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Compensatory glomerular growth after unilateral nephrectomy is VEGF dependent
Allan Flyvbjerg1, Bieke F Schrijvers, An S De Vriese
1Medical Department M, Medical Research Laboratories, Institute of Experimental Clinical Research, Aarhus University, DK-8000 Aarhus, Denmark. allan.fyvbjerg@dadlnet.dk
Summary
Compensatory kidney growth after uninephrectomy (kidney removal) is dependent on vascular endothelial growth factor (VEGF). Blocking VEGF abolished glomerular enlargement and partially inhibited kidney hypertrophy, demonstrating VEGF
Area of Science:
- Nephrology
- Renal Physiology
- Molecular Biology
Background:
- Kidney enlargement involves various growth factors and cytokines.
- Vascular Endothelial Growth Factor (VEGF) is crucial for renal development and diabetic glomerular enlargement.
- Insulin-like Growth Factor I (IGF-I) is implicated in compensatory renal growth, with VEGF potentially mediating its effects.
Purpose of the Study:
- To investigate the role of VEGF in compensatory renal changes following uninephrectomy.
- To assess the impact of a neutralizing VEGF-antibody (VEGF-Ab) on glomerular volume and kidney weight.
- To examine the relationship between VEGF, IGF-I, and compensatory renal growth.
Main Methods:
- Uninephrectomized mice were treated with either a neutralizing VEGF-antibody (VEGF-Ab) or a placebo for 7 days.
- Kidney weight and glomerular volume were measured.
- Serum and kidney levels of Insulin-like Growth Factor I (IGF-I) were quantified.
Main Results:
- Placebo-treated mice showed increased kidney IGF-I, glomerular volume, and kidney weight post-uninephrectomy.
- VEGF-Ab treatment abolished increased glomerular volume and partially blocked renal hypertrophy.
- The renal effects of VEGF-Ab were observed without altering renal IGF-I levels.
Conclusions:
- Compensatory glomerular growth after uninephrectomy is dependent on VEGF.
- VEGF plays a significant role in renal hypertrophy following kidney removal.
- The compensatory renal growth mediated by VEGF occurs independently of changes in renal IGF-I levels.