This is a nice summary of the latest guidelines on diagnosis and management of mineral bone disease induced by chronic kidney disease. Kidney anomaly can be classified functionally via estimated GFR or structurally via proteinuria.
Guidelines emphasize the need for bone density scan, bone biopsy, parathyroid hormone, calcium and phosphorus measures in the right context. Vitamin D analogs and phosphate binders are also discussed. See below for detailed recommendations.
Annals of Internal Medicine
In patients with CKD G3a–G5D:
- With evidence of CKD–MBD (mineral bone disorder) and/or risk factors for osteoporosis, we suggest BMD (bone mineral density) testing to assess fracture risk if results will impact treatment decisions.
- It is reasonable to perform a bone biopsy if knowledge of the type of renal osteodystrophy will impact treatment decisions.
- Treatments of CKD–MBD should be based on serial assessments of phosphate, calcium, and PTH levels, considered together.
- We suggest lowering elevated phosphate levels toward the normal range.
- We suggest avoiding hypercalcemia.
- Decisions about phosphate-lowering treatment should be based on progressively or persistently elevated serum phosphate.
- Receiving phosphate-lowering treatment, we suggest restricting the dose of calcium-based phosphate binders.
- We suggest limiting dietary phosphate intake in the treatment of hyperphosphatemia alone or in combination with other treatments. It is reasonable to consider phosphate source (e.g., animal, vegetable, additives) in making dietary recommendations.
- 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.
- Not on dialysis, we suggest that calcitriol and vitamin D analogues NOT be routinely used.
- It is reasonable to reserve the use of calcitriol and vitamin D analogues for patients with CKD G4–G5 with severe and progressive hyperparathyroidism.
- 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.
In patients with CKD G5D:
- We suggest using a dialysate calcium concentration between 1.25-1.50 mmol/L.
- Requiring PTH-lowering therapy, we suggest calcimimetics, calcitriol, or vitamin D analogues, or a combination of calcimimetics with calcitriol or vitamin D analogues.
More from the publication:
Chronic kidney disease (CKD) is defined as abnormalities in kidney structure or function that are present for more than 3 months and have health implications. The disease is classified on the basis of cause and category of glomerular filtration rate (GFR) (G1 to G5) and albuminuria (A1 to A3).
As kidney function decreases, marked changes in bone mineral metabolism occur, resulting in increased risk for fractures, cardiovascular disease, and overall mortality. In 2009, Kidney Disease: Improving Global Outcomes (KDIGO) published the Clinical Practice Guideline for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD–MBD). Based on evidence from new clinical trials, an updated clinical practice guideline was published in 2017.
The 2017 update provides recommendations for diagnosis of bone abnormalities in CKD–MBD, treatment of CKD–MBD by decreasing serum phosphate levels and maintaining serum calcium levels, treatment of parathyroid hormone (PTH) abnormalities in CKD–MBD, treatment of bone abnormalities using antiresorptive agents and other osteoporosis therapies, and evaluation and treatment of kidney transplant bone disease.
This synopsis focuses on diagnosis of CKD–MBD and management of serum phosphate, calcium, and PTH levels in adults—areas in which controversy and knowledge gaps exist. Recommendations for children and kidney transplant recipients are not addressed in this synopsis, but interested readers can refer to the guideline update for details.
The data support use of DXA BMD testing if the results will affect future treatment. Because such testing does not distinguish among types of renal osteodystrophy, bone biopsy remains the diagnostic gold standard. For patients at high risk for fracture, facilities that lack the ability to perform bone biopsy or evaluate the results should not withhold antiresorptive therapy.
The interplay among biochemical variables (serum phosphate, calcium, and PTH) in patients with CKD–MBD received considerable attention during the review of the current evidence. It is apparent that therapeutic maneuvers aimed at improving one variable often have unintended effects on others. Thus, treatment approaches for CKD–MBD should be based on serial assessments of these variables taken together.
Current evidence does not show benefit to maintaining normal serum phosphate levels in patients not receiving dialysis, and there are safety concerns associated with aggressive phosphate-lowering therapy. Thus, treatment should focus on patients with overt hyperphosphatemia. In the case of calcium, new evidence suggests that hypercalcemia may be harmful in all GFR categories of CKD, prompting the recommendation to avoid inappropriate calcium loading in adults whenever possible. Use of calcium-based phosphate binders should also be restricted in patients with hyperphosphatemia across the CKD spectrum.
The 2009 recommendations for treatment of SHPT were expanded to reflect that modest increases in PTH may represent an appropriate adaptive response to decreasing kidney function. The current recommendation is to treat patients with PTH values that are progressively increasing or persistently above the upper limit of normal and not to base treatment on a single elevated value. Treatment approaches for SHPT in patients not receiving dialysis should not include routine use of calcitriol or vitamin D analogues due to the increased risk for hypercalcemia. Calcimimetics, calcitriol, and vitamin D analogues are acceptable first-line options in patients receiving dialysis.
Future RCTs should be conducted to compare the ability of calcium-containing and calcium-free phosphate binders to promote bone accrual, as well as their effect on arterial calcification. Studies on dietary phosphate intake should compare phosphate sources (vegetable, meat, or “hidden” sources, such as food additives). Prospective trials should use a benefit–risk–cost ratio to identify the most effective phosphate-lowering approach across all CKD GFR categories; such studies should include patient-centered and surrogate end points, including vascular calcification, FGF23 levels, and LVH. Multicenter studies examining patient-level outcomes are needed to determine the benefits and risks of treatment with calcitriol or vitamin D analogues in patients with CKD stage G3a-G5 and mild or severe SHPT. Placebo-controlled trials are also needed to compare calcimimetics with standard therapy in patients with CKD stage G5D and SHPT, with an emphasis on FGF23 reduction as a therapeutic end point.