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CKD-MBD KDIGO guidelines: how difficult is reaching the 'target'?
1Department of Health Sciences, Renal Division, San Paolo Hospital, University of Milan, Milan, Italy.
Insights
Chronic kidney disease-mineral and bone disorder (CKD-MBD) causes abnormal mineral levels and increases mortality risk. Current treatments for CKD-MBD, like phosphate binders and vitamin D, show limited survival benefits due to incomplete understanding of the disease's molecular pathways.
Area of Science:
- Nephrology
- Endocrinology
- Molecular Biology
Background:
- Chronic kidney disease (CKD) is frequently associated with mineral and bone disorder (MBD).
- CKD-MBD involves dysregulation of serum calcium (Ca), phosphorus (P), and parathyroid hormone (PTH).
- Mineral metabolism derangements in CKD correlate with increased all-cause and cardiovascular mortality.
Purpose of the Study:
- To highlight the challenges in managing CKD-MBD.
- To emphasize the need for a deeper understanding of molecular pathways in CKD-MBD.
Main Methods:
- Review of existing literature on CKD-MBD pathophysiology and treatment.
- Analysis of the impact of mineral imbalances on patient outcomes.
Main Results:
- Patients on haemodialysis often have 1,25-dihydroxyvitamin D (calcitriol) deficiency, exacerbating secondary hyperparathyroidism (SHPT).
- Established treatments like phosphate binders, vitamin D, and calcimimetics offer limited survival advantages.
- Incomplete understanding of CKD-MBD molecular mechanisms hinders effective therapeutic strategies.
Conclusions:
- CKD-MBD is a complex, multifactorial condition requiring further research into its underlying molecular pathways.
- Addressing P overload and SHPT remains a clinical challenge with current therapeutic options.
- Enhanced comprehension of molecular processes is crucial for developing improved treatments and improving survival in CKD patients.
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.