This month KDIGO published an executive conclusions paper on CKD-Mineral and Bone Disorder, covering management of calcium, phosphorus, PTH and vitamin D. So in today’s post, I am pulling out all the key info that dietitians need to know.
To read the full article check out the full reference:
Background
CKD-MBD occurs across all stages of CKD and impacts two systems:
- Skeletal
- Cardiovascular
People living with CKD may experience all the traditional risk factors of developing the disorders associated with cardiovascular and/or skeletal disease (osteoporosis). However, in addition to this, CKD-specific risk factors for developing these disorders include:
- Impacts on the immune system related to CKD
- Changes to the Gut ecosystem
- Endocrine changes
- Uremic toxins
- Neurohormonal system changes
Recognizing the complexity of these disorders, the 2025 guidelines acknowledge that prior recommendations lacked comprehensive coverage. As a result, these guidelines divide recommendations based on two overarching clinical syndromes.
- CKD-associated osteoporosis
- CKD-associated CVD
Part 1: CKD-Associated Osteoporosis
Do we still use the term Renal Osteodystrophy?
in the past, clinicians used the term Renal Osteodystrophy (ROD) to describe CKD-related changes to bones. ROD causes global defects in bone quality and strength, increasing fracture risk independently of other bone health markers, such as bone mineral density.
However, the concern with this term is that it takes a relatively narrow focus – specifically monitoring and correcting parathyroid hormone (PTH), calcium and phosphorus while ignoring other components of bone health. Therefore, these guidelines use broader terminology to encourage clinicians to consider bone health beyond the PTH/calcium/phosphorus axis.
What is osteoporosis?
Osteoporosis is a disorder of bone that involves decreasing bone strength and increasing fracture risk. Bone strength encompasses both:
- Amount of bone
- Quality of bone
DXA and CT scans can assess bone quantity. Evaluating bone geometry, microarchitecture, and tissue properties helps assess bone quality. Physicians diagnose osteoporosis by identifying Bone Mineral Density (BMD) scores below 2.5 on DXA scans.
Clinicians should recognize that CKD-associated osteoporosis is a distinct form of osteoporosis that requires unique management strategies.
What role does PTH play in development of bone disease?
High PTH levels may increase bone formation and resorption. This results in changes to the microarchitecture of the bones. Low PTH, related to over supplementation of activated Vitamin D, results in low bone turnover.
What is the right PTH to target?
The previous guidelines recommended targeting a PTH of 2-9 times the upper limit of normal for those with stage 5 CKD. However, it is not clear if this is actually the right target. Unfortunately, these new guidelines do not provide a new target as there is a lack of evidence for what target is right.
What treatments are suggested for high PTH?
While calcimimetics (such as cinacalcet) are effective at lowering PTH, it is important to note that there is no data to suggest that these medications offer survival benefit, reduce fracture risk or cardiovascular events.
Low-dose activated Vitamin D can help lower PTH, but clinicians should avoid high doses, as they increase the risk of hypercalcemia and do not reduce cardiovascular events.
The guidelines also recommend a dietary phosphate restriction, however they do not go further into this recommendations.
What about serum phosphorus?
Hyperphosphatemia has been found to:
- Increase bone resistance to PTH
- Correlates with increased PTH
- Decrease osteocyte viability
- Affect bone quality
Hypophosphatemia is associated with impaired mineralization. The authors recommend maintaining adequate levels. There are no other specifics provided.
What about serum calcium?
Hypercalcemia suppresses PTH and decreases osteocyte viability. Hypocalcemia stimulates PTH and favors mineralization deficits. The authors recommend maintaining adequate levels and ensuring adequate calcium intake.
There are no other specifics provided.
What about Vitamin D?
It is unclear if regular vitamin D supplement impacts clinical outcomes in CKD for people with normal Vitamin D status. Recent studies have not found that routine supplementation improves outcomes.
However, it is recommended to avoid and correct Vitamin D deficiencies.
What about parathyroidectomy?
Evidence suggests that parathyroidectomy improves bone mineral density and reduces mortality more effectively than calcimimetics.
Part 2: CKD-associated CVD
What conditions encompass CKD associated CVD?
Vascular calcification and hyperphosphatemia characterize CKD-associated CVD. However, serum calcium and phosphorus levels do not directly correlate with vascular pathology.
Other CVD conditions include arterial calcification, left ventricular hypertrophy and congestive heart failure.
What about phosphorus?
No new trials since 2017 have necessitated adjustments to serum phosphorus targets. However, studies such as the PHOSPHATE trial, when published may lead to adjustment of targets.
Studies using phosphorus binders in patients (both pre-dialysis and on dialysis) with normal serum levels have failed to demonstrate clinical benefit. Therefore, guidelines do not recommend starting phosphorus binders in people with normal serum levels.
There are no comments here about dietary patterns to control phosphorus levels.
What about calcium?
We do not know the optimal range for serum calcium levels in CKD. However, experts recommend aiming for 800-1000mg of dietary calcium intake for optimal bone health.
4o mini Many patients are likely not getting enough calcium in their diets.
Measuring ionized calcium is preferred over measuring serum calcium values because albumin-adjusting formula calculations do not consistently correlate with ionized calcium values.
Symptoms of hypocalcemia include:
- Muscle spasms
- Myalgia (muscle aches)
- Paresthesis (numbness, tingling)
- Hypoesthesia (reduced sensation)
The guidelines recommend determining the cause of hypocalcemia and correcting it. This differs from the previous guidelines, which considered permissive hypocalcemia acceptable.
What about calcium baths?
Optimal calcium baths for those on dialysis are 1.25-1.50mmol/L. Baths below this tend to result in a negative calcium balance leading to intradialytic cardiovascular instability and hospitalization. Calcium baths above 1.5mmol/L are associated with vascular calcification and increased morality.
Are calcium-free binders better for patient outcomes?
Lanthanum and sevelamer do not reduce vascular calcification compared to calcium. Therefore, the latest guidelines differ from the 2017 recommendation to avoid or limit calcium-based binders.
What about PTH?
When PTH is very high and bone turnover is high, hyperphosphatemia may occur. In these cases, therapies targeting PTH lowering can improve hyperphosphatemia.
What about Vitamin K?
In small studies, Vitamin K and MK-7 appear safe in CKD populations. Results do not suggest that they consistently reduced calcification. (For more about Vitamin K – check out my previous post here).
What about Magnesium?
In animal models, magnesium was found to prevent phosphate-induced vascular calcification. To date, clinical trials on magnesium have been contradictory. The Canadian Dial-Mag study is currently investigating the impact of Magnesium in the dialysate at 0.5 or 0.75mmol/L and may help improve our understanding on the relationship between magnesium and vascular calcification.
Key Take Aways
While there wasn’t much specific to nutrition in these guidelines, I think the key points for dietitians are:
- Ensure Vitamin D deficiencies are treated
- Ensure patients are getting 800-1000mg of calcium, avoid excessive dietary calcium restrictions
- Dietary phosphorus restriction may help with hyperphosphatemia, though how it relates to hard outcomes remains an area under active investigation
- Phosphorus binders do not benefit patients with normophosphatemia
- If indicated, non-calcium based binders haven’t been found to offer consistent vascular protection over calcium-based binders
- If PTH is very high, hyperphosphatemia may be related to bone turnover as opposed to dietary intake.
- Parathyroidectomies appear to have been outcomes for our patients compared to calcimimetics.
