Executive summary of the 2017 KDIGO Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD) Guideline Update: what’s changed and why it matters
Authors: Markus Ketteler, Geoffrey A. Block, Pieter Evenepoel, Masafumi Fukagawa, Charles A. Herzog, Linda McCann, Sharon M. Moe, Rukshana Shroff, Marcello A. Tonelli, Nigel D. Toussaint, Marc G. Vervloet, Mary B. Leonard
Journal: Kidney International (2017)

The KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of CKD-MBD represents a selective update of the prior CKD-MBD Guideline published in 2009. This update, along with the 2009 publication, is intended to assist the practitioner caring for adults and children with chronic kidney disease (CKD), those on chronic dialysis therapy, or individuals with a kidney transplant. This review highlights key aspects of the 2017 CKD-MBD Guideline Update, with an emphasis on the rationale for the changes made to the original guideline document. Topic areas encompassing updated recommendations include diagnosis of bone abnormalities in CKD–mineral and bone disorder (MBD), treatment of CKD-MBD by targeting phosphate lowering and calcium maintenance, treatment of abnormalities in parathyroid hormone in CKD-MBD, treatment of bone abnormalities by antiresorptives and other osteoporosis therapies, and evaluation and treatment of kidney transplant bone disease. The KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of CKD-MBD represents a selective update of the prior CKD-MBD Guideline published in 2009. This update, along with the 2009 publication, is intended to assist the practitioner caring for adults and children with chronic kidney disease (CKD), those on chronic dialysis therapy, or individuals with a kidney transplant. This review highlights key aspects of the 2017 CKD-MBD Guideline Update, with an emphasis on the rationale for the changes made to the original guideline document. Topic areas encompassing updated recommendations include diagnosis of bone abnormalities in CKD–mineral and bone disorder (MBD), treatment of CKD-MBD by targeting phosphate lowering and calcium maintenance, treatment of abnormalities in parathyroid hormone in CKD-MBD, treatment of bone abnormalities by antiresorptives and other osteoporosis therapies, and evaluation and treatment of kidney transplant bone disease. In 2009, Kidney Disease: Improving Global Outcomes (KDIGO) published the KDIGO Clinical Practice Guideline for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD).1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar At that time, the Work Group acknowledged the lack of high-quality evidence on which to base recommendations. Over the years that followed, multiple randomized controlled trials (RCTs) and prospective cohort studies examined some of the key issues underlying the assessment, development, progression, and treatment of CKD-MBD. KDIGO recognizes the need to reexamine the currency of its guidelines on a periodic basis, and therefore convened a Controversies Conference in 2013, titled "CKD-MBD: Back to the Future."2Ketteler M. Elder G.J. Evenepoel P. 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: 502-528Abstract Full Text Full Text PDF PubMed Scopus (110) Google Scholar The conference participants concluded that most of the 2009 recommendations1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar were still applicable in current practice; however, a total of 12 recommendations were identified for revision, based on new data. As a result, a Work Group was convened to undertake a "selective update"3Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work GroupKDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF PubMed Scopus (887) Google Scholar of the 2009 KDIGO CKD-MBD Guideline (Table 1).1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar Notably, despite the availability of results from several new key clinical trials, large gaps of knowledge still remained. Accordingly, many of the "opinion-based" recommendation statements from the 2009 Guideline1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar remain unchanged (see summary of KDIGO CKD-MBD recommendations).Table 1Comparison of the 2017 and 2009 KDIGO CKD-MBD Guideline recommendations2017 revised KDIGO CKD-MBD recommendations3Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work GroupKDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF PubMed Scopus (887) Google Scholar2009 KDIGO CKD-MBD recommendations1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google ScholarBrief rationale for updating3.2.1. In patients with CKD G3a–G5D with evidence of CKD-MBD and/or risk factors for osteoporosis, we suggest BMD testing to assess fracture risk if results will impact treatment decisions (2B).3.2.2. In patients with CKD G3a–G5D with evidence of CKD-MBD, we suggest that BMD testing not be performed routinely, because BMD does not predict fracture risk as it does in the general population, and BMD does not predict the type of renal osteodystrophy (2B).Multiple new prospective studies have documented that lower DXA BMD predicts incident fractures in patients with CKD G3a–G5D. The order of these first 2 recommendations was changed because a DXA BMD result might impact the decision to perform a bone biopsy.3.2.2. In patients with CKD G3a–G5D, it is reasonable to perform a bone biopsy if knowledge of the type of renal osteodystrophy will impact treatment decisions (Not Graded).3.2.1. In patients with CKD G3a–G5D, it is reasonable to perform a bone biopsy in various settings including, but not limited to: unexplained fractures, persistent bone pain, unexplained hypercalcemia, unexplained hypophosphatemia, possible aluminum toxicity, and prior to therapy with bisphosphonates in patients with CKD-MBD (Not Graded).The primary motivation for this revision was the growing experience with osteoporosis medications in patients with CKD, low BMD, and a high risk of fracture. The inability to perform a bone biopsy may not justify withholding antiresorptive therapy from patients at high risk of fracture.4.1.1. In patients with CKD G3a–G5D, treatments of CKD-MBD should be based on serial assessments of phosphate, calcium, and PTH levels, considered together (Not Graded).This new recommendation was provided in order to emphasize the complexity and interaction of CKD-MBD laboratory parameters.4.1.2. In patients with CKD G3a–G5D, we suggest lowering elevated phosphate levels toward the normal range (2C).4.1.1. In patients with G3a–G5, we suggest maintaining serum phosphate in the normal range (2C). In patients with CKD G5D, we suggest lowering elevated phosphate levels toward the normal range (2C).There is an absence of data supporting that efforts to maintain phosphate in the normal range are of benefit to CKD G3a–G4 patients, including some safety concerns. Treatment should be aimed at overt hyperphosphatemia.4.1.3. In adult patients with CKD G3a–G5D, we suggest avoiding hypercalcemia (2C). In children with CKD G3a–G5D, we suggest maintaining serum calcium in the age-appropriate normal range (2C).4.1.2. In patients with CKD G3a–G5D, we suggest maintaining serum calcium in the normal range (2D).Mild and asymptomatic hypocalcemia (e.g., in the context of calcimimetic treatment) can be tolerated in order to avoid inappropriate calcium loading in adults.4.1.4. In patients with CKD G5D, we suggest using a dialysate calcium concentration between 1.25 and 1.50 mmol/l (2.5 and 3.0 mEq/l) (2C).4.1.3. In patients with CKD G5D, we suggest using a dialysate calcium concentration between 1.25 and 1.50 mmol/l (2.5 and 3.0 mEq/l) (2D).Additional studies of better quality are available; however, these do not allow for discrimination of benefits and harm between calcium dialysate concentrations of 1.25 and 1.50 mmol/l (2.5 and 3.0 mEq/l). Hence, the wording is unchanged, but the evidence grade is upgraded from 2D to 2C.4.1.5. In patients with CKD G3a–G5D, decisions about phosphate-lowering treatment should be based on progressively or persistently elevated serum phosphate (Not Graded).4.1.4. In patients with CKD G3a–G5 (2D) and G5D (2B), we suggest using phosphate-binding agents in the treatment of hyperphosphatemia. It is reasonable that the choice of phosphate binder takes into account CKD stage, presence of other components of CKD-MBD, concomitant therapies, and side effect profile (Not Graded).Emphasizes the perception that early "preventive" phosphate-lowering treatment is currently not supported by data (see Recommendation 4.1.2). The broader term "phosphate-lowering" treatment is used instead of phosphate-binding agents since all possible approaches (i.e., binders, diet, dialysis) can be effective.4.1.6. In adult patients with CKD G3a–G5D receiving phosphate-lowering treatment, we suggest restricting the dose of calcium-based phosphate binders (2B). In children with CKD G3a–G5D, it is reasonable to base the choice of phosphate-lowering treatment on serum calcium levels (Not Graded).4.1.5. In patients with CKD G3a–G5D and hyperphosphatemia, we recommend restricting the dose of calcium-based phosphate binders and/or the dose of calcitriol or vitamin D analog in the presence of persistent or recurrent hypercalcemia (1B). In patients with CKD G3a–G5D and hyperphosphatemia, we suggest restricting the dose of calcium-based phosphate binders in the presence of arterial calcification (2C) and/or adynamic bone disease (2C) and/or if serum PTH levels are persistently low (2C).New evidence from 3 RCTs supports a more general recommendation to restrict calcium-based phosphate binders in hyperphosphatemic patients across all severities of CKD.4.1.8. In patients with CKD G3a–G5D, we suggest limiting dietary phosphate intake in the treatment of hyperphosphatemia alone or in combination with other treatments (2D). It is reasonable to consider phosphate source (e.g., animal, vegetable, additives) in making dietary recommendations (Not Graded).4.1.7. In patients with CKD G3a–G5D, we suggest limiting dietary phosphate intake in the treatment of hyperphosphatemia alone or in combination with other treatments (2D).New data on phosphate sources were deemed important to include as an additional qualifier to the previous recommendation.4.2.1. In patients with CKD G3a–G5 not on dialysis, the optimal PTH level is not known. However, we suggest that patients with levels of intact PTH progressively rising or persistently above the upper normal limit for the assay be evaluated for modifiable factors, including hyperphosphatemia, hypocalcemia, high phosphate intake, and vitamin D deficiency (2C).4.2.1. In patients with CKD G3a–G5 not on dialysis, the optimal PTH level is not known. However, we suggest that patients with levels of intact PTH above the upper normal limit of the assay are first evaluated for hyperphosphatemia, hypocalcemia, and vitamin D deficiency (2C). It is reasonable to correct these abnormalities with any or all of the following: reducing dietary phosphate intake and administering phosphate binders, calcium supplements, and/or native vitamin D (Not Graded).The Work Group felt that modest increases in PTH may represent an appropriate adaptive response to declining kidney function and has revised this statement to include "persistently" above the upper normal PTH level as well as "progressively rising" PTH levels, rather than "above the upper normal limit." That is, treatment should not be based on a single elevated value.4.2.2. In adult patients with CKD G3a–G5 not on dialysis, we suggest that calcitriol and vitamin D analogs not be routinely used (2C). It is reasonable to reserve the use of calcitriol and vitamin D analogs for patients with CKD G4–G5 with severe and progressive hyperparathyroidism (Not Graded).4.2.2. In patients with CKD G3a–G5 not on dialysis, in whom serum PTH is progressively rising and remains persistently above the upper limit of normal for the assay despite correction of modifiable factors, we suggest treatment with calcitriol or vitamin D analogs (2C).Recent RCTs of vitamin D analogs failed to demonstrate improvements in clinically relevant outcomes but demonstrated increased risk of hypercalcemia.In children, calcitriol and vitamin D analogs may be considered to maintain serum calcium levels in the age-appropriate normal range (Not Graded).4.2.4. In patients with CKD G5D requiring PTH-lowering therapy, we suggest calcimimetics, calcitriol, or vitamin D analogs, or a combination of calcimimetics with calcitriol or vitamin D analogs (2B).4.2.4. In patients with CKD G5D and elevated or rising PTH, we suggest calcitriol, or vitamin D analogs, or calcimimetics, or a combination of calcimimetics and calcitriol or vitamin D analogs be used to lower PTH (2B).•It is reasonable that the initial drug selection for the treatment of elevated PTH be based on serum calcium and phosphate levels and other aspects of CKD-MBD (Not Graded).•It is reasonable that calcium or non–calcium-based phosphate binder dosage be adjusted so that treatments to control PTH do not compromise levels of phosphate and calcium (Not Graded).•We recommend that, in patients with hypercalcemia, calcitriol or another vitamin D sterol be reduced or stopped (1B).•We suggest that, in patients with hyperphosphatemia, calcitriol or another vitamin D sterol be reduced or stopped (2D).•We suggest that, in patients with hypocalcemia, calcimimetics be reduced or stopped depending on severity, concomitant medications, and clinical signs and symptoms (2D).•We suggest that, if the intact PTH levels fall below 2 times the upper limit of normal for the assay, calcitriol, vitamin D analogs, and/or calcimimetics be reduced or stopped (2C).This recommendation originally had not been suggested for updating by the KDIGO Controversies Conference in 2013. However, due to a subsequent series of secondary and post hoc publications of the EVOLVE trial, the Work Group decided to reevaluate Recommendation 4.2.4 as well. Although EVOLVE did not meet its primary endpoint, the majority of the Work Group members were reluctant to exclude potential benefits of calcimimetics for G5D patients based on subsequent prespecified analyses. The Work Group, however, decided not to prioritize any PTH-lowering treatment at this time because calcimimetics, calcitriol, or vitamin D analogs are all acceptable first-line options in G5D patients.4.3.3. In patients with CKD G3a–G5D with biochemical abnormalities of CKD-MBD and low BMD and/or fragility fractures, we suggest that treatment choices take into account the magnitude and reversibility of the biochemical abnormalities and the progression of CKD, with consideration of a bone biopsy (2D).4.3.3. In patients with CKD G3a–G3b with biochemical abnormalities of CKD-MBD and low BMD and/or fragility fractures, we suggest that treatment choices take into account the magnitude and reversibility of the biochemical abnormalities and the progression of CKD, with consideration of a bone biopsy (2D).Recommendation 3.2.2 now addresses the indications for a bone biopsy prior to antiresorptive and other osteoporosis therapies. Therefore, 2009 Recommendation 4.3.4 has been removed and 2017 Recommendation 4.3.3 is broadened from CKD G3a–G3b to CKD G3a–G5D.4.3.4. In patients with CKD G4–G5D having biochemical abnormalities of CKD-MBD, and low BMD and/or fragility fractures, we suggest additional investigation with bone biopsy prior to therapy with antiresorptive agents (2C).5.5. In patients with G1T–G5T with risk factors for osteoporosis, we suggest that BMD testing be used to assess fracture risk if results will alter therapy (2C).5.5. In patients with an estimated glomerular filtration rate greater than approximately 30 ml/min/1.73 m2, we suggest measuring BMD in the first 3 months after kidney transplant if they receive corticosteroids, or have risk factors for osteoporosis as in the general population (2D).2009 Recommendations 5.5 and 5.7 were combined to yield 2017 Recommendation 5.5.5.7. In patients with CKD G4T–G5T, we suggest that BMD testing not be performed routinely, because BMD does not predict fracture risk as it does in the general population and BMD does not predict the type of kidney transplant bone disease (2B).5.6. In patients in the first 12 months after kidney transplant with an estimated glomerular filtration rate greater than approximately 30 ml/min/1.73 m2 and low BMD, we suggest that treatment with vitamin D, calcitriol/alfacalcidol, and/or antiresorptive agents be considered (2D).•We suggest that treatment choices be influenced by the presence of CKD-MBD, as indicated by abnormal levels of calcium, phosphate, PTH, alkaline phosphatases, and 25(OH)D (2C).•It is reasonable to consider a bone biopsy to guide treatment (Not Graded).There are insufficient data to guide treatment after the first 12 months.5.6. In patients in the first 12 months after kidney transplant with an estimated glomerular filtration rate greater than approximately 30 ml/min/1.73 m2 and low BMD, we suggest that treatment with vitamin D, calcitriol/alfacalcidol, or bisphosphonates be considered (2D).•We suggest that treatment choices be influenced by the presence of CKD-MBD, as indicated by abnormal levels of calcium, phosphate, PTH, alkaline phosphatases, and 25(OH)D (2C).•It is reasonable to consider a bone biopsy to guide treatment, specifically before the use of bisphosphonates due to the high incidence of adynamic bone disease (Not Graded).There are insufficient data to guide treatment after the first 12 months.The second bullet point is revised, consistent with the new bone biopsy recommendation (i.e., 2017 Recommendation 3.2.2).25(OH)D, 25-hydroxyvitamin D; BMD, bone mineral density; CKD, chronic kidney disease; DXA, dual-energy X-ray absorptiometry; MBD, mineral bone disorder; PTH, parathyroid hormone, RCT, randomized controlled trial.Changes to the above summarized recommendations resulted in renumbering of several adjacent guideline statements. Specifically, 2009 Recommendation 4.1.6 now becomes 2017 Recommendation 4.1.7; 2009 Recommendation 4.1.8 now becomes 2017 Recommendation 4.1.9; 2009 Recommendation 4.3.5 now becomes 2017 Recommendation 4.3.4; and 2009 Recommendation 5.8 now becomes 2017 Recommendation 5.7. Open table in a new tab 25(OH)D, 25-hydroxyvitamin D; BMD, bone mineral density; CKD, chronic kidney disease; DXA, dual-energy X-ray absorptiometry; MBD, mineral bone disorder; PTH, parathyroid hormone, RCT, randomized controlled trial. Changes to the above summarized recommendations resulted in renumbering of several adjacent guideline statements. Specifically, 2009 Recommendation 4.1.6 now becomes 2017 Recommendation 4.1.7; 2009 Recommendation 4.1.8 now becomes 2017 Recommendation 4.1.9; 2009 Recommendation 4.3.5 now becomes 2017 Recommendation 4.3.4; and 2009 Recommendation 5.8 now becomes 2017 Recommendation 5.7. Similar to the original 2009 KDIGO CKD-MBD Guideline,1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar development of the 2017 Update3Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work GroupKDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF PubMed Scopus (887) Google Scholar followed a rigorous process of evidence review and appraisal, based on systematic reviews of results from clinical trials. The structured approach was modeled after the GRADE system,4Guyatt G. Oxman A.D. Akl E.A. et al.GRADE guidelines: 1. Introduction-GRADE evidence profiles and summary of findings tables.J Clin Epidemiol. 2011; 64: 383-394Abstract Full Text Full Text PDF PubMed Scopus (5016) Google Scholar which ascribes grades to the quality of the overall evidence and strength for each recommendation. Where appropriate, the Work Group issued "not graded" recommendations, based on general advice, that were not part of a systematic evidence review. Despite the dearth of high-quality evidence identified in several areas pertaining to CKD-MBD, the Work Group was committed to developing a comprehensive guideline document that is of highest value to the nephrology community. The list of research recommendations in each chapter of the 2017 CKD-MBD Guideline Update3Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work GroupKDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF PubMed Scopus (887) Google Scholar should guide future investigations, which in turn will help advance the evidence base in CKD-MBD. At the time of publication of the 2009 KDIGO CKD-MBD Guideline,1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar the literature addressing the ability to estimate fracture risk in CKD from bone mineral density (BMD) measurements by dual-energy X-ray absorptiometry (DXA) was limited to cross-sectional studies that compared BMD in CKD patients with and without a prevalent fracture. These results were variable across studies and across skeletal sites. Due to the lack of evidence that DXA BMD predicted fractures in CKD patients as it does in the general population, and the inability of DXA to indicate the histological type of bone disease, the 2009 Guideline1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar recommended that BMD testing not be performed routinely in patients with CKD G3a to G5D and CKD-MBD. The evidence-based review for the 2017 KDIGO CKD-MBD Guideline Update3Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work GroupKDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF PubMed Scopus (887) Google Scholar identified 4 prospective cohort studies in adults demonstrating that DXA BMD predicted fractures across the spectrum from CKD G3a to G5D. These studies represent a substantial advance since the original 2009 Guideline was published.1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar Despite the fact that the studies were conducted across a range of CKD severity, the finding that hip BMD predicted fractures was consistent across studies, and 2 studies demonstrated associations comparable to those seen in the absence of CKD. Based on these insights, the Work Group concluded that DXA BMD assessment is reasonable if a low or declining BMD will lead to additional interventions to reduce falls or use osteoporosis medications. Renal osteodystrophy is defined as abnormal bone histology and is 1 component of the bone abnormalities of CKD-MBD. Bone biopsy is the gold standard for the diagnosis and classification of renal osteodystrophy. The 2009 KDIGO CKD-MBD Guideline1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar noted that DXA BMD does not distinguish among types of renal osteodystrophy. Further, it concluded that the diagnostic utility of biochemical markers was limited by their poor sensitivity and specificity. Differences in parathyroid hormone (PTH) assays have also contributed to conflicting results across studies. For the 2017 Update,3Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work GroupKDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF PubMed Scopus (887) Google Scholar the Work Group encouraged the continued use of PTH trends, rather than 1-time values, to guide therapy. When PTH trends are inconsistent, a bone biopsy is a reasonable consideration if the results may lead to changes in therapy. The 2009 Guideline1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar recommended a bone biopsy prior to antiresorptive therapy in patients with CKD G4 to G5D and evidence of biochemical abnormalities of CKD-MBD, low BMD, and/or fragility fractures. However, the Work Group is well aware that clinical experience concerning performance and evaluation of bone biopsies may be limited. There is growing evidence that antiresorptive therapies are effective in patients with CKD G3a to G3b and G4, and no robust evidence that these medications induce adynamic bone disease. Therefore, the 2017 Update3Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work GroupKDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD).Kidney Int Suppl. 2017; 7: 1-59Abstract Full Text Full Text PDF PubMed Scopus (887) Google Scholar no longer suggests performing a bone biopsy prior to initiation of these medications. The previous Recommendation 4.1.1 from the 2009 KDIGO CKD-MBD Guideline1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar provided guidance regarding treatment based on serum phosphate levels in different glomerular filtration rate (GFR) categories of CKD. The accumulated evidence did not lead to a substantially different conclusion in that there is an increasing risk of all-cause mortality with increasing levels of serum phosphate in a consistent and direct fashion. For GFR decline and cardiovascular event rate, results were less conclusive. The Work Group considered it reasonable to take the context of therapeutic interventions into account when assessing values of phosphate, calcium, and PTH. Further, it is important to emphasize the interdependency of these biochemical parameters. Based on these assumptions, the Work Group also decided to split the previous 2009 Recommendation 4.1.1 into 2 new Recommendations: 4.1.1 (diagnostic recommendation based on accumulated observational evidence) and 4.1.2 (therapeutic recommendation based mostly on RCTs). Following the publication of the 2009 KDIGO CKD-MBD Guideline,1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar additional high-quality evidence now links higher concentrations of phosphate with mortality among patients with CKD G3a to G5 or after transplantation. However, there is still a lack of trial data demonstrating that therapeutic approaches to lower serum phosphate will improve patient-centered outcomes. The 2009 Guideline1Kidney Disease: Improving Global Outcomes (KDIGO) CKD–MBD Work GroupKDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease–mineral and bone disorder (CKD–MBD).Kidney Int Suppl. 2009; : S1-S130Google Scholar suggested maintaining serum phosphate in the normal range for patients with CKD G3a to G3b and G4. On reevaluating the evidence for the 2