scholarly journals Mineral and bone disorders secondary to chronic kidney disease (renal osteodystrophy)

2015 ◽  
Vol 5 (2) ◽  
pp. 91
Author(s):  
Alphonsus N. Onyiriuka ◽  
Olubunmi B. Fakeye-Udeogu ◽  
Mohammad Abdullahi ◽  
Chiedozie J. Achonwa ◽  
Isaac O. Oluwayemi ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Renal Osteodystrophy ◽  
Bone Disorders

scholarly journals CLINICAL PROFILE OF MINERAL BONE DISORDERS (RENAL OSTEODYSTROPHY) IN CHRONIC KIDNEY DISEASE PATIENTS

2021 ◽  
pp. 107-110
Author(s):  
ASHISH KHATTAR ◽  
KARTHIK RAO N ◽  
RAVINDRA PRABHU ◽  
BUDDHI RAJ POKHREL ◽  
SHANTI GURUNG ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Radial Artery ◽  
Renal Osteodystrophy ◽  
Clinical Profile ◽  
Biochemical Tests ◽  
Bone Disorders ◽  
Ckd Stage ◽  
High Prevalence ◽  
The Mean

Objective: The objective of the study was to evaluate the clinical profile of mineral bone disorders (renal osteodystrophy) in chronic kidney disease (CKD) patients. Methods: A retrospective study was performed involving 100 patients above 15 years of age with previously diagnosed chronic renal failure. A series of tests such as biochemical, radiological, and arterial calcifications were monitored. The mean age of subjects in our study was 52.54 years. Results: Biochemical tests revealed that hypocalcemia was present in 54% of the patients, and hyperphosphatemia was seen in 84% of the participants, while only 22% of the participants had high alkaline phosphate (ALP) levels. Radiological tests revealed that 39 patients had aortic calcification, 42 patients had radial artery calcification, and 27 patients had both. Subperiosteal resorption was seen on 29 participants. The majority of the vascular calcification and subperiosteal resorption was seen in patients with CKD Stage 5, and both aortic and radial artery calcifications were significantly associated with subperiosteal bone resorption. Conclusion: The results point toward a high prevalence of derangement in the mineral, vascular and valvular calcifications. Serum total ALP can serve as a biochemical marker to identify a pattern of bone turnover where intact parathyroid hormone is not available. The results highlight that serum phosphorus and Ca × P product levels were significantly associated with both aortic and radial artery calcifications. There was no significant association of these calcifications with serum calcium and ALP levels.

Renal Osteodystrophy in Peritoneal Dialysis: Special Considerations

2008 ◽  
Vol 28 (2_suppl) ◽  
pp. 11-19 ◽  
Author(s):  
Ronen Levy ◽  
Anca Gal-Moscovici
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Peritoneal Dialysis ◽  
Kidney Disease ◽  
Renal Osteodystrophy ◽  
Bone Disease ◽  
Bone Lesion ◽  
Phosphate Binders ◽  
Vitamin D Metabolites ◽  
Bone Disorder

Bone disease is one of the most challenging complications in patients with chronic kidney disease. Today, it is considered to be part of a complex systemic disorder manifested by disturbances of mineral metabolism and vascular calcifications called chronic kidney disease – mineral bone disorder (CKD-MBD). The term renal osteodystrophy is reserved to define the specific bone lesion in CKD-MBD, whose spectrum ranges from high turnover to low turnover disease. Phosphate retention, decreased serum calcium, and 1,25-dihydroxy vitamin D synthesis are involved in the pathogenesis of high bone turnover. However, the various therapeutic approaches (calcium supplements, phosphate binders, and vitamin D metabolites, among others), the renal replacement modality (hemodialysis or continuous ambulatory peritoneal dialysis), and the types of patients to whom dialysis is offered (more patients who are diabetic or older, or both) may influence the evolution of the bone disorder. As a result, recent studies have reported a greater prevalence of adynamic forms of renal osteodystrophy, especially in diabetic and peritoneal dialysis patients. The present article reviews, for patients treated with peritoneal dialysis, the pathophysiologic mechanisms involved in the evolution and perpetuation of this bone disease and the therapeutic modalities for treating and preventing adynamic bone.

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.

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