Abstract

Chronic Kidney Disease (CKD) provokes biochemical and systemic alterations, causing bone fragility with an increase in bone fracture risk, extraskeletal calcifications, increased morbidity, and cardiovascular mortality. The complex pathophysiological mechanism causes a syndrome called CKD-MBD (Chronic Kidney Disease – Mineral and Bone Disorders), which includes mineral and bone alterations leading to renal osteodystrophy (ROD). An early diagnosis is therefore essential to prevent the onset of more severe complications. A precise diagnosis of bone disorders and the subsequent administration of the best therapy is difficult without performing a bone biopsy. However, lately, the diagnostic focus is shifting to a series of molecules, the bone turnover markers (BTM), generated by the same bone tissue during the remodeling process, which is proving to be a useful diagnostic tool in the definition of ROD. BTMs are divided into bone formation molecules (amino-terminal propeptide of type 1 procollagen, P1NP; osteocalcin, OC; bone alkaline phosphatase, bALP) and bone resorption molecules (carboxy-terminal cross-linked telopeptide of type 1 collagen, CTX; isoform 5b tartrate-resistant acid phosphatase, TRAP-5b). There are also biomarkers of bone metabolism such as parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and sclerostin. Although PTH is one of the most used molecules, P1NP, bALP, CTX, and TRAP-5b have proven to be superior in the discrimination of low turnover pathologies. The diagnostic capability of these molecules and their potential still require further studies, but clinicians must include BTMs in the diagnostic process of CKD-MBD.