Chronic Kidney Disease Mineral and Bone Disorders
Summary
Chronic kidney disease mineral and bone disorders (CKD-MBD) encompass a spectrum of systemic complications arising from impaired renal function and disrupted mineral homoeostasis. As nephron loss progresses, the kidneys’ capacity to excrete phosphate and to generate active vitamin D diminishes, leading to hyperphosphataemia, hypocalcaemia and secondary hyperparathyroidism. Altered levels of regulatory hormones—parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23) and the co-receptor Klotho—drive bone turnover abnormalities, ranging from high-turnover osteitis fibrosa to low-turnover adynamic bone disease. Biochemical disturbances also promote vascular and soft-tissue calcification, which is closely linked to cardiovascular morbidity and mortality. Diagnosis relies on a combination of blood and urine indices, bone imaging and, in selected cases, histomorphometry. Management strategies include phosphate binders, vitamin D analogues, calcimimetics and individualised dietary counselling. Understanding the complex interplay between bone health, vascular function and systemic inflammation remains essential for improving patient outcomes and guiding the development of targeted therapies.
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Chronic Kidney Disease Mineral and Bone Disorders publication trend
The graph below shows the total number of articles in chronic kidney disease mineral and bone disorders across all publications each year (not limited to Nature Index journals).
Technical terms
Estimated glomerular filtration rate (eGFR): A calculated index of kidney filtering capacity, used to stage CKD.
Fibroblast growth factor 23 (FGF23): A bone-derived hormone that lowers serum phosphate by reducing renal reabsorption and suppressing vitamin D activation.
Parathyroid hormone (PTH): A peptide hormone from the parathyroid glands that maintains calcium and phosphate balance.
Klotho: A membrane and soluble protein that partners with FGF23 in mineral metabolism and exerts vasculo-protective effects.
Osteoprotegerin (OPG): A decoy receptor inhibiting osteoclast differentiation, implicated in both bone remodelling and vascular calcification.
Vascular calcification: Pathological deposition of calcium phosphate in blood vessel walls, contributing to arterial stiffness and cardiovascular risk.
References
- Association of mineral and bone biomarkers with adverse cardiovascular outcomes and mortality in the German Chronic Kidney Disease (GCKD) cohort. Bone Research (2023).
- Is controlling phosphorus by decreasing dietary protein intake beneficial or harmful in persons with chronic kidney disease?. American Journal of Clinical Nutrition (2008).
- A Decreased Level of Serum Soluble Klotho Is an Independent Biomarker Associated with Arterial Stiffness in Patients with Chronic Kidney Disease. PLOS ONE (2013).
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