intensity in the ATN kidneys with respect to the sham control kidneys reflected the corresponding changes in renal TSC. The sodium images clearly demonstrated the inability of the ATN kidneys to maintain the corticomedullary sodium gradient; the slope of the cortico-outer medullary gradient declined and the inner medulla to cortex sodium ratio decreased. Declining corticomedullary sodium gradient conceivably reflects a functional derangement of the countercurrent system, related to tubular damage or malfunction, and perhaps to evolving regional endothelial dysfunction. The fact that water deprivation did not affect the sodium gradient19.Maril N. Margalit R. Mispelter J. et al.Functional sodium magnetic resonance imaging of the intact rat kidney.Kidney Int. 2004; 65: 927-935Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar illustrates the potential of this technique to distinguish between pre-renal azothemia and ATN. Hypoxic tubular necrosis, in models of distal tubular injury, is very limited initially, but gradually develops over 24 h after insult.22.Heyman S.N. Brezis M. Epstein F.H. et al.Early renal medullary hypoxic injury from radiocontrast and indomethacin.Kidney Int. 1991; 40: 632-642Abstract Full Text PDF PubMed Scopus (272) Google Scholar Indeed, only 4% of mTALs in the mid-inner stripe were necrotic by 6 h, the time the MRI study was performed. However, apoptotic cells and tubules with mild, potentially reversible features of morphologic hypoxic tubular injury were previously shown to transiently coexist at that stage,22.Heyman S.N. Brezis M. Epstein F.H. et al.Early renal medullary hypoxic injury from radiocontrast and indomethacin.Kidney Int. 1991; 40: 632-642Abstract Full Text PDF PubMed Scopus (272) Google Scholar, 23.Beeri R. Symon Z. Brezis M. et al.Rapid DNA fragmentation from hypoxia along the thick ascending limb of rat kidneys.Kidney Int. 1995; 47: 1806-1810Abstract Full Text PDF PubMed Scopus (126) Google Scholar and presumably contribute to the impaired regional concentrating capacity. A widespread expression of hypoxia-inducible factors both in tubular segments and in endothelial cells in the renal medulla illustrates the extent of regional hypoxic stress produced in this model.24.Rosenberger C. Heyman S.N. Rosen S. et al.Up-regulation of HIF in experimental acute renal failure: evidence for a protective transcriptional response to hypoxia.Kidney Int. 2005; 67: 531-542Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar Furthermore, the loop diuretic furosemide inhibits the mTAL sodium transporter and consequently abolishes outer medullary hypoxic injury.25.Heyman S.N. Brezis M. Greenfeld Z. et al.Protective role of furosemide and saline in radiocontrast-induced acute renal failure in the rat.Am J Kidney Dis. 1989; 14: 377-385Abstract Full Text PDF PubMed Scopus (86) Google Scholar We have previously shown that indeed the cortico-outer medullary sodium gradient almost disappears in the presence of furosemide,20.Maril N. Margalit R. Mispelter J. et al.Sodium magnetic resonance imaging of diuresis: spatial and kinetic response.Magn Reson Med. 2005; 53: 545-552Crossref PubMed Scopus (37) Google Scholar whereas no change in this gradient is observed in mannitol-induced diuresis, where mTAL pumps maintain their function. Thus, a direct coupling exists between tubular transport dysfunction, induced by either hypoxic insults or by transport inhibition, and a reduction in the cortico-outer medullary sodium gradient. Collectively, our sodium MRI studies indicate that altered cortico-outer medullary sodium gradient selectively represents a malfunctioning countercurrent system, whereas a reduction in the inner medullary sodium is non-specific.19.Maril N. Margalit R. Mispelter J. et al.Functional sodium magnetic resonance imaging of the intact rat kidney.Kidney Int. 2004; 65: 927-935Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar, 20.Maril N. Margalit R. Mispelter J. et al.Sodium magnetic resonance imaging of diuresis: spatial and kinetic response.Magn Reson Med. 2005; 53: 545-552Crossref PubMed Scopus (37) Google Scholar The observed reduction in the inner medulla sodium in ATN probably reflects regional structural damage, also quite prevalent in this model,24.Rosenberger C. Heyman S.N. Rosen S. et al.Up-regulation of HIF in experimental acute renal failure: evidence for a protective transcriptional response to hypoxia.Kidney Int. 2005; 67: 531-542Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar, 23.Beeri R. Symon Z. Brezis M. et al.Rapid DNA fragmentation from hypoxia along the thick ascending limb of rat kidneys.Kidney Int. 1995; 47: 1806-1810Abstract Full Text PDF PubMed Scopus (126) Google Scholar and in the hydronephrotic kidney.19.Maril N. Margalit R. Mispelter J. et al.Functional sodium magnetic resonance imaging of the intact rat kidney.Kidney Int. 2004; 65: 927-935Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar A similar pattern of flattened inner medullary sodium gradient is also seen following diuretics,20.Maril N. Margalit R. Mispelter J. et al.Sodium magnetic resonance imaging of diuresis: spatial and kinetic response.Magn Reson Med. 2005; 53: 545-552Crossref PubMed Scopus (37) Google Scholar presumably representing the washout of papillary sodium content. In summary, we have demonstrated the ability of 23Na MRI to quantify changes in the corticomedullary sodium gradient at early stages of ATN when morphologic tubular injury is still focal and very limited. This noninvasive technique may enable the detection of evolving ATN in the setup of acute renal failure, and to differentiate it from the pre-renal phase, where tubular function is well maintained. The study was performed on female 2–4-months-old Lewis rats (250–300 g), and was approved and conducted in accordance with the guidelines of the Institutional Committee on Animals of the Weizmann Institute of Science. Medullary hypoxic ATN was induced by the administration of the radiocontrast sodium iothalamate (Angio-Conray 80%, Mallinckrodt, St Louis, MO, USA; 6 ml/kg intraarterial) following the inhibition of prostaglandin synthesis with indomethacin (Sigma Chemical Co., St Louis, MO, USA; 2 mg/kg, intravenous) and of nitric oxide synthesis with Nω-nitro-L-arginine methyl ester (Sigma Chemical Co., St Louis, MO, USA; 1 mg/kg, intravenous), as described previously.26.Agmon Y. Peleg H. Greenfeld Z. et al.Nitric oxide and prostanoids protect the renal outer medulla from radiocontrast toxicity in the rat.J Clin Invest. 1994; 94: 1069-1075Crossref PubMed Scopus (304) Google Scholar Outer medullary hypoxic stress and tubular damage have been documented early after the induction of ATN in similar24.Rosenberger C. Heyman S.N. Rosen S. et al.Up-regulation of HIF in experimental acute renal failure: evidence for a protective transcriptional response to hypoxia.Kidney Int. 2005; 67: 531-542Abstract Full Text Full Text PDF PubMed Scopus (140) Google Scholar and comparable experimental setups.22.Heyman S.N. Brezis M. Epstein F.H. et al.Early renal medullary hypoxic injury from radiocontrast and indomethacin.Kidney Int. 1991; 40: 632-642Abstract Full Text PDF PubMed Scopus (272) Google Scholar Rats were anesthetized by exposure to 1% isoflurane (Medeva Pharmaceuticals, Inc., Rochester, NY, USA), in an O2/N2O (3:7) mixture, applied through a nose cone. In seven rats (ATN group) indomethacin, Nω-nitro-L-arginine methyl ester and sodium iothalamate were sequentially injected at 15-min intervals through the rat-tail veins and artery. Five additional animals injected with vehicles served as sham controls. After 6 h MR images were recorded, as described below. Subsequently, plasma samples were obtained for the determination of creatinine. In seven different rats, the kidneys were perfusion-fixed 6 h after the insult and processed for morphologic assessment, as detailed elsewhere.22.Heyman S.N. Brezis M. Epstein F.H. et al.Early renal medullary hypoxic injury from radiocontrast and indomethacin.Kidney Int. 1991; 40: 632-642Abstract Full Text PDF PubMed Scopus (272) Google Scholar, 23.Beeri R. Symon Z. Brezis M. et al.Rapid DNA fragmentation from hypoxia along the thick ascending limb of rat kidneys.Kidney Int. 1995; 47: 1806-1810Abstract Full Text PDF PubMed Scopus (126) Google Scholar, 27.Heyman S.N. Brezis M. Reubinoff C.A. et al.Acute renal failure with selective medullary injury in the rat.J Clin Invest. 1988; 82: 401-412Crossref PubMed Scopus (225) Google Scholar The study was performed on a 4.7-T Biospec spectrometer (Bruker, Rheinstetten, Germany) using a home-built 3 cm 1H/23Na double-tuned surface coil. The rats were anesthetized by sodium pentobarbital (0.04 mg/g, intraperitoneal), and were placed on the coil in a supine position. The location of the kidney along the axial axis was chosen by carefully positioning the height of the rat, to avoid dislocation of the center of the kidney in the sodium image due to the small number of axial sampling points (n=16). This was achieved by localizing the exact position of the kidney center using axial 3D 1H gradient echo images acquired at high resolution,19.Maril N. Margalit R. Mispelter J. et al.Functional sodium magnetic resonance imaging of the intact rat kidney.Kidney Int. 2004; 65: 927-935Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar and then setting the height of the medulla from the magnet center to be an integer (between 0 to 3) times the slice thickness. After this fine positioning of the rat, an oblique coronal–sagittal field of view (FOV) was assigned for the sodium image so that the angle of the oblique plane was equal to that of the corticomedullary axis. The 3D 23Na gradient echo image was then recorded, using a 90° sine/cosine adiabatic pulse,28.Ugurbil K. Garwood M. Rath A. Optimization of modulation functions to improve insensitivity of adiabatic pulses to variation in B1 magnitude.J Magn Reson. 1988; 80: 448-469Google Scholar a echo-time/repetition-time (TE/TR) of 1.7/60 ms, FOV 12 × 12 × 5–8 cm3, and a matrix of 128 × 128 × 16 with 10 scans (20 min). The conversion of the relative signal intensity units to TSC units was based on sodium imaging of a reference saline solution, taking into account the sodium relaxation rates in the reference solution and in the rat kidney, measured previously,19.Maril N. Margalit R. Mispelter J. et al.Functional sodium magnetic resonance imaging of the intact rat kidney.Kidney Int. 2004; 65: 927-935Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar and correcting for coil sensitivity.20.Maril N. Margalit R. Mispelter J. et al.Sodium magnetic resonance imaging of diuresis: spatial and kinetic response.Magn Reson Med. 2005; 53: 545-552Crossref PubMed Scopus (37) Google Scholar In order to define the exact boundaries of the kidney regions (cortex, outer and inner medulla) in the sodium image, an oblique 3D 1H MR image was also acquired with the same FOV and spatial resolution as that of the sodium image.19.Maril N. Margalit R. Mispelter J. et al.Functional sodium magnetic resonance imaging of the intact rat kidney.Kidney Int. 2004; 65: 927-935Abstract Full Text Full Text PDF PubMed Scopus (47) Google Scholar Results are presented as the mean±s.e.m. Two-tailed unpaired Student's t-test was used for the comparison of control and ATN kidney and linear regression fitting was applied to assess MRI and functional correlations. This work was supported by the Israel Science Foundation (801/04) and by the estate of Julie Osler. H Degani is the incumbent of the Fred and Andrea Fallek Professorial Chair in Breast Cancer Research." @default.
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• W2019975627 title "Detection of evolving acute tubular necrosis with renal 23Na MRI: Studies in rats" @default.
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