Is Adynamic Bone Always a Disease? Lessons from Patients with Chronic Kidney Disease

Nagy, Eman; Sobh, Mahmoud; Abdalbary, Mohamed; Elnagar, Sherouk; Elrefaey, Rabab; Shabaka, Shimaa; Elshabrawy, Nehal; Shemies, Rasha; Tawfik, Mona K.; Santos, Cássia Gomes S.; Barreto, Fellype Carvalho; El-Husseini, Amr

doi:10.3390/jcm11237130

Cited by 6 publications

(7 citation statements)

References 197 publications

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“…Vascular and soft tissue calcification are integral aspects of CKD MBD, intricately connected to ROD, particularly adynamic bone disease [ 101 , 102 ]. Numerous studies highlight a high prevalence of VC with increased severity and rapid progression in CKD, spanning both early stages and ESKD [ 103 , 104 , 105 , 106 ].…”

Section: Vascular Calcificationmentioning

confidence: 99%

Chronic Kidney Disease with Mineral Bone Disorder and Vascular Calcification: An Overview

Izzo,

Secondulfo,

Bilancio

et al. 2024

Life

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Chronic kidney disease (CKD) is a global health issue with a rising prevalence, affecting 697.5 million people worldwide. It imposes a substantial burden, contributing to 35.8 million disability-adjusted life years (DALYs) and 1.2 million deaths in 2017. The mortality rate for CKD has increased by 41.5% between 1990 and 2017, positioning it as a significant cause of global mortality. CKD is associated with diverse health complications, impacting cardiovascular, neurological, nutritional, and endocrine aspects. One prominent complication is CKD–mineral and bone disorder (MBD), a complex condition involving dysregulation of bone turnover, mineralization, and strength, accompanied by soft tissue and vascular calcification. Alterations in mineral metabolism, including calcium, phosphate, parathyroid hormone (PTH), vitamin D, fibroblast growth factor-23 (FGF-23), and Klotho, play pivotal roles in CKD-MBD. These disturbances, observed early in CKD, contribute to the progression of bone disorders and renal osteodystrophy (ROD). Vascular calcification (VC) is a key component of CKD-MBD, accelerated by CKD. The pathophysiology involves complex processes in vascular smooth muscle cells and the formation of calciprotein particles (CPP). VC is closely linked to cardiovascular events and mortality, emphasizing its prognostic significance. Various serum markers and imaging techniques, including lateral plain X-ray, Kauppila Score, Adragao Score, and pulse wave velocity, aid in VC detection. Additionally, pQCT provides valuable information on arterial calcifications, offering an advantage over traditional scoring systems. CKD poses a substantial global health burden, and its complications, including CKD-MBD and VC, significantly contribute to morbidity and mortality. Understanding the intricate relationships between mineral metabolism, bone disorders, and vascular calcification is crucial for effective diagnosis and therapeutic interventions.

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Section: Vascular Calcificationmentioning

confidence: 99%

Chronic Kidney Disease with Mineral Bone Disorder and Vascular Calcification: An Overview

Izzo,

Secondulfo,

Bilancio

et al. 2024

Life

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“…Frontiers in Physiology frontiersin.org 07 formation, low cellularity, and thin osteoid seams, the lastmentioned being the most important difference with osteomalacia (wide osteoid volume) since mineralization is normal in ABD (Parfitt et al, 1987;Moe et al, 2006;Nagy et al, 2022). Minimodeling has been shown to potentially contribute to bone formation in dialysis patients with ABD, in the absence of remodelling stimulated by PTH, and this is especially the case in young patients with positive activities of daily living (Ubara et al, 2005).…”

Section: Adynamic Bone Diseasementioning

confidence: 99%

Pathophysiology of Bone and Mineral Metabolism

2024

Frontiers Research Topics

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Frontiers is more than just an open access publisher of scholarly articles: it is a pioneering approach to the world of academia, radically improving the way scholarly research is managed. The grand vision of Frontiers is a world where all people have an equal opportunity to seek, share and generate knowledge. Frontiers provides immediate and permanent online open access to all its publications, but this alone is not enough to realize our grand goals. Frontiers journal seriesThe Frontiers journal series is a multi-tier and interdisciplinary set of openaccess, online journals, promising a paradigm shift from the current review, selection and dissemination processes in academic publishing. All Frontiers journals are driven by researchers for researchers; therefore, they constitute a service to the scholarly community. At the same time, the Frontiers journal series operates on a revolutionary invention, the tiered publishing system, initially addressing specific communities of scholars, and gradually climbing up to broader public understanding, thus serving the interests of the lay society, too. Dedication to qualityEach Frontiers article is a landmark of the highest quality, thanks to genuinely collaborative interactions between authors and review editors, who include some of the world's best academicians. Research must be certified by peers before entering a stream of knowledge that may eventually reach the public -and shape society; therefore, Frontiers only applies the most rigorous and unbiased reviews. Frontiers revolutionizes research publishing by freely delivering the most outstanding research, evaluated with no bias from both the academic and social point of view. By applying the most advanced information technologies, Frontiers is catapulting scholarly publishing into a new generation. What are Frontiers Research Topics?Frontiers Research Topics are very popular trademarks of the Frontiers journals series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area.

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“…Aluminum intoxication was previously the most frequent cause of low-turnover bone disease (aluminum-induced osteomalacia) since aluminum decreases the activation of OB and OC and causes an important defective mineralization ( Malluche and Faugere, 1986 ; Nebeker and Coburn, 1986 ). ABD is characterized by suppressed bone formation, low cellularity, and thin osteoid seams, the last-mentioned being the most important difference with osteomalacia (wide osteoid volume) since mineralization is normal in ABD ( Parfitt et al, 1987 ; Moe et al, 2006 ; Nagy et al, 2022 ). Minimodeling has been shown to potentially contribute to bone formation in dialysis patients with ABD, in the absence of remodelling stimulated by PTH, and this is especially the case in young patients with positive activities of daily living ( Ubara et al, 2005 ).…”

Section: Adynamic Bone Diseasementioning

confidence: 99%

“…The prevalence of ABD used to be much lower than that of osteitis fibrosa, but this pattern of bone damage has increased significantly, and in most recent studies it is described as the most prevalent ( Frazão and Martins, 2009 ; Malluche et al, 2011 ; Nagy et al, 2022 ). It has even been proposed that ABD may be the predominant bone pattern in early stages of CKD ( Massy and Drueke, 2017 ).…”

Section: Adynamic Bone Diseasementioning

confidence: 99%

“…In any case, the implications of drug-induced suppression of bone turnover for bone strength are intensely debated ( Evenepoel et al, 2021a ). As we mentioned previously, low PTH levels as a proxy of low-bone turnover in CKD patients have been associated with increased fracture risk ( Coco and Rush, 2000 ; Nitta et al, 2004 ) but it remains a matter of debate whether low bone turnover per se or the disease causing low bone turnover accounts for the perceived ABD-induced risk of fracture or adverse outcomes ( Evenepoel et al, 2021a ; Nagy et al, 2022 ).…”

Section: Adynamic Bone Diseasementioning

confidence: 99%

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Pathophysiology of bone disease in chronic kidney disease: from basics to renal osteodystrophy and osteoporosis

Aguilar,

Gifre,

Ureña-Torres

et al. 2023

Front. Physiol.

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Chronic kidney disease (CKD) is a highly prevalent disease that has become a public health problem. Progression of CKD is associated with serious complications, including the systemic CKD-mineral and bone disorder (CKD-MBD). Laboratory, bone and vascular abnormalities define this condition, and all have been independently related to cardiovascular disease and high mortality rates. The “old” cross-talk between kidney and bone (classically known as “renal osteodystrophies”) has been recently expanded to the cardiovascular system, emphasizing the importance of the bone component of CKD-MBD. Moreover, a recently recognized higher susceptibility of patients with CKD to falls and bone fractures led to important paradigm changes in the new CKD-MBD guidelines. Evaluation of bone mineral density and the diagnosis of “osteoporosis” emerges in nephrology as a new possibility “if results will impact clinical decisions”. Obviously, it is still reasonable to perform a bone biopsy if knowledge of the type of renal osteodystrophy will be clinically useful (low versus high turnover-bone disease). However, it is now considered that the inability to perform a bone biopsy may not justify withholding antiresorptive therapies to patients with high risk of fracture. This view adds to the effects of parathyroid hormone in CKD patients and the classical treatment of secondary hyperparathyroidism. The availability of new antiosteoporotic treatments bring the opportunity to come back to the basics, and the knowledge of new pathophysiological pathways [OPG/RANKL (LGR4); Wnt-ß-catenin pathway], also affected in CKD, offers great opportunities to further unravel the complex physiopathology of CKD-MBD and to improve outcomes.

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Is Adynamic Bone Always a Disease? Lessons from Patients with Chronic Kidney Disease

Cited by 6 publications

References 197 publications

Chronic Kidney Disease with Mineral Bone Disorder and Vascular Calcification: An Overview

Chronic Kidney Disease with Mineral Bone Disorder and Vascular Calcification: An Overview

Pathophysiology of Bone and Mineral Metabolism

Pathophysiology of bone disease in chronic kidney disease: from basics to renal osteodystrophy and osteoporosis

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