Cossettini Althea, Re Sartò Giulia Vanessa, Aghi Andrea, Gallieni Maurizio, Cosmai Laura, Tripepi Giovanni, Plebani Mario, Giannini Sandro, Simioni Paolo, Stella Stefania, Arcidiacono Gaetano Paride, Marino Carmela, Fusaro Maria
Scuola di Specializzazione in Nefrologia, Università degli Studi di Milano, Milano, Italia.
UOC Nefrologia e Dialisi, Azienda Socio-Sanitaria Territoriale (ASST) Fatebenefratelli-Sacco, Ospedale Fatebenefratelli, Milano, Italia.
G Ital Nefrol. 2024 Oct 9;41(Suppl 83):2024-S83.
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.
慢性肾脏病(CKD)会引发生化和全身改变,导致骨脆性增加,骨折风险升高,出现骨外钙化、发病率增加以及心血管死亡率上升。这种复杂的病理生理机制会引发一种名为CKD-MBD(慢性肾脏病 - 矿物质和骨异常)的综合征,其中包括导致肾性骨营养不良(ROD)的矿物质和骨改变。因此,早期诊断对于预防更严重并发症的发生至关重要。如果不进行骨活检,很难对骨疾病进行准确诊断并随后给予最佳治疗。然而,最近诊断重点正转向一系列分子,即骨转换标志物(BTM),它们是在重塑过程中由同一骨组织产生的,事实证明这是在定义ROD方面有用的诊断工具。BTM分为骨形成分子(I型前胶原氨基端前肽,P1NP;骨钙素,OC;骨碱性磷酸酶,bALP)和骨吸收分子(I型胶原羧基端交联端肽,CTX;5b型抗酒石酸酸性磷酸酶异构体,TRAP-5b)。还有骨代谢生物标志物,如甲状旁腺激素(PTH)、成纤维细胞生长因子23(FGF23)和硬化蛋白。尽管PTH是最常用的分子之一,但P1NP、bALP、CTX和TRAP-5b在区分低转换病变方面已被证明更具优势。这些分子的诊断能力及其潜力仍需要进一步研究,但临床医生必须将BTM纳入CKD-MBD的诊断过程中。