Mineral Bone Disorders in Kidney Disease Patients: The Ever-Current Topic

Abstract

Chronic kidney disease (CKD) is a complex and multifactorial disease, and one of the most prevalent worldwide. Chronic kidney disease-mineral bone disorders (CKD-MBD) with biochemical and hormonal alterations are part of the complications associated with the progression of CKD. Pathophysiology of CKD-MBD focused on abnormalities in serum levels of several biomarkers (such as FGF-23, klotho, phosphate, calcium, vitamin D, and PTH) which are discussed in this review. We therefore examine the prognostic association between CKD-MBD and the increased risk for cardiovascular events, mortality, and CKD progression to end-stage kidney disease (ESKD). Lastly, we present specific treatments acting on CKD to prevent and treat the complications associated with secondary hyperparathyroidism (SHPT): control of hyperphosphatemia (with dietary restriction, intestinal phosphate binders, and adequate dialysis), the use of calcimimetic agents, vitamin D, and analogues, and the use of bisphosphonates or denosumab in patients with osteoporosis.

Keywords: CKD–MBD; ESKD; cardiovascular; epidemiology; kidney; prognosis.

Figure 1

The interplay among FGF-23, PTH, vitamin D3, and phosphorus in CKD. Secretion of FGF-23 is stimulated by increased levels of PTH, 1,25(OH)D3 and phosphorus from diet loading. On the other side, FGF-23 inhibits PTH secretion, decreases levels of 1,25(OH)D3, reduces intestinal absorption of alimentar phosphorus, inhibits phosphorus reabsorption in the proximal tubule leading to increased urinary excretion. Furthermore, 1,25(OH)D3 suppresses PTH, and hyperphosphatemia reduces CASR sensibility, directly affecting PTH synthesis.

Figure 2

Correlations between serum levels of Klotho, FGF-23, vitamin D, phosphate, and PTH during CKD progression.