Beyond hemoglobin: Critical role of 2,3‐bisphosphoglycerate mutase in kidney function and injury
2025

The Role of BPGM in Kidney Function and Injury

Sample size: 32 publication 10 minutes Evidence: high

Author Information

Author(s): Vera A. Kulow, Kameliya Roegner, Robert Labes, Mumtaz Kasim, Susanne Mathia, Claudia S. Czopek, Nikolaus Berndt, Philipp N. Becker, Gohar Ter‐Avetisyan, Friedrich C. Luft, Philipp Enghard, Christian Hinze, Jan Klocke, Kai‐Uwe Eckardt, Kai M. Schmidt‐Ott, Pontus B. Persson, Christian Rosenberger, Michael Fähling

Primary Institution: Charité—Universitätsmedizin Berlin

Hypothesis

We hypothesized that kidney BPGM could be renoprotective by balancing glucose metabolism and preventing ROS formation.

Conclusion

BPGM is crucial for maintaining glucose metabolism in the distal nephron, and its absence leads to metabolic imbalances and kidney injury.

Supporting Evidence

  • BPGM expression was localized to the distal nephron and was absent in proximal tubules.
  • Inducible knockout of Bpgm resulted in rapid kidney injury within 4 days.
  • Proteomic analyses revealed involvement of BPGM in key metabolic pathways, including glycolysis and oxidative stress response.
  • Bpgm knockdown led to enhanced glycolysis and increased apoptosis under osmotic stress.

Takeaway

BPGM helps keep our kidneys healthy by managing sugar levels, and without it, the kidneys can get hurt.

Methodology

The study used a tubular-specific, doxycycline-inducible Bpgm-knockout mouse model and various analyses including histological, immunofluorescence, and proteomic methods.

Potential Biases

Potential bias in the interpretation of results due to the specific model used and the focus on certain pathways.

Limitations

The study primarily focused on a specific mouse model, which may not fully represent human kidney function.

Participant Demographics

The study involved murine models and urine samples from 32 AKI patients.

Statistical Information

P-Value

p<0.05

Statistical Significance

p<0.05

Digital Object Identifier (DOI)

10.1111/apha.14242

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