The glomerular filtration barrier (GFB) has three main cellular components: fenestrated endothelial cells; basement membrane; and podocyte foot processes. In health the GFB is highly permeable to water and small solutes but almost entirely impermeable to proteins. Vascular endothelial growth factor A (VEGF-A) is produced by podocytes. Tight regulation of VEGF-A expression is critical for the establishment and maintenance of the GFB¹, and glomerular VEGF expression is disrupted in many glomerular diseases². Differential splicing of the VEGF-A gene forms two families of isoforms: the pro-angiogenic family (VEGF-A_xxx), and the anti-angiogenic families (VEGF-A_xxxb). VEGF-A₁₆₅ contributes to the high permeability of glomeruli to water³. We sought to determine the effects of VEGF-A₁₆₅b on glomerular permeability by examining permeability coefficients in glomeruli harvested from transgenic mice with podocyte specific heterozygosity (^+/-) for VEGF-A₁₆₅b. The water permeability of isolated mouse glomeruli (normalised ultrafiltration co-efficient: L_pA/V_i) was assessed using a previously described oncometric technique³. L_pA/V_i is calculated from the rate of change of glomerular volume after introduction of an oncotic pressure gradient of known magnitude. VEGF-A₁₆₅b over-expression reduced glomerular L_pA/V_i as compared with wild-type littermate controls (VEGF-A₁₆₅b^+/-: 1.44±0.11, n=18; controls: 1.93± 0.16, n=8; unpaired t-test: p=0.017). We have modified this methodology to estimate the reflection co-efficient to albumin (σ_alb)⁴. The volume of a glomerulus incubated in dextran solution, expressed as a fraction of the volume of the same glomerulus when incubated in an iso-oncotic solution of albumin, describes σ_alb. Compared with wild-type littermate controls, there was no significant difference in the σ_alb in glomeruli harvested from VEGF-A₁₆₅b^+/- mice (VEGF-A₁₆₅b^+/-: 0.975±0.011, n=9; controls: 0.998± 0.02, n=11; unpaired t-test p=0.32). These results suggest that a higher concentration of podocyte VEGF-A₁₆₅b does not reduce the ability of the barrier to retain macromolecules. Altering the balance of VEGF-A_xxx and VEGF-A_xxxb in disease states may be of therapeutic interest.