While glomerular HS may participate in the glomerular barrier to fluid and protein (e.g., heparanase may contribute to the proteinuria characteristic of chronic kidney diseases) (Szymczak et al. 2010; Salmon and Satchell 2012), the relevance of this barrier function to septic AKI is uncertain, as we found no evidence of endothelial hyperpermeability (no change in kidney wet/dry ratio, urine protein/creatinine ratio, or kidney EBD-albumin extravasation) 4 h after CLP (Fig. 3). This evidence concerns the gene ALB and chronic kidney disease.