INTRODUCTION AND AIMS: Low-protein diet is recommended to slow down chronic kidney disease progression because each protein load leads to a detrimental glomerular hyperfiltration. All protein preparations used to demonstrate protein-mediated renal hemodynamic effects were rich in Advanced Glycation End Products (AGE). The aim of our study was to evaluate if the AGE content of a protein load is responsible for the protein-induced renal hyperfiltration.

METHODS: Ten healthy subjects were assigned to a high-protein (1g/kg) low-AGE (3.000 kU AGE) versus high-AGE (30.000 kU AGE) meal, during imaging sessions performed at two different days. Renal perfusion assessed by PET using [15O]H2O, renal oxidative metabolism measured by PET using 11C labeled acetate, and oxygen content using BOLD-MRI, were measured before and 120- minutes after each meal.

RESULTS: Renal perfusion increased significantly (3.16 ± 0.55 vs 3.80 ± 0.42 mL/min/g (p=0.0002)) after the high-AGE meal whereas it was not modified after the low-AGE meal (3.35±0.65 vs 3.38±0.53 ml/min/g, p=0.88) (Figure 1). Oxidative metabolism increased significantly after the high-AGE meal (0.3 ± 0.04 vs 0.36 ± 0.08 min-1, p=0.005) compared to the low-AGE meal (0.30 ± 0.02 vs 0.31 ± 0.06 min-1, p=0.76) for both cortices (Figure 2). We did not find any difference in oxygen content between the two diets.

CONCLUSIONS: Our results demonstrate that this is not the high protein content of a meal that increases renal perfusion and oxidative metabolism but its high-AGE content. Therefore, this study suggests that prevention of CKD progression should aim predominantly at reducing food AGE content.

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