Worldwide chronic kidney disease (CKD) is a fast-growing public health and socioeconomic problem1,2. It is a multifaceted disease often coinciding with cardiovascular pathology and metabolic disorders and recognized as a cardiovascular risk factor1. Degradation of the endothelial glycocalyx (glx) is associated with CKD and disease progression. A final pathological progression of CKD is renal fibrosis which arises from glx damage and dysfunction3. Although many studies have demonstrated glx destruction in several pathological conditions4, 5 a link between glx integrity and kidney function needs to be established in relation to CKD. The aim of the study was to assess the renal hemodynamics and oxygen homeostasis with and without the glx barrier. The hypothesis is the renal function and oxygen consumption will be altered. Male Wistar Rats (250-350g, n=3) were anaesthetised with Isoflurane (inhaled, 2.5%), cannulas were placed in the left femoral artery for blood pressure (BP) and in the vein for saline/FITC-inulin infusion for glomerular filtration rate (GFR) measurements; the left ureter was cannulated for left kidney urine collection. The glx removal was accomplished by venous infusion of an enzyme bolus mix (chondroitinase 0.087mU/g and hyaluronidase 15mU/g, a final volume of 200 µl in saline (0.9%)) 30 minutes before the experimental period. Blood and urine samples were collected before and after the enzyme mix bolus infusion. Spike2 Software was used to record BP, renal blood flow (RBF, Doppler flow probe placed around the left renal artery) and heart rate (HR). Renal oxygen consumption (QO2) was calculated from the arterio-venous difference in oxygen content and the oxygen delivery rate was obtained using the product of arterial oxygen content and RBF. Comparisons before and after enzyme mix bolus was performed using paired ttest. Values are means and ± S.E.M. Glycocalyx destruction did not seem to affect BP (95.0±1.7 vs 87.1±4.1 mmHg, p>0.05), HR (313.4±22.2 vs 301.7±21.2 bpm, p>0.05), RBF (4.5±0.3 vs 5.5±0.9 ml/min, p>0.05), oxygen delivery rate (89.7±5.4 vs. 102.9±16.5 mmol/ml/min, p>0.05) and left kidney GFR (0.5±0.1 vs 0.7±0.1 ml/min, p>0.05). However, QO2 (6.3±0.7 vs 16.1±4.1 mmol/min, p>0.05) was numerical higher for each animal before and after enzyme mix bolus, although not significantly (P=0.x). These preliminary data demonstrate that we have an experimental model in which we can quantify basic kidney physiology, i.e. renal hemodynamics and oxygen consumption. Although further experiments are needed (and currently ongoing) to elucidate the link between glx degradation and renal function the data is suggesting that glx destruction could increase renal oxygen consumption and hence alters oxygen homeostasis in healthy kidneys.