Phosphate handling in CKD-MBD from stage 3 to dialysis and the three strengths of lanthanum carbonate

Abstract

Lanthanum carbonate, being the most potent calcium-free phosphate binder available in clinical practice, could be decisive for those cases where controlling phosphate load is complicated by poor compliance to medications, stubborn high phosphorus intake, extended VC and bone disorders.

Which Vitamin D in CKD-MBD? The Time of Burning Questions

“…On the contrary, its suspension or reduction is suggested in the case of hypercalcemia or hyperphosphatemia [6]. The risks related to high doses of vitamin D are mainly due to phosphate and calcium overload which are both associated with worse survival in dialysis patients [56, 57]. Furthermore, the achievement of the suggested calcium and phosphate targets is still suboptimal in the European dialysis population, as reported by the recent COSMOS investigation [58].…”

Magnesium: a renewed player of vascular ageing in diabetic CKD patients?

“…Consistent results from the basic and clinical research showed that cardiovascular susceptibility in CKD is due, partially at least, to a considerable acceleration of the vascular ageing processes in the context of chronic kidney disease-mineral bone disorder syndrome (CKD-MBD) [ 2 ]. This premature cardiovascular senescence is mainly characterized by altered endothelial reactivity, followed by pathologic calcification of cardiac valves and medial layer in the arteries [ 3 ]. The consequent increase of arterial stiffness worsens the cardiac afterload, contributing to the onset of left ventricular hypertrophy and to the progressive increase of pulse pressure (PP) leading to a significant reduction of diastolic tissue perfusion.…”

“…The consequent increase of arterial stiffness worsens the cardiac afterload, contributing to the onset of left ventricular hypertrophy and to the progressive increase of pulse pressure (PP) leading to a significant reduction of diastolic tissue perfusion. The metabolic pathways linked to this premature ageing involve the dysregulation of several systems such as inflammation, oxydative stress, insulin resistance and mineral metabolism [ 3 ]. The alterations of calcium (Ca) and phosphate (P) homeostasis in renal patients, mainly driven by a derangement of Klotho/fibroblast growth factor 23 (FGF23)—parathormone (PTH)—vitamin D axis, are considered pivotal triggers and regulators of vascular ageing rather than mere biomarkers of CKD-MBD syndrome [ 3 ].…”

“…The metabolic pathways linked to this premature ageing involve the dysregulation of several systems such as inflammation, oxydative stress, insulin resistance and mineral metabolism [ 3 ]. The alterations of calcium (Ca) and phosphate (P) homeostasis in renal patients, mainly driven by a derangement of Klotho/fibroblast growth factor 23 (FGF23)—parathormone (PTH)—vitamin D axis, are considered pivotal triggers and regulators of vascular ageing rather than mere biomarkers of CKD-MBD syndrome [ 3 ]. Thus, P overload and hyperparathyroidism 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 in renal patients [ 3 , 4 ].…”

“…The alterations of calcium (Ca) and phosphate (P) homeostasis in renal patients, mainly driven by a derangement of Klotho/fibroblast growth factor 23 (FGF23)—parathormone (PTH)—vitamin D axis, are considered pivotal triggers and regulators of vascular ageing rather than mere biomarkers of CKD-MBD syndrome [ 3 ]. Thus, P overload and hyperparathyroidism 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 in renal patients [ 3 , 4 ]. The tough hedge that is still keeping nephrologists far from a conclusive and winning approach against vascular ageing is reasonably related to the still partial comprehension of the molecular pathways involved in a so complex, multifactorial and extreme process.…”