Opinion - (2025) Volume 15, Issue 4
Received: 01-Jul-2025, Manuscript No. jnt-26-178947;
Editor assigned: 03-Jul-2025, Pre QC No. P-178947;
Reviewed: 17-Jul-2025, QC No. Q-178947;
Revised: 22-Jul-2025, Manuscript No. R-178947;
Published:
29-Jul-2025
, DOI: 10.37421/2161-0959.2025.15.574
Citation: O’Connell, Benjamin. ”CKD-MBD: Complex Factors, Management, and Complications.” J Nephrol Ther 15 (2025):574.
Copyright: © 2025 O’Connell B. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.
Mineral and bone disorders (CKD-MBD) in chronic kidney disease (CKD) constitute a complex systemic condition characterized by biochemical, endocrine, and structural abnormalities that significantly impact patient health and outcomes. This multifaceted disorder encompasses alterations in mineral metabolism, including calcium and phosphate, alongside disturbances in bone turnover, mineralization, and calcification of both vascular and extraskeletal tissues [1].
The primary drivers of CKD-MBD are well-established and include the kidney's impaired ability to excrete phosphate, leading to hyperphosphatemia, and a deficiency in vitamin D due to reduced synthesis and activation, which subsequently fuels secondary hyperparathyroidism [1].
Recent research has illuminated the critical role of fibroblast growth factor 23 (FGF23) in the pathogenesis of CKD-MBD. This hormone acts as a key regulator of phosphate homeostasis and vitamin D metabolism, and its dysregulation is increasingly recognized as central to the progression of this disorder [1].
Effective management of hyperphosphatemia is a cornerstone of CKD-MBD treatment due to its strong association with increased cardiovascular events and mortality. Therapies primarily involve phosphate binders, which are categorized into calcium-based, non-calcium-based, and polymeric agents, to reduce dietary phosphate absorption [2].
Novel phosphate binders with improved tolerability and efficacy are continuously being developed, aiming to mitigate the risks of hypercalcemia and gastrointestinal side effects, which are common with older formulations. Dietary phosphate restriction remains a vital component of management, although patient adherence can be a significant challenge [2].
Secondary hyperparathyroidism (SHPT) is a defining feature of CKD-MBD, arising from reduced calcitriol production and impaired calcium sensing by the parathyroid glands. Treatment strategies are directed at suppressing parathyroid hormone (PTH) levels while maintaining calcium and phosphate within recommended target ranges [3].
The principal therapeutic modalities for SHPT include calcimimetics, which enhance calcium sensing by the parathyroid glands, and vitamin D sterols, often used in combination. Close monitoring for adverse effects such as hypocalcemia and gastrointestinal disturbances is essential when utilizing these agents [3].
Vascular calcification represents a particularly serious complication of CKD-MBD, substantially elevating cardiovascular risk. This process involves intricate cellular and molecular mechanisms, including the transformation of vascular smooth muscle cells into osteoblast-like cells, driven by factors like elevated phosphate and imbalanced calcium-phosphate levels [4].
Bone disease in CKD presents with diverse histological patterns, such as adynamic bone disease, osteomalacia, and hyperparathyroid bone disease. While bone biopsy is the gold standard for definitive diagnosis, clinical parameters and biochemical markers can guide therapeutic decisions aimed at optimizing bone health and reducing fracture risk [5].
Extraskeletal calcification, extending beyond the vasculature to other soft tissues, contributes significantly to the morbidity associated with CKD-MBD. Understanding the underlying risk factors, the complex interplay of mineral metabolism, and the role of calcification inhibitors is crucial for developing effective preventive and therapeutic strategies [8].
Mineral and bone disorders (CKD-MBD) in chronic kidney disease (CKD) encompass a complex array of biochemical, endocrine, and structural abnormalities affecting mineral metabolism, bone health, and calcification [1].
The pathogenesis is largely driven by impaired phosphate excretion, leading to hyperphosphatemia, and vitamin D deficiency, which stimulates secondary hyperparathyroidism [1].
Emerging research highlights the pivotal role of fibroblast growth factor 23 (FGF23) in CKD-MBD, influencing phosphate and vitamin D regulation and contributing to the overall disease process [1].
The management of hyperphosphatemia is critical due to its strong association with cardiovascular complications and increased mortality in CKD patients. Phosphate binders, including calcium-based, non-calcium-based, and polymeric types, are central to reducing phosphate absorption from the diet [2].
Recent advancements in phosphate binder therapy focus on developing agents with improved tolerability and efficacy, aiming to minimize side effects like hypercalcemia and gastrointestinal distress. Dietary phosphate restriction is also a key strategy, although achieving consistent patient adherence can be challenging [2].
Secondary hyperparathyroidism (SHPT) is a hallmark of CKD-MBD, resulting from diminished calcitriol levels and altered calcium sensing. Treatment goals are to suppress parathyroid hormone (PTH) while maintaining calcium and phosphate within target ranges, utilizing therapies such as calcimimetics and vitamin D sterols [3].
Calcimimetics and vitamin D sterols are principal treatment modalities for SHPT, often employed in combination. Careful monitoring for potential adverse effects, including hypocalcemia and gastrointestinal symptoms, is essential during treatment with these agents [3].
Vascular calcification is a significant complication of CKD-MBD, contributing substantially to the elevated cardiovascular risk observed in these patients. This process involves complex cellular events, such as the transition of vascular smooth muscle cells to osteoblast-like cells, influenced by mineral imbalances and FGF23 [4].
Therapeutic strategies for vascular calcification are continuously evolving, with ongoing research exploring agents capable of inhibiting or potentially reversing the calcification process. Understanding the intricate mechanisms underlying vascular calcification is paramount for developing effective interventions [4].
Bone disease in CKD manifests in various histological forms, including adynamic bone disease, osteomalacia, and hyperparathyroid bone disease. Treatment selection often depends on the specific bone histology, which can be difficult to ascertain without a bone biopsy, although clinical and biochemical markers can guide management [5].
Extraskeletal calcification, notably vascular calcification, poses a serious threat in CKD-MBD, escalating cardiovascular risk. Beyond the vasculature, calcification can affect other soft tissues, contributing to patient morbidity. Identifying risk factors and understanding the mechanisms, including mineral metabolism alterations, are key to prevention and treatment [8].
Iron deficiency is highly prevalent in CKD and often coexists with and exacerbates CKD-MBD. Iron deficiency can negatively impact mineral metabolism and bone health by impairing erythropoiesis, increasing hepcidin, and promoting inflammation. Addressing iron deficiency through supplementation is an important aspect of comprehensive CKD management [7].
Mineral and bone disorders (CKD-MBD) in chronic kidney disease (CKD) involve complex biochemical, endocrine, and structural abnormalities. Key factors include impaired phosphate excretion, vitamin D deficiency, and secondary hyperparathyroidism, with FGF23 playing a crucial role. Management focuses on controlling hyperphosphatemia with phosphate binders and dietary restriction, and treating secondary hyperparathyroidism with calcimimetics and vitamin D sterols. Vascular calcification is a significant complication increasing cardiovascular risk. Bone disease in CKD presents with various histological patterns, requiring tailored management. Iron deficiency often exacerbates CKD-MBD. Therapeutic strategies aim to mitigate these complications and improve patient outcomes.
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