scholarly journals THE SPECTRUM OF RENAL OSTEODYSTROPHY – NOVEL AND OLD PARADIGMS

2016 ◽  
Vol 25 (1) ◽  
pp. 5-13
Author(s):  
Violeta Bojinca ◽  
◽  
Daria Popescu ◽  
Cristina Capusa ◽  
◽  
...  

“Chronic kidney disease-related mineral and bone disorder” is a newly introduced concept which replaced the former term of “renal osteodystrophy” or “renal bone disease”. It highlights the need for understanding the complex relationships among calcium-phosphate axis, bone metabolism, ectopic calcification and cardiovascular morbidity and mortality in patients with chronic kidney disease. It has the merit to shift the focus from monitoring and treating separate biochemical abnormalities at all costs to the greater aim of improvement survival and reducing major cardiovascular events. However, mainly because of the lack of reliable assessment tools, the bone disorders component is discussed to a much lesser extent even it accounts for major physical disabilities and result in significant impairment of the quality of life. Therefore, the current review aimed to briefly remind the older and newer knowledge in the field of bone changes that occur during the course of chronic kidney disease.

Author(s):  
Stuart M. Sprague ◽  
Menaka Sarav

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.


Author(s):  
Diego Ennes Gonzalez ◽  
Renato Demarchi Foresto ◽  
Ana Luiza Santos Maldonado ◽  
Wallace Stwart Carvalho Padilha ◽  
Fernanda Badiani Roberto ◽  
...  

ABSTRACT Introduction: The clinical impact of vascular calcification is well established in the context of cardiovascular morbidity and mortality, but other clinical syndromes, such as calciphylaxis, although less frequent, have a significant impact on chronic kidney disease. Methods: Case report of a 27-year-old woman, who had complained of bilateral pain in her toes for 3 days, with the presence of small necrotic areas in the referred sites. She had a history of type 1 diabetes (25 years ago), with chronic kidney disease, on peritoneal dialysis, in addition to rheumatoid arthritis. She was admitted to the hospital, which preceded the current condition, due to exacerbation of rheumatoid arthritis, evolving with intracardiac thrombus due to venous catheter complications, when she started using warfarin. Ischemia progressed to her feet, causing the need for bilateral amputations. Her chirodactyls were also affected. Thrombophilia, vasculitis, endocarditis or other embolic sources were investigated and discarded. Her pathology report evidenced skin necrosis and superficial soft parts with recent arterial thrombosis, and Monckeberg's medial calcification. We started treatment with bisphosphonate and sodium thiosulfate, conversion to hemodialysis and replacement of warfarin with unfractionated heparin. Despite all the therapy, the patient died after four months of evolution. Discussion: Calciphylaxis is a rare microvasculature calcification syndrome that results in severe ischemic injuries. It has pathogenesis related to the mineral and bone disorder of chronic kidney disease combined with the imbalance between promoters and inhibitors of vascular calcification, with particular importance to vitamin K antagonism. Conclusion: The preventive strategy is fundamental, since the therapy is complex with poorly validated effectiveness.


2019 ◽  
Vol 2019 ◽  
pp. 1-9 ◽  
Author(s):  
Kittrawee Kritmetapak ◽  
Chatlert Pongchaiyakul

Accurate measurement of parathyroid hormone (PTH) is crucial for therapeutic decision-making in patients with chronic kidney disease-mineral and bone disorder (CKD-MBD). The second-generation PTH assays, often referred to as “intact PTH” assays, are the current standard and most available assays in clinical practice. However, intact PTH assays measure both full-length biologically active PTH and heterogeneous PTH fragments in the circulation, providing the equivocal value of PTH measurement in patients with CKD-MBD. Due to the variability of PTH assays, preanalytical sample errors, and the phenomenon of end-organ PTH hyporesponsiveness, current CKD-MBD guidelines recommend a wide range for serum PTH targets (2–9 the upper normal limit of the intact PTH assay) in dialysis patients to diminish the risk of developing adynamic bone disease. Nevertheless, a sizeable proportion of CKD patients still experience renal osteodystrophy despite having serum PTH levels within the recommended range. The primary cause of this inconsistency is the analytical interference of various PTH fragments and oxidized PTH forms that considerably accumulate in CKD patients. Therefore, a new mass spectrometry-based assay, which is capable of specifically measuring the whole spectra of PTH fragments, can potentially improve diagnostic accuracy for renal osteodystrophy. However, the effects of different PTH fragments on bone metabolism, vascular calcification, and mortality in CKD patients warrant further research.


Author(s):  
Iulia-Daniela Vladu ◽  
Daniela Cana ◽  
Cristina Vaduva ◽  
Corina Grauntanu ◽  
Sorin Zaharie ◽  
...  

Chronic Kidney Disease-Mineral Bone Disorder in Diabetes Mellitus PatientsDiabetes mellitus (DM) and chronic kidney disease (CKD) are two diseases with increasing prevalence and adverse outcomes that represent an international health problem. Chronic kidney disease- mineral and bone disorder (CKD-MBD) is defined as a systemic disorder of mineral and bone metabolism due to CKD manifested by either one or a combination of the following: abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism; abnormalities in bone turnover, mineralization, volume, linear growth, or strength and vascular or other soft-tissue calcification. Disturbances in mineral and bone metabolism are prevalent in CKD and are an important cause of decreased quality of life, cardiovascular morbidity and mortality; these disturbances settle in earlier and have a more severe evolution in DM patients.


2018 ◽  
Author(s):  
Antonis Bartsiokas ◽  
Juan Luis Arsuaga

Both animal hibernation (heterothermy) and human renal osteodystrophy are characterized by high levels of serum parathyroid hormone. To test the hypothesis of hibernation in an extinct human species, we examined the hominin skeletal collection from Sima de los Huesos, Cave Mayor, Atapuerca, Spain, for evidence of hyperparathyroidism. We studied the morphology of the fossilized bones by using macrophotography, microscopy, histology and CT scanning. We found trabecular tunneling and osteitis fibrosa, subperiosteal resorption,‘rotten fence post’ signs,brown tumours, subperiosteal new bone, chondrocalcinosis, rachitic osteoplaques and empty gaps between them, craniotabes, and beading in ribs mostly in the adolescent population of these hominins. Since many of the above lesions are pathognomonic, these extinct hominins suffered annually from renal rickets, secondary hyperparathyroidism, and renal osteodystrophy associated with Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). We suggest these diseases were caused by non-tolerated hibernation in dark cavernous hibernacula. This is evidenced by the rachitic osteoplaques and the gaps between them mainly in the adolescent individuals along with the evidence of healing mainly in the adults. The sublayers in the rachitic osteoplaques point to bouts of arousal from hibernation. The strong projection of the external lip of the femoral trochlea, the rachitic osteoplaques with the empty gaps between them,the “rotten fence post sign”, and the evidence of annual healing caused by non-tolerated hibernation in adolescent individuals, also point to the presence of annually intermittent puberty in this population. The hypothesis of hibernation is consistent with the genetic evidence and the fact that the SH hominins lived during a glacial period. The present work will provide a new insight into the physiological mechanism of early human metabolism which could help in determining the life histories and physiologies of extinct human species.


2008 ◽  
Vol 28 (2_suppl) ◽  
pp. 5-10
Author(s):  
Sharon M. Moe

The definition, evaluation, and classification of the mineral abnormalities and bone disease in chronic kidney disease (CKD) should encompass all three clinical components: • Abnormalities in serum biochemistries • Vascular calcification • Bone abnormalities This principle was discussed at a Kidney Disease: Improving Global Outcomes consensus conference, resulting in a recognition of the shortcomings of the current classification and a recommendation for the development of new terminology. The recommendation was that the term “renal osteodystrophy” be used exclusively to define the bone pathology associated with CKD. The many clinical, biochemical, and imaging abnormalities that have heretofore been identified as correlates of renal osteodystrophy should be defined more broadly as a clinical entity or syndrome called “chronic kidney disease – mineral and bone disorder.” The hope is that this new terminology will enhance communication and facilitate research worldwide.


Author(s):  
Maria Fusaro ◽  
Rachel Holden ◽  
Charmaine Lok ◽  
Giorgio Iervasi ◽  
Mario Plebani ◽  
...  

Abstract In chronic kidney disease (CKD), phosphate homoeostasis plays a central role in the development of mineral and bone disorder (MBD) together with decreased serum calcium and elevated serum parathyroid hormone, fibroblast growth factor 23 and sclerostin levels. Today there are only a few data exploring the direct role of abnormal phosphate homoeostasis and hyperphosphataemia in the development of CKD-MBD. On the other hand, several studies have looked at the link between hyperphosphataemia and cardiovascular morbidity and mortality in CKD, but there is a lack of evidence to indicate that lowering phosphate levels improves cardiovascular outcomes in this population. Furthermore, the impact of liberalizing phosphate targets on CKD-MBD progression and bone fracture is currently not known. In this review we discuss the central role of phosphate in the pathogenesis of CKD-MBD and how it may be associated with fracture risk, both in hyper- and hypophosphataemia.


2019 ◽  
Vol 7 (1) ◽  
pp. 18 ◽  
Author(s):  
Ronald B. Brown

An association between periodontal disease and cancer has been established in recent studies, but no common etiology has been identified in the hopes of reducing the global burden of these non-communicable diseases. This perspective article hypothesizes that the determinant mediating the association of periodontal disease with cancer is dysregulated phosphate metabolism. Phosphate, an essential dietary micronutrient, is dysregulated in chronic kidney disease, and both cancer and periodontal disease are associated with chronic kidney disease. Reviewed evidence includes the association between phosphate toxicity and cancer development, and the association between periodontal disease and chronic kidney disease-mineral and bone disorder includes conditions such as ectopic calcification and bone resorption, which may be indirectly related to periodontal disease. Dental calculus in periodontal disease contains calcium phosphate crystals that are deposited from excess calcium and phosphate in saliva. Alveolar bone resorption may be linked systemically to release of parathyroid hormone in response to hypocalcemia induced by hyperphosphatemia. More research is needed to examine the role of dysregulated phosphate metabolism in periodontal disease.


2018 ◽  
Author(s):  
Antonis Bartsiokas ◽  
Juan Luis Arsuaga

Both animal hibernation (heterothermy) and human renal osteodystrophy are characterized by high levels of serum parathyroid hormone. To test the hypothesis of hibernation in an extinct human species, we examined the hominin skeletal collection from Sima de los Huesos, Cave Mayor, Atapuerca, Spain, for evidence of hyperparathyroidism. We studied the morphology of the fossilized bones by using macrophotography, microscopy, histology and CT scanning. We found trabecular tunneling and osteitis fibrosa, subperiosteal resorption,‘rotten fence post’ signs,brown tumours, subperiosteal new bone, chondrocalcinosis, rachitic osteoplaques and empty gaps between them, craniotabes, and beading in ribs mostly in the adolescent population of these hominins. Since many of the above lesions are pathognomonic, these extinct hominins suffered annually from renal rickets, secondary hyperparathyroidism, and renal osteodystrophy associated with Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). We suggest these diseases were caused by non-tolerated hibernation in dark cavernous hibernacula. This is evidenced by the rachitic osteoplaques and the gaps between them mainly in the adolescent individuals along with the evidence of healing mainly in the adults. The sublayers in the rachitic osteoplaques point to bouts of arousal from hibernation. The strong projection of the external lip of the femoral trochlea, the rachitic osteoplaques with the empty gaps between them,the “rotten fence post sign”, and the evidence of annual healing caused by non-tolerated hibernation in adolescent individuals, also point to the presence of annually intermittent puberty in this population. The hypothesis of hibernation is consistent with the genetic evidence and the fact that the SH hominins lived during a glacial period. The present work will provide a new insight into the physiological mechanism of early human metabolism which could help in determining the life histories and physiologies of extinct human species.


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