scholarly journals Evaluation of prevalence, biochemical profile, and drugs associated with chronic kidney disease-mineral and bone disorder in 11 dialysis centers

2018 ◽  
Vol 40 (1) ◽  
pp. 26-34 ◽  
Author(s):  
Rodrigo Reis Abrita ◽  
Beatriz dos Santos Pereira ◽  
Neimar da Silva Fernandes ◽  
Renata Abrita ◽  
Rosalia Maria Nunes Henriques Huaira ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Linear Regression Analysis ◽  
Laboratory Data ◽  
Diabetic Patients ◽  
Biochemical Profile ◽  
Mineral And Bone Disorder ◽  
Significant Positive Association ◽  
Bone Disorder

ABSTRACT Introduction: The diagnosis and treatment of mineral and bone disorder of chronic kidney disease (CKD-MBD) is a challenge for nephrologists and health managers. The aim of this study was to evaluate the prevalence, biochemical profile, and drugs associated with CKD-MBD. Methods: Cross-sectional study between July and November 2013, with 1134 patients on dialysis. Sociodemographic, clinical, and laboratory data were compared between groups based on levels of intact parathyroid hormone (iPTH) (< 150, 150-300, 301-600, 601-1000, and > 1001 pg/mL). Results: The mean age was 57.3 ± 14.4 years. The prevalence of iPTH < 150 pg/mL was 23.4% and iPTH > 601 pg/mL was 27.1%. The comparison between the groups showed that the level of iPTH decreased with increasing age. Diabetic patients had a higher prevalence of iPTH < 150 pg/mL (27.6%). Hyperphosphatemia (> 5.5 mg/dL) was observed in 35.8%. Calcium carbonate was used by 50.5%, sevelamer by 14.7%, 40% of patients had used some form of vitamin D and 3.5% used cinacalcet. Linear regression analysis showed a significant negative association between iPTH, age, and diabetes mellitus and a significant positive association between iPTH and dialysis time. Conclusion: The prevalence of patients outside the target for iPTH was 50.5%. There was a high prevalence of hyperphosphatemia (35.8%), and the minority of patients were using active vitamin D, vitamin D analogs, selective vitamin D receptor activators, and cinacalcet. These data indicate the need for better compliance with clinical guidelines and public policies on the supply of drugs associated with CKD-MBD.

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.

Die totale Parathyreoidektomie ohne Autotransplantation und Thymektomie

2009 ◽  
Vol 18 (02) ◽  
pp. 125-127
Author(s):  
F. Keller ◽  
D. Henne-Bruns ◽  
G. Steinbach ◽  
P. Würl ◽  
S. Stracke
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Mineral And Bone Disorder ◽  
Oder Eine ◽  
Bone Disorder ◽  
Pathologische Frakturen

ZusammenfassungDer sekundäre Hyperparathyreoidismus führt zu renaler Osteodystrophie („chronic kidney disease-mineral and bone disorder” [CKDMBD]) und progredienten Gefäßverkalkungen. Indikationen für eine Parathyreoidektomie (PTX) umfassen ein Versagen der medikamentösen Therapie bestehend aus Phosphatbindern, aktivem Vitamin D und Kalzimimetika sowie eine knochenbioptisch nachgewiesene hyperparathyreoide Knochenerkrankung, sonografisch vergrößerte Epithelkörperchen, pathologische Frakturen, therapierefraktärer Juckreiz und/oder eine Kalziphylaxie. Die PTX kann als subtotale oder totale PTX mit und ohne Thymektomie und mit und ohne Autotransplantation von Nebenschilddrüsengewebe erfolgen. Wir favorisieren die totale Parathyreoidektomie ohne Autotransplantation und ohne Thymektomie. Dieses ist ein sicheres, rezidivarmes und kosteneffektives Verfahren, postoperativ einfach substituierbar und ermöglicht die adäquate Dosierung von aktivem Vitamin D.

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.

Vitamin D status and its association with mineral and bone disorder in a multi-ethnic chronic kidney disease population

2014 ◽  
Vol 82 (2014) (10) ◽  
pp. 231-239 ◽  
Author(s):  
Melissa Ngai ◽  
Valerie Lin ◽  
Hung Chew Wong ◽  
Anantharaman Vathsala ◽  
Priscilla How
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vitamin D Status ◽  
Mineral And Bone Disorder ◽  
Bone Disorder ◽  
Chronic Kidney Disease Population

Management of chronic kidney disease-mineral and bone disorder

2018 ◽  
Author(s):  
Alexandra Voinescu ◽  
Nadia Wasi Iqbal ◽  
Kevin J. Martin
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Vascular Calcifications ◽  
Mineral And Bone Disorder ◽  
Natural Form ◽  
Bone Disorder ◽  
P Removal

In all patients with chronic kidney disease (CKD) stages 3–5, regular monitoring of serum markers of CKD-mineral and bone disorder, including calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25-hydroxyvitamin D, and alkaline phosphatase, is recommended. Target ranges for these markers are endorsed by guidelines. The principles of therapy for secondary hyperparathyroidism include control of hyperphosphataemia, correction of hypocalcaemia, use of vitamin D sterols, use of calcimimetics, and parathyroidectomy. of hyperphosphataemia is crucial and may be achieved by means of dietary P restriction, use of P binders, and P removal by dialysis. Dietary P restriction requires caution, as it may be associated with protein malnutrition. Aluminium salts are effective P binders, but they are not recommended for long-term use, as Aluminium toxicity (though from contaminated dialysis water rather than oral intake) may cause cognitive impairment, osteomalacia, refractory microcytic anaemia, and myopathy. Ca-based P binders are also quite effective, but should be avoided in patients with hypercalcaemia, vascular calcifications, or persistently low PTH levels. Non-aluminium, non-Ca binders, like sevelamer and lanthanum carbonate, may be more adequate for such patients; however, they are expensive and may have several side effects. Furthermore, comparative trials have failed so far to provide conclusive evidence on the superiority of these newer P binders over Ca-based binders in terms of preventing vascular calcifications, bone abnormalities, and mortality. P removal is about 1800–2700 mg per week with conventional thrice-weekly haemodialysis, but may be increased by using haemodiafiltration or intensified regimens, such as short daily, extended daily or three times weekly nocturnal haemodialysis. Several vitamin D derivatives are currently used for the treatment of secondary hyperparathyroidism. In comparison with the natural form calcitriol, the vitamin D analogue paricalcitol seems to be more fast-acting and less prone to induce hypercalcaemia and hyperphosphataemia, but whether these advantages translate into better clinical outcomes is unknown. Calcimimetics such as cinacalcet can significantly reduce PTH, Ca, and P levels, but they have failed to definitively prove any benefits in terms of mortality and cardiovascular events in dialysis patients. Parathyroidectomy is often indicated in CKD patients with severe persistent hyperparathyroidism, refractory to aggressive medical treatment with vitamin D analogues and/or calcimimetics. This procedure usually leads to rapid improvements in biochemical markers (i.e. significant lowering of serum Ca, P, and PTH) and clinical manifestations (such as pruritus and bone pain); however, the long-term benefits are still unclear.

scholarly journals Canadian Society of Nephrology Commentary on the Kidney Disease Improving Global Outcomes 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder

2020 ◽  
Vol 7 ◽  
pp. 205435812094427
Author(s):  
Rachel M. Holden ◽  
Reem A. Mustafa ◽  
R. Todd Alexander ◽  
Marisa Battistella ◽  
Micheli U. Bevilacqua ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Clinical Practice ◽  
Kidney Disease ◽  
Clinical Practice Guideline ◽  
Practice Guideline ◽  
Mineral And Bone Disorder ◽  
Bmd Testing ◽  
Prevention And Treatment ◽  
Bone Disorder

Purpose of review: (1) To provide commentary on the 2017 update to the Kidney Disease Improving Global Outcomes (KDIGO) 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD); (2) to apply the evidence-based guideline update for implementation within the Canadian health care system; (3) to provide comment on the care of children with chronic kidney disease (CKD); and (4) to identify research priorities for Canadian patients. Sources of information: The KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of CKD-MBD. Methods: The commentary committee co-chairs selected potential members based on their knowledge of the Canadian kidney community, aiming for wide representation from relevant disciplines, academic and community centers, and different geographical regions. Key findings: We agreed with many of the recommendations in the clinical practice guideline on the diagnosis, evaluation, prevention, and treatment of CKD-MBD. However, based on the uncommon occurrence of abnormalities in calcium and phosphate and the low likelihood of severe abnormalities in parathyroid hormone (PTH), we recommend against screening and monitoring levels of calcium, phosphate, PTH, and alkaline phosphatase in adults with CKD G3. We suggest and recommend monitoring these parameters in adults with CKD G4 and G5, respectively. In children, we agree that monitoring for CKD-MBD should begin in CKD G2, but we suggest measuring ionized calcium, rather than total calcium or calcium adjusted for albumin. With regard to vitamin D, we suggest against routine screening for vitamin D deficiency in adults with CKD G3-G5 and G1T-G5T and suggest following population health recommendations for adequate vitamin D intake. We recommend that the measurement and management of bone mineral density (BMD) be according to general population guidelines in CKD G3 and G3T, but we suggest against routine BMD testing in CKD G4-G5, CKD G4T-5T, and in children with CKD. Based on insufficient data, we also recommend against routine bone biopsy in clinical practice for adults with CKD or CKD-T, or in children with CKD, although we consider it an important research tool. Limitations: The committee relied on the evidence summaries produced by KDIGO. The CSN committee did not replicate or update the systematic reviews.

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