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Table of Contents
CLINICAL PRACTICE
Year : 2019  |  Volume : 5  |  Issue : 4  |  Page : 91-92

At glance translating clinical practice guidelines for mineral bone disease in chronic kidney disease into practice


1 Associate Professor, Department of Nephrology, RML Institiute of Medical Sciences, Lucknow, Uttar Pradesh, India
2 Professor, Department of Nephrology, Sanjay Gabdhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Submission04-May-2020
Date of Acceptance04-May-2020
Date of Web Publication09-Jun-2020

Correspondence Address:
Dr. Abhilash Chandra
Dr. Ram Manohar Lohia Institute of Medical Sciences, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrnm.jrnm_9_20

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How to cite this article:
Chandra A, Saxena A. At glance translating clinical practice guidelines for mineral bone disease in chronic kidney disease into practice. J Renal Nutr Metab 2019;5:91-2

How to cite this URL:
Chandra A, Saxena A. At glance translating clinical practice guidelines for mineral bone disease in chronic kidney disease into practice. J Renal Nutr Metab [serial online] 2019 [cited 2020 Jul 14];5:91-2. Available from: http://www.jrnm.in/text.asp?2019/5/4/91/286282


  Introduction Top


The Kidney Disease Improving Global Outcomes (KDIGO) in 2006 defined mineral and bone disorder (MBD) in chronic kidney disease (CKD) as a systemic disorder of mineral and bone metabolism manifested by one or a combination of the following: (i) abnormalities of calcium, phosphorus, parathyroid hormone (PTH), or Vitamin D metabolism; (ii) abnormalities in bone turnover, mineralization, volume, linear growth, or strength; and (iii) vascular or other soft-tissue calcification.[1]

KDIGO put forth the Clinical Practice Guideline Update in 2017[2] for the diagnosis, evaluation, prevention, and treatment of CKD-MBD, which is a selective update of the prior guideline published in 2009. This article enumerates the simplicity of KDIGO guidelines on CKD-MBD.


  How to Diagnose and Monitor Chronic Kidney Disease-Mineral and Bone Disorder Top


The first step is to test for the presence of biochemical abnormalities.

The guidelines suggest that monitoring of serum levels of calcium, phosphate, PTH, and alkaline phosphatase should begin in CKD G3a. In children, monitoring should begin in CKD G2, and thereafter, monitoring should be continued based on the abnormalities and the rate of progression of CKD [Table 1], [Table 2].
Table 1: Diagnosing and monitoring chronic kidney disease-mineral and bone disorder at glance

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Table 2: KDIGO guide to phosphorus-lowering agents

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In the CKD population, low bone mineral density (BMD) is associated with an increased risk of fractures. In CKD G3a–G5D, if the clinician so deems that BMD testing will influence the intervention to mitigate osteoporotic changes, BMD testing is advisable (provided evidence exists of CKD-MBD and/or risk factors). In the absence of noninvasive biochemical tests' availability for the assessment of the bone disorder despite standard therapy, bone biopsy is a viable option.


  Why Treat Chronic Kidney Disease-Mineral and Bone Disorder? Salient Features for Dietary Counseling Top


The treatment of CKD-MBD is aimed at lowering high serum phosphate and maintaining serum calcium level in both adults and children. High phosphorus values are linked with higher mortality.[3] In CKD G3a–G5D, KDIGO recommends lowering elevated phosphate levels toward the normal range with dietary modifications, phosphate binders, and if required, by intensifying the dialysis sessions. In case of a continuously increasing trend of serum phosphorus level and persistent hyperphosphatemia, phosphate-lowering therapies should be resorted to [Table 3]. Limiting dietary phosphate intake is important. Sources of phosphorus are natural raw unprocessed food, additives, supplements, and medications. Organic phosphorus comes from animal and plant sources. It is less readily absorbed as compared to the inorganic phosphorus from processed food. The bioavailability of plant-based phosphorus is lower than the animal-based phosphorus. Even while restricting dietary phosphate, ensure the provision of adequate protein. High calcium levels have been linked to higher cardiovascular mortality.[4] According to the KDIGO guidelines, low calcium levels can put patients at risk of low BMD, hyperparathyroidism (HPT), and QTc prolongation. Individualize appropriate calcium levels targets.
Table 3: KDIGO recommendations for infants and children

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In CKD, causes of secondary HPT are hypocalcemia, hyperphosphatemia, and Vitamin D deficiency. Evaluate these factors, if levels of intact PTH (iPTH) are progressively rising or persistently above the upper normal limit in patients with CKD G3a–G5 not on dialysis. Use calcitriol and other Vitamin D analogs in patients with CKD G4–G5 with severe and progressive HPT with caution. High PTH values are a compensatory response to several correctable factors. According to the KDIGO, in patients with CKD G5D, maintain iPTH levels in the range of approximately 2–9 times the upper normal limit. Marked changes in the iPTH levels call for an active intervention. In children, maintain serum calcium levels in the age-appropriate range and treat high PTH levels with calcitriol or other Vitamin D analogs. To avoid hypercalcemia, start at a low dose (titrate based on the PTH response). Avoid hypocalcemia also. In patients with CKD G5D requiring PTH-lowering therapy, calcimimetics, calcitriol, or Vitamin D analogs or a combination of calcimimetics with calcitriol or Vitamin D analogs can be used, guided by the current therapy and serum calcium and phosphate values. In patients with CKD G3a–G5D with severe HPT, parathyroidectomy is indicated in case pharmacological therapy fails.

KDIGO recommends the same management as for the general population in patients with CKD G1–G2 with osteoporosis and/or high risk of fracture and also for G3a–G3b with normal PTH and osteoporosis and/or high risk of fracture.

Keeping in view the magnitude of biochemical abnormalities of CKD-MBD and low BMD and/or fragility fractures, bisphosphonates, other osteoporosis medications, and growth hormone therapy should be considered in patients with CKD G3a–G5D. Rule out osteomalacia due to Vitamin D deficiency or endemic fluorosis before the commencement of any therapy. Antiresorptive or anabolic therapy warrants a careful evaluation of the side effect profile and cost.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Ketteler M, Elder GJ, Evenepoel P, Ix JH, Jamal SA, Lafage-Proust MH, et al. Revisiting KDIGO clinical practice guideline on chronic kidney disease-mineral and bone disorder: A commentary from a kidney disease: Improving global outcomes controversies conference. Kidney Int 2015;87:502-28.  Back to cited text no. 1
    
2.
Isakova T, Nickolas TL, Denburg M, Yarlagadda S, Weiner DE, Gutiérrez OM, et al. KDOQI US commentary on the 2017 KDIGO Clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD). Am J Kidney Dis 2017;70:737-51.  Back to cited text no. 2
    
3.
Eddington H, Hoefield R, Sinha S, Chrysochou C, Lane B, Foley RN, et al. Serum phosphate and mortality in patients with chronic kidney disease. Clin J Am Soc Nephrol 2010;5:2251-7.  Back to cited text no. 3
    
4.
Moe SM. Calcium as a cardiovascular toxin in CKD-MBD. Bone 2017;100:94-9.  Back to cited text no. 4
    



 
 
    Tables

  [Table 1], [Table 2], [Table 3]



 

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