Early monitoring of acute tubular necrosis in the rat kidney by 23Na-MRI

Bharath K. Atthe, Andriy M. Babsky, Paige N. Hopewell, Carrie Phillips, Bruce Molitoris, Navin Bansal

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Reabsorption of water and other molecules is dependent on the corticomedullary sodium concentration gradient in the kidney. During the early course of acute tubular necrosis (ATN), this gradient is altered. Therefore, 23Na magnetic resonance imaging (MRI) was used to study the alterations in renal sodium distribution in the rat kidney during ischemia and reperfusion (IR) injury, which induces ATN. In-magnet ischemia was induced for 0 (control), 10, 20, 30 or 50 min in Wistar rats. 23Na images were collected every 10 min during baseline, ischemia, and 60-min reperfusion periods. T1 and T2 relaxation times were measured by both 23Na-MRI and -MRS on a separate cohort of animals during ischemia and reperfusion for correction of relaxation-related tissue sodium concentration (TSC). A marked decrease was observed in the medulla and cortex 23Na-MRI signal intensity (SI) during the early evolution of ATN caused by IR injury, with the sodium reabsorption function of the kidney being irreversibly damaged after 50 min of ischemia. Sodium relaxation time characteristics were similar in the medulla and cortex of normal kidney, but significantly decreased with IR. The changes in relaxation times in both compartments were identical; thus the medulla-to-cortex sodium SI ratio represents the TSC ratio of both compartments. The extent of IR damage observed with histological examination correlated with the 23Na-MRI data. 23Na-MRI has great potential for noninvasive, clinical diagnosis of evolving ATN in the setup of acute renal failure and in differentiating ATN from other causes of renal failure where tubular function is maintained.

Original languageEnglish
JournalAmerican Journal of Physiology - Renal Physiology
Volume297
Issue number5
DOIs
StatePublished - Nov 2009

Fingerprint

Necrosis
Sodium
Magnetic Resonance Imaging
Ischemia
Kidney
Reperfusion Injury
Reperfusion
Kidney Cortex
Magnets
Acute Kidney Injury
Renal Insufficiency
Wistar Rats
Water

Keywords

  • Ischemia-reperfusion injury
  • Relaxation times
  • Sodium concentration
  • Tissue

ASJC Scopus subject areas

  • Physiology
  • Urology

Cite this

Early monitoring of acute tubular necrosis in the rat kidney by 23Na-MRI. / Atthe, Bharath K.; Babsky, Andriy M.; Hopewell, Paige N.; Phillips, Carrie; Molitoris, Bruce; Bansal, Navin.

In: American Journal of Physiology - Renal Physiology, Vol. 297, No. 5, 11.2009.

Research output: Contribution to journalArticle

Atthe, Bharath K. ; Babsky, Andriy M. ; Hopewell, Paige N. ; Phillips, Carrie ; Molitoris, Bruce ; Bansal, Navin. / Early monitoring of acute tubular necrosis in the rat kidney by 23Na-MRI. In: American Journal of Physiology - Renal Physiology. 2009 ; Vol. 297, No. 5.
@article{2f1283bf83104fd9954b375fbabece4a,
title = "Early monitoring of acute tubular necrosis in the rat kidney by 23Na-MRI",
abstract = "Reabsorption of water and other molecules is dependent on the corticomedullary sodium concentration gradient in the kidney. During the early course of acute tubular necrosis (ATN), this gradient is altered. Therefore, 23Na magnetic resonance imaging (MRI) was used to study the alterations in renal sodium distribution in the rat kidney during ischemia and reperfusion (IR) injury, which induces ATN. In-magnet ischemia was induced for 0 (control), 10, 20, 30 or 50 min in Wistar rats. 23Na images were collected every 10 min during baseline, ischemia, and 60-min reperfusion periods. T1 and T2 relaxation times were measured by both 23Na-MRI and -MRS on a separate cohort of animals during ischemia and reperfusion for correction of relaxation-related tissue sodium concentration (TSC). A marked decrease was observed in the medulla and cortex 23Na-MRI signal intensity (SI) during the early evolution of ATN caused by IR injury, with the sodium reabsorption function of the kidney being irreversibly damaged after 50 min of ischemia. Sodium relaxation time characteristics were similar in the medulla and cortex of normal kidney, but significantly decreased with IR. The changes in relaxation times in both compartments were identical; thus the medulla-to-cortex sodium SI ratio represents the TSC ratio of both compartments. The extent of IR damage observed with histological examination correlated with the 23Na-MRI data. 23Na-MRI has great potential for noninvasive, clinical diagnosis of evolving ATN in the setup of acute renal failure and in differentiating ATN from other causes of renal failure where tubular function is maintained.",
keywords = "Ischemia-reperfusion injury, Relaxation times, Sodium concentration, Tissue",
author = "Atthe, {Bharath K.} and Babsky, {Andriy M.} and Hopewell, {Paige N.} and Carrie Phillips and Bruce Molitoris and Navin Bansal",
year = "2009",
month = "11",
doi = "10.1152/ajprenal.00388.2009",
language = "English",
volume = "297",
journal = "American Journal of Physiology",
issn = "0193-1857",
publisher = "American Physiological Society",
number = "5",

}

TY - JOUR

T1 - Early monitoring of acute tubular necrosis in the rat kidney by 23Na-MRI

AU - Atthe, Bharath K.

AU - Babsky, Andriy M.

AU - Hopewell, Paige N.

AU - Phillips, Carrie

AU - Molitoris, Bruce

AU - Bansal, Navin

PY - 2009/11

Y1 - 2009/11

N2 - Reabsorption of water and other molecules is dependent on the corticomedullary sodium concentration gradient in the kidney. During the early course of acute tubular necrosis (ATN), this gradient is altered. Therefore, 23Na magnetic resonance imaging (MRI) was used to study the alterations in renal sodium distribution in the rat kidney during ischemia and reperfusion (IR) injury, which induces ATN. In-magnet ischemia was induced for 0 (control), 10, 20, 30 or 50 min in Wistar rats. 23Na images were collected every 10 min during baseline, ischemia, and 60-min reperfusion periods. T1 and T2 relaxation times were measured by both 23Na-MRI and -MRS on a separate cohort of animals during ischemia and reperfusion for correction of relaxation-related tissue sodium concentration (TSC). A marked decrease was observed in the medulla and cortex 23Na-MRI signal intensity (SI) during the early evolution of ATN caused by IR injury, with the sodium reabsorption function of the kidney being irreversibly damaged after 50 min of ischemia. Sodium relaxation time characteristics were similar in the medulla and cortex of normal kidney, but significantly decreased with IR. The changes in relaxation times in both compartments were identical; thus the medulla-to-cortex sodium SI ratio represents the TSC ratio of both compartments. The extent of IR damage observed with histological examination correlated with the 23Na-MRI data. 23Na-MRI has great potential for noninvasive, clinical diagnosis of evolving ATN in the setup of acute renal failure and in differentiating ATN from other causes of renal failure where tubular function is maintained.

AB - Reabsorption of water and other molecules is dependent on the corticomedullary sodium concentration gradient in the kidney. During the early course of acute tubular necrosis (ATN), this gradient is altered. Therefore, 23Na magnetic resonance imaging (MRI) was used to study the alterations in renal sodium distribution in the rat kidney during ischemia and reperfusion (IR) injury, which induces ATN. In-magnet ischemia was induced for 0 (control), 10, 20, 30 or 50 min in Wistar rats. 23Na images were collected every 10 min during baseline, ischemia, and 60-min reperfusion periods. T1 and T2 relaxation times were measured by both 23Na-MRI and -MRS on a separate cohort of animals during ischemia and reperfusion for correction of relaxation-related tissue sodium concentration (TSC). A marked decrease was observed in the medulla and cortex 23Na-MRI signal intensity (SI) during the early evolution of ATN caused by IR injury, with the sodium reabsorption function of the kidney being irreversibly damaged after 50 min of ischemia. Sodium relaxation time characteristics were similar in the medulla and cortex of normal kidney, but significantly decreased with IR. The changes in relaxation times in both compartments were identical; thus the medulla-to-cortex sodium SI ratio represents the TSC ratio of both compartments. The extent of IR damage observed with histological examination correlated with the 23Na-MRI data. 23Na-MRI has great potential for noninvasive, clinical diagnosis of evolving ATN in the setup of acute renal failure and in differentiating ATN from other causes of renal failure where tubular function is maintained.

KW - Ischemia-reperfusion injury

KW - Relaxation times

KW - Sodium concentration

KW - Tissue

UR - http://www.scopus.com/inward/record.url?scp=70350708144&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=70350708144&partnerID=8YFLogxK

U2 - 10.1152/ajprenal.00388.2009

DO - 10.1152/ajprenal.00388.2009

M3 - Article

C2 - 19726545

AN - SCOPUS:70350708144

VL - 297

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0193-1857

IS - 5

ER -