CKD-MBD KDIGO guidelines: how difficult is reaching the ‘target’?

Abstract

Patients with chronic kidney disease (CKD) are affected by mineral and bone disorder (MBD), resulting in abnormalities in serum calcium (Ca), phosphorous (P) and parathyroid hormone (PTH). Changes in mineral metabolism have also been associated with higher rates of both all-cause and cardiovascular-related mortality. The majority of haemodialysis patients are also deficient in the endogenous hormone 1,25-dihydroxyvitamin D (calcitriol), often contributing to increased secondary hyperparathyroidism (SHPT) and consequently to abnormal levels of Ca, P and PTH. Thus P overload and SHPT are well-known targets of medical treatments, such as P binders, vitamin D and calcimimetics, although with still limited evidence-based advantages in terms of survival. The tough hedge that is still keeping nephrologists far from a conclusive and winning approach against CKD-MBD is reasonably related to the still partial comprehension of the molecular pathways involved in a complex, multifactorial and extreme process.