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Do sodium-glucose cotransporter-2 inhibitors affect renal hemodynamics by different mechanisms in type 1 and type 2
Petter Bjornstad1, Robert G Nelson2, Meda E Pavkov3
1Section of Endocrinology, Department of Pediatrics, Division of Nephrology, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado, USA.
Abstract:
Cardiovascular and renal outcome trials demonstrate nephroprotection with sodium-glucose cotransporter-2 inhibitors in people with type 2 diabetes. Attenuation of hyperfiltration is believed to be responsible for the nephroprotection, and studies in young adults with type 1 diabetes suggest that afferent arteriolar vasoconstriction induced by a tubuloglomerular feedback mechanism may be responsible for this effect. The study by van Bommel et al. suggests that this mechanism may not hold true in older adults with type 2 diabetes, who instead attenuate elevated glomerular filtration rate via post-glomerular vasodilation.
Insights
Sodium-glucose cotransporter-2 inhibitors protect kidneys in type 2 diabetes by reducing hyperfiltration. This effect in older adults may involve post-glomerular vasodilation, differing from mechanisms in younger patients.
Area of Science:
- Nephrology
- Endocrinology
- Pharmacology
Background:
- Sodium-glucose cotransporter-2 inhibitors (SGLT2i) show nephroprotective effects in type 2 diabetes (T2D).
- Hyperfiltration attenuation is a proposed mechanism for SGLT2i-induced nephroprotection.
- In type 1 diabetes, afferent arteriolar vasoconstriction via tubuloglomerular feedback is implicated in young adults.
Purpose of the Study:
- To investigate the mechanism of glomerular filtration rate (GFR) attenuation by SGLT2i in older adults with T2D.
- To determine if the mechanism observed in type 1 diabetes applies to older adults with T2D.
Main Methods:
- The study by van Bommel et al. examined hemodynamic changes in the glomerulus.
- Analysis focused on the role of afferent versus efferent arteriolar tone.
Main Results:
- Older adults with T2D undergoing SGLT2i treatment showed attenuation of elevated GFR.
- This attenuation was achieved through post-glomerular vasodilation, not afferent arteriolar vasoconstriction.
- The findings suggest a different nephroprotective mechanism in this population compared to younger individuals with type 1 diabetes.
Conclusions:
- The mechanism of SGLT2i-mediated nephroprotection in older adults with T2D differs from that observed in younger individuals with type 1 diabetes.
- Post-glomerular vasodilation appears to be the key factor in attenuating hyperfiltration in this specific demographic.
- These findings have implications for understanding and optimizing SGLT2i therapy in diverse patient groups.
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