scholarly journals Biological and Clinical Effects of Calciprotein Particles on Chronic Kidney Disease-Mineral and Bone Disorder

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Kenichi Akiyama ◽  
Takaaki Kimura ◽  
Kazuhiro Shiizaki
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Studies ◽  
Inflammatory Responses ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Clinical Effects ◽  
Mineral And Bone Disorder ◽  
Calciprotein Particles ◽  
Bone Disorder

Calciprotein particles (CPPs) are a new biological marker of chronic kidney disease-mineral and bone disorder (CKD-MBD). CPPs consist of phosphate, calcium, and some proteins, with phosphate being the major contributor to the level and biological activity of CPPs. Recent studies have shown the physiological and pathological significance of CPPs, including contributions to bone and mineral metabolism, and to tissue and organ impairments such as cardiovascular damage and inflammatory responses. These actions are well known as important aspects of CKD-MBD. Fibroblast growth factor 23 (FGF23), which is secreted from the bone as the phosphaturic hormone, is markedly elevated in CKD-MBD. Many clinical studies have shown significant relationships between the level of FGF23 and outcomes such as mortality, prevalence of cardiovascular disease, bone fracture, and levels of inflammatory markers. Basic and clinical studies have suggested that CPPs contribute to synthesis and secretion of FGF23. Surgical treatments such as renal transplantation and parathyroidectomy for patients with CKD-MBD suppress excess levels of phosphate, calcium, parathyroid hormone (PTH), and FGF23, which are related to the CPP level. Therefore, suppression of CPPs might also contribute to improved clinical outcomes after these treatments.

Chronic kidney disease-mineral and bone disorder

2018 ◽  
Author(s):  
Stuart M. Sprague ◽  
Menaka Sarav
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Osteodystrophy ◽  
Mineral Metabolism ◽  
Bone Biopsy ◽  
Fibroblast Growth Factor 23 ◽  
Critical Role ◽  
Specific Treatment ◽  
Mineral And Bone Disorder ◽  
Bone Disorder

The kidneys play a critical role in maintaining normal serum calcium and phosphorus concentrations, under the regulation of three main hormones: parathyroid hormone, calcitriol, and fibroblast growth factor 23. With the progression of chronic kidney disease (CKD), most patients develop CKD–mineral and bone disorder (CKD-MBD), which is a systemic disorder involving derangement in mineral metabolism, renal osteodystrophy, and extraskeletal calcification. Disturbances in mineral metabolism develop early in CKD and include phosphate retention, hypocalcaemia, vitamin D deficiency, and hyperparathyroidism. Renal osteodystrophy involves pathologic changes of bone morphology related to progressive CKD and is quantifiable by histomorphometry, based on bone biopsy. CKD-MBD is associated with significant morbidity, including bone loss, fractures, cardiovascular disease, immune suppression, as well as increased mortality. As the disorder begins early in the course of CKD, a proactive approach with intervention is important. Therapeutic strategies could then be employed to prevent and correct these disturbances, aiming to improve cardiovascular outcomes and survival. Current practice guidelines for CKD-MBD are based on insufficient data and high-quality studies are required before specific treatment can be advocated strongly.

Pathophysiology of chronic kidney disease-mineral and bone disorder

2015 ◽  
Author(s):  
Alexandra Voinescu ◽  
Nadia Wasi Iqbal ◽  
Kevin J. Martin
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Parathyroid Hormone ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Serum Levels ◽  
Mineral And Bone Disorder ◽  
Vitamin D Metabolism ◽  
Bone Disorder ◽  
Calcium Phosphorus

Chronic kidney disease is associated with the inability to control normal mineral homeostasis, resulting in abnormalities in serum levels of calcium, phosphorus, parathyroid hormone, fibroblast growth factor 23 (FGF23) and vitamin D metabolism. These disturbances lead to the development of secondary hyperparathyroidism, skeletal abnormalities, vascular calcifications, and other systemic manifestations. Traditionally, mineral and bone abnormalities seen in chronic kidney disease were included in the term ‘renal osteodystrophy’. More recently, the term chronic kidney disease-mineral and bone disorder was introduced to define the biochemical abnormalities of phosphorus, parathyroid hormone, FGF23, calcium, or vitamin D metabolism, abnormalities in bone remodelling and mineralization, and vascular or other soft tissue calcifications.

scholarly journals Adverse Effects of Autoclaved Diets on the Progression of Chronic Kidney Disease and Chronic Kidney Disease-Mineral Bone Disorder in Rats

2020 ◽  
Vol 51 (5) ◽  
pp. 381-389
Author(s):  
Annabel Biruete ◽  
Shruthi Srinivasan ◽  
Kalisha D. O’Neill ◽  
Colby J. Vorland ◽  
Kathleen M. Hill Gallant ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Kidney Function ◽  
Fibroblast Growth Factor 23 ◽  
Laboratory Animals ◽  
Casein Diet ◽  
Mineral And Bone Disorder ◽  
Bone Disorder ◽  
And Oxidative Stress

Background: Autoclaving rodent diets is common in laboratory animals, but autoclaving increases the formation of dietary advanced glycation end-products (AGE). We studied the effect of autoclaved (AC) diet alone or in combination with a diet high in bioavailable phosphorus on biochemistries of chronic kidney disease-mineral and bone disorder (CKD-MBD), intestinal gene expression, and oxidative stress. Methods: Male CKD rats (Cy/+) and normal littermates were fed 1 of 3 diets: AC 0.7% phosphorus grain-based diet for 28 weeks (AC); AC diet for 17 weeks followed by non-autoclaved (Non-AC) 0.7% phosphorus casein diet until 28 weeks (AC + Casein); or Non-AC diet for 16 weeks followed by a Non-AC purified diet until 30 weeks (Non-AC + Casein). Results: AC diets contained ~3× higher AGEs and levels varied depending on the location within the autoclave. Rats fed the AC and AC + Casein diets had higher total AGEs and oxidative stress, irrespective of kidney function. Kidney function was more severely compromised in CKD rats fed AC or AC + Casein compared to Non-AC + Casein. There was a disease-by-diet interaction for plasma phosphorus, parathyroid hormone, and c-terminal fibroblast growth factor-23, driven by high values in the CKD rats fed the AC + Casein diet. Compared to Non-AC + Casein, AC and AC + Casein-fed groups had increased expression of receptor of AGEs and intestinal NADPH oxidase dual oxidase-2, independent of kidney function. Conclusions: Autoclaving rodent diets impacts the progression of CKD and CKD-MBD, highlighting the critical importance of standardizing diets in experiments.

THE ROLE OF FBROBLAST GROWTH FACTOR 23 (FGF 23) IN THE MINERAL AND BONE DISORDER (MBD) OF THE PATENTS WITH CHRONIC KIDNEY DISEASE

2016 ◽  
pp. 9-14
Author(s):  
Huu Vu Quang Nguyen ◽  
Tam Vo
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Kidney Function ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Normal Kidney ◽  
Mineral And Bone Disorder ◽  
Normal Kidney Function ◽  
Fgf 23

Fibroblast growth factor 23 (FGF23) is a key regulator of phosphorus metabolism whose effects in patients with chronic kidney disease (CKD) have only recently begun to be appreciated. Recent study of this phosphaturic hormone has revealed new path-ways of mineral regulation in both individuals with normal kidney function and in patients with CKD. While the effects of FGF23 on mineral metabolism in CKD appears to be similar to its effects in individuals with normal kidney function, elevated levels of the protein in the CKD population have also been linked to kidney disease progression, altered skeletal histology, and increased mortality rates, relationships that have not been examined in the general population.Thus, potential differences in FGF23 metabolism accompany the elevated levels found in CKD patients and, although the exact pathophysiological consequences remain mostly unknown, elevated FGF23 levels appear to contribute to major complications of CKD that plague both adults and children. Key words: FGF23, chronic kidney

scholarly journals Recent advances in understanding and managing secondary hyperparathyroidism in chronic kidney disease

F1000Research ◽  
2020 ◽  
Vol 9 ◽  
pp. 1077 ◽  
Author(s):  
María E. Rodríguez-Ortiz ◽  
Mariano Rodríguez
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Mineral Metabolism ◽  
Mineral And Bone Disorder ◽  
Parathyroid Function ◽  
Vitamin D Levels ◽  
Bone Disorder ◽  
New Evidence ◽  
Shed Light

Secondary hyperparathyroidism is a complex pathology that develops as chronic kidney disease progresses. The retention of phosphorus and the reductions in calcium and vitamin D levels stimulate the synthesis and secretion of parathyroid hormone as well as the proliferation rate of parathyroid cells. Parathyroid growth is initially diffuse but it becomes nodular as the disease progresses, making the gland less susceptible to be inhibited. Although the mechanisms underlying the pathophysiology of secondary hyperparathyroidism are well known, new evidence has shed light on unknown aspects of the deregulation of parathyroid function. Secondary hyperparathyroidism is an important feature of chronic kidney disease–mineral and bone disorder and plays an important role in the development of bone disease and vascular calcification. Thus, part of the management of chronic kidney disease relies on maintaining acceptable levels of mineral metabolism parameters in an attempt to slow down or prevent the development of secondary hyperparathyroidism. Here, we will also review the latest evidence regarding several aspects of the clinical and surgical management of secondary hyperparathyroidism.

Current Approaches in the Treatment of Chronic Kidney Disease Mineral and Bone Disorder

2008 ◽  
Vol 21 (3) ◽  
pp. 196-213 ◽  
Author(s):  
Priscilla P. How ◽  
Darius L. Mason ◽  
Alan H. Lau
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Mineral Metabolism ◽  
High Morbidity ◽  
Mineral And Bone Disorder ◽  
Vitamin D Analogs ◽  
Bone Disorder ◽  
Stage Renal Disease

Patients with chronic kidney disease (CKD) develop mineral and bone disorder (MBD), a common and important complication, as a result of impaired phosphorus excretion and reduced vitamin D activation. Altered mineral metabolism is now recognized as an independent cardiovascular risk factor in end-stage renal disease patients and contributes to the risk for accelerating vascular calcification. CKD patients are at high risk for cardiovascular disease and vascular calcification which account for the high morbidity and mortality in this patient population. Pharmacotherapeutic interventions are necessary to manage and treat the condition. Multiple classes of agents including phosphorus binders, vitamin D analogs, and calcimimetics are now available to treat CKD-MBD. Recent data have shown that treatment with sevelamer and vitamin D analogs are associated with a reduction in calcification and cardiovascular mortality and improved survival. This article provides an overview of the strategies and considerations for the management of CKD-MBD, as well as their implications on clinical outcomes.

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