Kidney Week

Abstract: TH-PO334

Sodium Magnetic Resonance Imaging Shows Impairment of the Counter-Current Multiplication System in the Diabetic Model Mice Kidney

Session Information

• Fluid, Electrolyte, and Acid-Base Disorders: Basic
  November 03, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
  Abstract Time: 10:00 AM - 12:00 PM

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

• 1001 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Basic

Authors

• Nakagawa, Yusuke, Niigata University, Niigata, Japan

Yusuke Nakagawa,

• Kaseda, Ryohei, Niigata University, Niigata, Japan

Ryohei Kaseda,

• Suzuki, Yuya, Niigata University, Niigata, Japan

Yuya Suzuki,

• Terada, Yasuhiko, Tsukuba University, Tsukuba, Japan

Yasuhiko Terada,

• Haishi, Tomoyuki, International University of Health and Welfare, Narita, Japan

Tomoyuki Haishi,

• Sasaki, Susumu, Niigata University, Niigata, Japan

Susumu Sasaki,

• Narita, Ichiei, Niigata University, Niigata, Japan

Ichiei Narita,

Background

Sodium Magnetic Resonance Imaging (²³Na-MRI) is a technique for imaging ²³Na. It is possible to non-invasively assess sodium distributions, especially sodium concentration in the counter-current multiplication system in the kidney, which forms a sodium concentration gradient from the cortex to the medulla, enabling efficient water reabsorption. Although knowledge regarding the mechanisms of sodium reabsorption through channels or transporters has been accumulated, the distribution of the sodium concentration in the entire kidney has not been delineated in kidney diseases. Applying ²³Na-MRI to disease model mice may expand the scope of prior studies and elucidate the pathogenesis of sodium gradient impairments. We investigated whether ²³Na-MRI can detect changes in sodium concentrations under normal conditions in mice and in disease models such as a mouse model with diabetes mellitus.

Methods

²³Na-MRI was performed with a 9.4T vertical standard-bore super-conducting magnet using C57BL/6JJcl administrated of furosemide (10 mg/kg BW), BKS.Cg-Lepr^db+/+ Lepr^db/Jcl (db/db) mice and its corresponding control BKS.Cg-m+/m+/Jcl (m+/m+) mice. The sodium gradient of the kidney between the cortex and medulla was compared.

Results

The corticomedullary sodium gradient of the kidney significantly decreased 20 min after administration of furosemide, an NKCC2 inhibitor involved in the formation of the counter-current multiplication system (pre-1.53±0.16, post-2.19±0.3, P<0.05, N=7). The signal intensity of the medullary region in the kidney was lower in db/db mice (db/db 209.6±42.4 mmol/L, m+/m+ 333.5±54.4 mmol/L, P<0.01, N=7 each) and the corticomedullary sodium gradient of db/db mice was significantly decreased compared to m+/m+ mice (db/db 1.64±0.36, m+m+ 2.28±0.21, P<0.01).

Conclusion

²³Na-MRI revealed reductions in the corticomedullary sodium gradients and impairment in the counter-current multiplication system in db/db mice at very early stages of diabetes mellitus. ²³Na-MRI may be useful for diagnosing diabetic kidney disease and elucidating the pathogenesis of sodium gradient impairments.

Funding

• Government Support – Non-U.S.