SP637PROFILING OSTEOCYTES IN RENAL OSTEODYSTROPHY FOR IDENTIFICATION OF POTENTIAL NEW BIOMAKERS OF CHRONIC KIDNEY DISEASE-INDUCED BONE LESIONS

Introduction and Aims: Renal osteodystrophy (ROD) affects bone remodeling and mineralisation and underlies osteoporosis mechanisms in patients with Chronic Kidney disease (CKD). ROD incudes 4 types of lesions: osteitis fibrosa (OF) adynamic osteopathy (OA) osteomalacia (OM) and mixed uremic lesions (MUO). ROD diagnosis is difficult because biomarkers such as serum Parathormone (PTH) are too weak to predict bone lesions. Osteocytes (ocy) express extracellular matrix SIBLINGS family members, such as DMP-1, MEPE and the peptide ASARM, which all regulate bone mineralisation. Ocy also express sclerostin (SOST), a potent inhibitor of bone formation, whose serum levels increase as CKD worsens. SOST expression is inhibited by PTH and may be linked to ocy apoptosis. In this context, our aim was to characterize ocy protein expression and apoptotic profile in ROD by immunohistochemistry (IHC) as a first step to identify potential new ROD biomarkers. Methods: We selected 48 iliac bone biopsies: 38 from CKD patients including all 4 ROD types defined by histomorphometry data and 10 from non uremic osteoporotic (OP) patients. Sections were decalcified and deplastified and IHC for ocy proteins was performed with anti-SOST, DMP1, MEPE and ASARM Antibodies. Nuclei were stained with DAPI. Quantitative (% of IHC or DAPI-stained ocy lacunae) and qualitative analyses were carried out. DAPI-negative ocy lacunae characterized apoptotic ocy. We counted 500 ocy per biopsy.