Calcium is a bit of a controversial topic in CKD – is it good for bone health or bad for calcification? As I have discussed before, calcification is problematic for those living with CKD and there is increasing interest in ways to help slow it down, but what about calcium? What should we say about that?
Well, fortunately, there was a recent publication from the European Renal Nutrition group to help us wade through what we should be telling people about calcium.
Today’s article:
What do we need calcium for?
Calcium is required for:
- Neuromuscular function
- Enzyme processes
- Blood Clotting
- Skeletal Rigidity (bone health)
Ionized calcium is the circulating form of calcium that is used for non-bone calcium jobs. In cases of low calcium intake, calcium will be taken from the bone to promote normal circulating levels.
In the 1990s there was increasing recognition of vascular calcification and increasing concern that excess calcium intake in CKD was contributing to cardiovascular death. This lead to the growing popularity of non-calcium based binders and medications like cinacalcet to suppress parathyroid hormone levels. This has lead the authors of the paper to ask:
Have we been so restrictive with calcium in CKD that we are causing calcium deficiencies?
The authors highlight that serum calcium levels are not reflective of calcium status. It isn’t a biomarker, like urine potassium is.
In my own practice, I haven’t seen such a shying away from calcium and activated Vitamin D. I am not sure if this is related to insurance programs that cover phosphorus binders in both Alberta and BC, where I have worked.
In Alberta there was very little coverage for non-calcium based binders, so we continued to rely heavily on calcium. In BC there is coverage for non-calcium based binders, but patients only qualify for coverage of these drugs if calcium is contra-indicated or failing to achieve therapeutic targets.
What are the dietary sources of calcium?
The authors highlight that the main sources of calcium come from dairy products, which are often restricted for people living with kidney disease because these foods are also high in phosphorus. They go on to discuss that many foods are also fortified with calcium, which can be an option for increasing dietary calcium intake.
My two cents: It was interesting to me in this section that they didn’t discuss the source of calcium used in fortification. In my experience, in Canada, a very common source of calcium for fortification is calcium phosphates. This leads me to worry that many calcium fortified sources would be worse for patients that naturally occurring calcium in an otherwise high phosphorus food (though that’s up for debate too!)
How is calcium intake assessed?
The authors highlight that several methods can be used to assess calcium intake and offer a few nutrition screeners that can be used. I found one from Osteoporosis Canada. I tried it on myself, but I found it difficult to use.
The authors also state that a rapid bedside estimation can be done by doing a diet history of a typical 24 hour period, though this statement isn’t referenced. Given what we know about the systematic errors that can occur in self-reporting of dietary intake, I was surprised to see that this method was recommended in this paper.
Several underlying mechanisms are discussed that likely lead to decreased calcium absorption in CKD:
- Altered gut physiology
- Hypovitaminonsis D
- Vitamin D hyporesponsiveness
- Hypogonadism
Adults living with CKD have decreased urinary calcium excretion as the disease progresses, though it is unknown if this is related to decreased absorption or decreased kidney function.
What about calcium balance for those on dialysis?
For patients on dialysis, the calcium concentration of the dialysate can impact calcium balance. HD bath concentrations of 1.25-1.5mmol/L are considered neutral (they neither contribute or take calcium). For PD patients, most solutions are considered calcium neutral, with the exception of Icodextran. Icodextran will contribute to positive calcium balance because it has a concentration of 1.75mmol/L calcium concentration.
How much calcium should we recommend?
The authors of this paper recommend aiming for a minimum total calcium intake of 800-1000mg (elemental) calcium. They suggest an upper limit of 1500mg elemental calcium per day, unless there is a clinical need for increased calcium, for example during hungry bone syndrome.
The authors highlight that intakes between 1500-2000mg (or higher) are likely to result in positive calcium balance. It is hypothesized that extra calcium will lead to calcification of soft tissues, though this hasn’t been proven.
What should we do when patient’s have hypercalcemia?
The most common causes of hypercalcemia are:
- Excess calcium (either from diet, supplements or the dialysate) or excess Vitamin D
- Tertiary hyperparathyroidism
- Malignancy(cancerous cells), granulomatous diseases (e.g. sarcoidosis), thyroid disease or immobilization.
The authors recommend that those with hypercalcemia should reduce their calcium and vitamin D containing medication and/or calcium dialysate. Pathological considerations, including malignancy and sarcoidosis should be investigated.
What should we do when patient’s have hypocalcemia?
Hypocalcemia is considered a life threatening condition. Acute, severe or symptomatic hypocalcemia requires prompt management, most often IV calcium or increases in the dialysate. The most common causes of hypocalcemia are:
- Hungry bone syndrome post parathyroidectomy.
- Anti-resorptive therapy (osteoporosis medications such as prolia)
- Calcimimetics (such as cinacalcet)
In cases of hungry bone, for example post parathyroidectomy, increasing calcium and vitamin D supplementation is suggested. Temporary increases in calcium dialysate to 1.75mmol/L are considered appropriate in these cases.
The article continues to reinforce that increases in the calcium dialysate should be considered a temporary measure. The authors do not make specific recommendations about whether or not calcium supplementation should go above 1500mg of elemental calcium in cases of chronic hypocalcemia.
Take Aways
I admit that this article left me with a number of unanswered questions. What do we do in cases of patients with chronic hypocalcemia with no obvious cause? The frequent mention of short-term high Ca dialysate leaves me wondering if chronic hypocalcemia is better than long term high calcium exposure. Though this wasn’t discussed.
That being said, here are my key take aways:
- Adequate calcium intake for CKD is recommended for health. Patients should be encouraged to get 800-1000mg of calcium each day, regardless of their serum calcium levels.
- For those with mild hypocalcemia treatment with calcium supplements, vitamin D, and potentially calcium-based phosphorus binders as appropriate. The maximum suggested calcium dose is 1500mg elemental calcium.
- For those with hypercalcemia, remove excess calcium sources (supplements, diet, vitamin D, dialysate). Consider medical work up for malignancy or sarcoidosis (this goes beyond nutrition).
- For those with persistent, chronic hypocalcemia – I remain at a loss of what to do. Does the risks of hypocalcemia outweigh the risks of high doses of calcium supplements or dialysate? Based on this article alone, I don’t know.
