- Pro: Should we correct vitamin D deficiency/insufficiency in chronic kidney disease patients with inactive forms of vitamin D or just treat them with active vitamin D forms?
- BACKGROUND—VITAMIN D DEFICIENCY—IT'S COMPLICATED!
- PLEIOTROPIC EFFECTS OF VITAMIN D—EXTRA-SKELETAL EFFECTS (THE ‘EVERYTHING ELSE’ FACTOR)
- CONFLICT OF INTEREST STATEMENT
- High Phosphorus (hyperphosphatemia)
- Vitamin D for Your Bones
- Vitamin D Deficiency
- Why do I need vitamin D and how do I get it?
- How much vitamin D do I need?
- What causes vitamin D deficiency?
- Who is at risk of vitamin D deficiency?
- What problems does vitamin D deficiency cause?
- How can I get more vitamin D?
- Can too much vitamin D be harmful?
- Excess Vitamin D Linked to Kidney Damage
- Supplements and Sunlight Triggered Toxicity
- How Vitamin D Improves Bone & Kidney Health
- Vitamin D for Bone & Kidney Health Snapshot
- Vitamin D Improves Bone Health
- Vitamin D Prevents Rickets and Osteomalacia
- Vitamin D Prevents Osteoporosis and Fractures
- Vitamin D & Kidney Health
- Read More
Pro: Should we correct vitamin D deficiency/insufficiency in chronic kidney disease patients with inactive forms of vitamin D or just treat them with active vitamin D forms?
Evidence for the usefulness of using vitamin D to treat ‘renal bone disease’ is now nearly six decades old. In regular clinical practice, however, it is more three decades, at most, that we have routinely been using vitamin D to try to prevent, or reverse, the impact of hyperparathyroidism on the skeleton of patients with chronic kidney disease (CKD).
The practice has been in the main to use high doses of synthetic vitamin D compounds, not naturally occurring ones. However, the pharmacological impacts of the different vitamin D species and of their different modes, and styles of administration cannot be assumed to be uniform across the spectrum.
It is disappointingly true to say that even in 2016 there is a remarkable paucity of evidence concerning the clinical benefits of vitamin D supplementation to treat vitamin D insufficiency in patients with stage 3b–5 CKD. This is even more so if we consider the non-dialysis population.
While there are a number of studies that report the impact of vitamin D supplementation on serum vitamin D concentrations (unsurprisingly, usually reporting an increase), and some variable evidence of parathyroid hormone concentration suppression, there has been much less focus on hard or semi-rigid clinical end point analysis (e.g.
fractures, hospitalizations and overall mortality).
Now, in 2016, with the practice pattern changes of first widespread clinical use of vitamin D and second widespread supplementation of cholecalciferol or ergocalciferol by patients (alone, or as multivitamins), it is now, in my view, next to impossible to run a placebo-controlled trial over a decent period of time, especially one which involved clinically meaningful (fractures, hospitalisation, parathyroidectomy, death) end-points. In this challenging situation, we need to ask what it is we are trying to achieve here, and how best to balance potential benefits with potential harm.
hyperparathyroidism, mineral and bone disorder, PTH, vitamin D
For the purpose of this debate, I am confining my remarks to patients with chronic kidney disease (CKD) stage 3b, 4 and 5 (5ND and 5D). I am not, in this essay, discussing earlier CKD (stages 1, 2 and 3a), mostly now managed by non-specialists, nor am I debating or discussing the complex matter of the ideal management of post-transplantation bone pathology.
My esteemed and learned opponent and I have no quarrel about the relevance of vitamin D to the health and well-being of patients with clinically significant CKD; we both agree that vitamin D plays an important role in the management of skeletal, and possibly other, complications of CKD. It would be hard indeed to find an opponent who could successfully rise to the task of opposing the use of vitamin D at all in this clinical situation, despite a lamentable lack of hard evidence to support this practice.
Where my opponent and I do differ, however, is not so much about what cards we need to have at our disposal, but the order in which these cards are best played.
Changing metaphors now, my opponent uses the most powerful weapons in his armamentarium as soon as he can. I prefer a more nuanced, subtle, approach to the same problem before deploying my heavier artillery, and only if I need to.
This is indeed one of the (many) distinguishing features between America and Great Britain.
It is important, therefore, to appreciate where the ‘fault line’ is between us. It is ly to reside around the issue of proportionality, and gradualness, as opposed to reliance on ‘shock and awe’. Let us now examine our dossier of evidence, to support the deployment of our weapons of mass distraction.
BACKGROUND—VITAMIN D DEFICIENCY—IT'S COMPLICATED!
Vitamin D, or calciferol, is a generic term and refers to a group of lipid soluble compounds with a four-ringed cholesterol backbone structure. 25-Hydroxyvitamin D [25(OH)D] is the major circulating form of vitamin D. It has a half-life of ∼3 weeks, compared with 24 h for parent vitamin D. It has activity at bone and intestine, but has 30 ng/mL) .
At 16 weeks of follow-up, more patients assigned to paricalcitol achieved a 30% reduction in PTH compared with patients assigned to ergocalciferol (53 versus 18%, respectively). The rates of hypercalcaemia and hyperphosphataemia were not different between groups.
However, this type of trial is only too reminiscent of the worst days of erythropoiesis-stimulating agent (‘ESA’) trials, where ESA ‘A’ was pitted against ESA ‘B’ to reveal a slew of irrelevant but often wildly over-interpreted differences in surrogate outcomes. Not very valuable information, except, perhaps, for the trial organizers.
For example, as with the previous 12-week study duration , just 16-week therapy in this study is without common sense as a reasonable time frame to correct a biochemical abnormality that ly has taken months to years to develop.
PLEIOTROPIC EFFECTS OF VITAMIN D—EXTRA-SKELETAL EFFECTS (THE ‘EVERYTHING ELSE’ FACTOR)
Perhaps if we were prepared, or able, to start the correction of vitamin D deficiency gently and early, using nutritional vitamin D from CKD stages 3a and 3b, and not leaving this matter until there is significant PTH elevation/resistance, the bone pathology associated with progressive CKD would be easier to manage (and patients would also have any benefit of pleiotropic benefits—remembering that probably two-thirds of deaths in CKD stage 3a are cardiovascular, not renal in origin).
It is often asserted, but not yet proven in a properly conducted RCT, that vitamin D supplementation is associated with better survival, in any patient cohort.
Effects on endothelial function, micro-circulation, arterial stiffness, blood pressure parameters, left ventricular hypertrophy (LVH) and function, numerous proxies for inflammation, glucose tolerance, insulin sensitivity, acute and chronic infection rates (bacterial, viral, other) and acute asthma have all been reported —but as yet, these glimmers are all too readily extinguished by the icy blasts of scepticism.
Several RCTs are currently investigating the potential effect of nutritional vitamin D on LVH (NCT01323712), insulin resistance (NCT00893451), erythropoietin dosing (NCT01395823), proteinuria (NCT01426724), immunity (NCT00892099), arteriovenous fistula maturation (NCT00912782), and physical and cognitive performance (NCT00511225, NCT01229878).
We will not be able to make a good judgement about this critically important point until we have the results from a number of well-conducted epidemiological trials, examining overall, cardiovascular and bone-related events. The VITAL study from the USA is the largest, and most eagerly awaited, of these mega-trials [1, 20].
Many of these trials are due to report in the next 24 months, and on these findings, we need to rest our case for vitamin D supplementation across the board, or, just selective patient treatment, or possibly even reservation of treatment for existing actual disease states (such as bone diseases) rather than just for a cluster of high-risk factors.
It is quite depressing seeing how little we actually know about the genesis, implications and potential impacts of vitamin D deficiency, and treatment, in CKD, even though for some decades, we have been busy deploying various vitamin D species in an effort to render certain biochemical analytes more acceptable to scrutiny. Certainly, there is little evidence of true patient-level benefit, in what is clearly a much more complex paradigm than we perhaps had ever imagined it to be.
Thus, in the spirit of primum non nocere, knowing first the propensity of active vitamin D compounds, especially deployed in large doses over long periods of time, to engender their own biochemical consequences—hypercalcaemia, hyperphosphataemia—and potentially also accelerate vascular calcification [21, 22], I think it is more prudent to start the fight against ‘bone disease’ using cheap, natural and safe interventions, such as ergocalciferol and cholecalciferol, at the very first signs of PTH elevation (CKD stage 3a/b). This might well mandate earlier (in CKD terms) testing of serum PTH calcium and 25(OH)D concentrations. This would need rigorous clinical testing of course, in different ways. I am happy to concede that, with appropriate attempts to control phosphate, calcium and PTH using diet, dialysis (where needed), phosphate binders and ‘natural’ vitamin D species, if the PTH is still deranged, and we feel compelled to continue to try to reduce its serum concentration, we can then swap the use of natural vitamin D species for one of the many alien, unnatural, ones.
In the end, neither my opponent nor I has been able to administer a knock-out blow on the other. Neither of us has the evidence at our disposal to do that. This is more the First World War than it is about the Nuclear Age.
Progress is slow, grindingly so at times, the terrain is unpromising, and the ‘promised land’ totally sight.
I truly believe in fact that we need to adopt a different approach to future trial design for this clinical paradigm—replicating the complex sequential series of interventions we use in the clinical situation—optimization of phosphate management, careful but sustained repletion of 25(OH)D, good dialysis for those patients in CKD 5D—selecting ‘real’ patients, across many units, and following their clinical progress in the real world to delineate real clinical outcomes of relevance—randomization under these circumstances is still possible, and of course, so is stratification for a number of potential confounders. We just first have to stop pretending that we have at our disposal a single miraculous intervention—be it drug ‘A’, ‘B’ or ‘C’—for a ‘simple’ clinical problem (elevated serum PTH), and that this wonder drug can be given over a short space of time, has no side effects, and thus that it is the nostrum, the panacea, the holy grail de nos jours.
CONFLICT OF INTEREST STATEMENT
D.G. has received speaking and consulting fees from Abbvie, Amgen, Genzyme, Sanofi and Shire.
(See related articles by Agarwal and Georgianos. Con: Nutritional vitamin D replacement in chronic kidney disease and end-stage renal disease. Nephrol Dial Transplant 2016; 31: 706–713; Zoccali and Mallamaci. Moderator's view: Vitamin D deficiency treatment in advanced chronic kidney disease: a close look at the emperor's clothes. Nephrol Dial Transplant 2016; 31: 714–716)
, , . The trials and tribulations of vitamin D: time for the ‘sunshine’ vitamin to come in the cold—or just more broken promises? Expert Rev Endocrinol Metab ; : –Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Work Group. KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). ; : –, , et al. . Changes in serum 25-hydroxyvitamin D and plasma intact PTH levels following treatment with ergocalciferol in patients with CKD. ; : , , et al. . Impact of ergocalciferol treatment of vitamin D deficiency on serum parathyroid hormone concentrations in chronic kidney disease. ; : , , et al. . Vitamin D supplementation in chronic kidney disease: a systematic review and meta-analysis of observational studies and randomized controlled trials. ; : , , et al. . Cholecalciferol supplementation alters calcitriol-responsive monocyte proteins and decreases inflammatory cytokines in ESRD. ; : , , . Effect of 18 months of treatment with alfacalcidol on bone in patients with mild to moderate chronic renal failure. ; : , , et al. . Paricalcitol versus ergocalciferol for secondary hyperparathyroidism in CKD stages 3 and 4: a randomized controlled trial. ; : ., , et al. . Ergocalciferol supplementation in hemodialysis patients with vitamin D deficiency: a randomized clinical trial. ; , , et al. . Paricalcitol versus ergocalciferol for secondary hyperparathyroidism in CKD stages 3 and 4: a randomised controlled trial. ; : –
High Phosphorus (hyperphosphatemia)
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Phosphorus is a common mineral. It is found in many foods, drinks and even some medicines.
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Phosphorus in your body comes from three places:
- The food you eat
- What you drink
- The medicines you take
Foods and drinks that are very high in phosphorus include:
- Milk and cheese
- Red meat
- Dried beans and peas
- Nuts and nut butters
- Whole grain bread
- Dark-colored sodas
Foods that are low in phosphorus include:
- Fresh fruits
- Fresh vegetables
Download the phosphorus food guide to find out about phosphorus in many common foods.
For more information on keeping track of phosphorus in the foods you eat, recipes low in phosphorus, and cooking demonstrations for low-phosphorus recipes, visit Kidney Kitchen.
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The normal amount of phosphorus in the blood (also called serum phosphorus) is between 2.5 – 4.5 mg/dL. This is for an otherwise healthy person. Click here for what your phosphorus numbers should be when you have kidney disease.
Having too much phosphorus in your blood is also called hyperphosphatemia. Too much phosphorus in your blood can cause problems. One of these problems is bone disease.
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Phosphorus works with calcium and vitamin D in your body to keep your bones healthy and strong.To do this, your body’s phosphorus, calcium and vitamin D all need to be in balance.
When you have too much phosphorus in your blood, it causes your body to pull calcium from your bones to try and keep your blood balanced. This can cause your bones to become weak and unhealthy. Unhealthy bones put you at higher risk of breaks (fractures) and other problems.
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Healthy kidneys also help keep your bones healthy. They do this in two ways:
- Your kidneys keep the right amounts of phosphorus and calcium in your body. When your kidneys are not working well, too much phosphorus can build up in your blood. This is called hyperphosphatemia.
- Your kidneys also help your body use vitamin D. When your kidneys are not working, your body may not be able to use vitamin D it should. This can also cause your bones to get weak.
Too much phosphorus or not enough vitamin D in your blood puts you balance. Your body tries to “fix” this using a hormone called parathyroid hormone (PTH). PTH pulls calcium from your bones to try and put your blood back in balance. This loss of calcium can eventually cause bone disease.
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As you read above, you need healthy kidneys to keep healthy bones. When you have kidney disease your bones are also at risk.
In the very early stages of CKD, you will probably not have any problems with how your body controls your phosphorus. However, if your kidney disease gets worse, you may also start to have problems controlling your phosphorus.
Talk to your doctor about what your phosphorus levels should be. Learn about the tests and symptoms of bone disease here
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As kidney disease gets worse, so do many other problems. When your kidneys fail and you need dialysis or a transplant, you will need to be very careful in how you manage your phosphorus. The good news is, there are many ways to manage your phosphorus through medicine and diet.
Talk to your healthcare team about how to best manage your phosphorus so that you prevent bone disease. How you manage your phosphorus will depend on several things, including:
- Your usual diet
- The kind of dialysis you are doing
- The medicines you are taking
- How your lab numbers are doing
If you are on dialysis, it is very important that you do not skip dialysis treatments! Your doctor may also suggest changing the number and length of dialysis sessions to get rid of extra phosphorus.
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Yes. Bone disease can still occur even after you have a kidney transplant. This can happen for several reasons, but the most common being:
- Damage to your bones from your kidney disease before the transplant
- Side effects of the medicines that stop your new kidney from being rejected (also called immunosuppressants).
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If you have kidney disease, it is important to manage your phosphorus levels. This can help prevent bone disease.
Steps you can take to manage your phosphorus levels include:
- Take a phosphate binder
- This is a pill you take with meals
- Keeps your body from absorbing the phosphorus from foods and drinks
- Help keep phosphorus from building up in your blood.
- Limit how much phosphorus you eat and drink each day.
- Ask your doctor or dietitian how much phosphorus you should have daily.
- Download our phosphorus food guide for information on amounts of phosphorus in common foods.
- Take a calcitriol supplement.
- A supplement that helps your body use the calcium and phosphorus it needs.
- Exercise and increase your daily activity. The more you do this, the more phosphorus your body gets rid of!
- Do not smoke or use tobacco.
- Take your all medicines exactly as your doctor prescribes.
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Bone disease often does not have any symptoms until your bones are very weak. The only way to know if you have, or are at risk for, bone disease is to be tested.
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Blood tests for bone health usually include the following:
|Phosphorus blood testNote: This is sometimes listed on lab results as “phosphate”||Checks the level of phosphorus in the blood. A high level means too much phosphorus is in your blood. This is called hyperphosphatemia.|
|Parathyroid hormone (PTH) blood test||Checks the level of PTH in your blood. Too much PTH in the blood can be a sign of a problem. Too much phosphorus or not enough vitamin D in your blood puts you balance. Your body tries to “fix” this using a hormone called parathyroid hormone (PTH). PTH pulls calcium from your bones to try and put your blood back in balance. This loss of calcium can eventually cause bone disease.|
|Calcium blood test||Checks the amount of calcium in your blood. Calcium levels tend to get lower as kidney function worsens. This occurs for many reasons. Calcium levels in your blood are looked at along with phosphorus, vitamin D and PTH levels to determine bone health.|
|Vitamin D blood test||Checks the level of vitamin D in the blood. Active Vitamin D is used by your body to keep bones strong and the right levels of phosphorus and calcium in the blood. Healthy kidneys activate vitamin D from food, vitamin D supplements and sunlight so your body can use it.|
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Bone disease, or damage to the bones, can be caused by having a high level of phosphorus in the blood over time. To prevent bone damage, your doctor may recommend a combination of medicines, diet changes, and exercise.
To know for certain whether your bones have been damaged, you may have to have more than blood tests. Other tests for bone health might include:
|Bone density scan||Uses X-rays to see how many grams of calcium and other bone minerals are packed into a segment bone.|
|X-ray||Creates a picture of a bone and is used to view and assess the bone for signs of damage.|
|Bone biopsy||A piece of tissue is removed from the bone and checked under a microscope for signs of bone damage.|
|Physical exam||Your body is checked carefully to find visible changes in bone structure.|
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Managing your phosphorus is one of many things your doctor might talk about when you are diagnosed with kidney disease.
Here are some questions you can bring with you to your appointment to ask your nephrologist:
- Do I need to worry about my phosphorus level at my stage of kidney disease?
- What should my phosphorus levels be?
- How often should I have my phosphorus blood levels checked?
- When should I start thinking about limiting the phosphorus in my diet?
- Should I take phosphate binders?
- Are there different types of phosphate binders?
- Which binder should I take?
- When do I need to take my phosphate binders? Before I eat a meal, after, or during?
- How often do I need to take phosphate binders?
- How many phosphate binders should I take?
- Would you recommend any other medicines?
- Can exercise help lower my phosphorus?
- Will dialysis remove any phosphorus?
- What happens if my phosphorus is not controlled? What symptoms should I look out for?
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- How much phosphorus do you recommend I eat every day/week?
- What's the best way to track the amount of phosphorus I eat?
- How do I find phosphorus on a food label?
- When do I need to take my phosphate binders? Before I eat a meal, after, or during?
- Do my blood test results show my phosphorus level at just that moment or over time?
- Are there any foods I should completely avoid?
- What is the difference between natural and added phosphorus? Is one type better than the other?
- Is there any way to remove or reduce phosphorus in food?
- What should I do when eating from a restaurant?
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For more information about managing phosphorus, check out our webinars on phosphorus for people with kidney disease.
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Take our free online continuing education (CE) course on Managing Hyperphosphatemia
The goals of this course are to:
- Identify and understand the challenges dietitians and other allied health professionals face in managing hyperphosphatemia in their patients.
- Describe the different metabolism and impact of organic and inorganic phosphorus sources and identify food sources of both.
- Identify effective tools and strategies health professionals can employ in their own practice.
CE credits: 1.00 Commission on Dietetic Registration (CDR); 1.20 NANT; 1.00 Attendance
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Vitamin D for Your Bones
Vitamin D has many important jobs in your body. It keeps your bones strong by helping your body absorb calcium and phosphorus, key minerals for bone health. Your muscles use it to move, and nerves need it to carry messages throughout your body.
But many people don’t get enough vitamin D. Find out the best ways to get what you need and whether a supplement might be a good idea for you.
The amount you need depends on your age:
- 600 IU (international units) a day for people ages 1 to 70, including women who are pregnant or breastfeeding
- 800 IU a day for anyone over 70
Some experts think that these recommendations are too low, especially for people who are more ly to get the bone-thinning disease osteoporosis. Ask your doctor how much vitamin D is best for you.
It is possible to get too much vitamin D. Doses above 4,000 IU a day can be harmful for people ages 9 and older. (Children ages 1 to 8 shouldn’t get more than 2,500-3,000 IU.) It’s hard to get that much from food, but it might happen if you take too many vitamin D supplements.
Your body makes the nutrient when the sun shines directly on your skin. Just 10 to 15 minutes of sunlight without sunscreen a couple of times a week usually gives you enough vitamin D.
But it’s also important to protect your skin, since too much time under the sun’s rays can cause skin cancer.
When you’re out in the sun for more than a few minutes, it’s best to wear sunscreen or clothing that covers you up.
So how else can you get this nutrient? A few foods have it naturally, including:
· Fatty fish salmon, tuna, and mackerel. They’re the best source of vitamin D.
· Beef liver, cheese, and egg yolks
· Mushrooms have a small amount
In the U.S., other foods are fortified with vitamin D, such as:
· Breakfast cereal
· Some orange juice, yogurt, and soy drinks
It’s best to get vitamin D from sunlight and food, but you can also get it in a supplement.
Vitamin D helps the body absorb calcium and phosphorus from the food you eat. So the nutrient is important for people with osteoporosis.
Studies show that calcium and vitamin D together can build stronger bones in women after menopause. It also helps with other disorders that cause weak bones, rickets.
If you’re concerned about your bone health, ask your doctor if you should think about taking a supplement.
People who have low levels of vitamin D also may need supplements. That includes those who:
- Are over 50
- Get very little sun
- Have kidney disease or conditions that affect how their bodies absorb minerals
- Have darker skin
- Are lactose intolerant, meaning they can’t digest the sugar in dairy foods
- Are vegan
- Are infants who eat only breast milk
- Those who take certain anticonvulsant drugs
Vitamin D deficiency is also common for people living in the northern parts of the U.S.
Studies have found prescription-strength vitamin D lotions can help people with psoriasis. Researchers have also studied how it affects other conditions from cancer to high blood pressure, but the evidence is unclear.
At normal doses, vitamin D seems to have few side effects. But if you take any medications, be careful — it can interact with many medicines, such as drugs for high blood pressure and heart problems. Ask your doctor if it's safe for you to take vitamin D supplements.
Too much vitamin D can cause loss of appetite, the need to pee a lot, nausea, and weight loss. High doses of vitamin D can also make you disoriented and lead to bone pain and kidney stones.
SOURCES:Institute of Medicine: “Dietary Reference Intakes for Calcium and vitamin D.”
Longe, J., ed. The Gale Encyclopedia of Alternative Medicine, second edition, 2004.
National Osteoporosis Foundation: “NOF Scientific Statement: National Osteoporosis Foundation's Updated Recommendations for Calcium and Vitamin D3 Intake.”Natural Standard Patient Monograph: “Vitamin D.”Office of Dietary Supplements: “Vitamin D.”
WebMD Feature: “Boning up on Calcium.”
National Institutes of Health: “Vitamin D.”
Mayo Clinic: “Vitamin D toxicity: What if you get too much?”
© 2019 WebMD, LLC. All rights reserved.
Vitamin D Deficiency
URL of this page: https://medlineplus.gov/vitaminddeficiency.html
Also called: Hypovitaminosis D, Low Vitamin D
Vitamin D deficiency means that you are not getting enough vitamin D to stay healthy.
Why do I need vitamin D and how do I get it?
Vitamin D helps your body absorb calcium. Calcium is one of the main building blocks of bone. Vitamin D also has a role in your nervous, muscle, and immune systems.
You can get vitamin D in three ways: through your skin, from your diet, and from supplements. Your body forms vitamin D naturally after exposure to sunlight. But too much sun exposure can lead to skin aging and skin cancer, so many people try to get their vitamin D from other sources.
How much vitamin D do I need?
The amount of vitamin D you need each day depends on your age. The recommended amounts, in international units (IU), are
- Birth to 12 months: 400 IU
- Children 1-13 years: 600 IU
- Teens 14-18 years: 600 IU
- Adults 19-70 years: 600 IU
- Adults 71 years and older: 800 IU
- Pregnant and breastfeeding women: 600 IU
People at high risk of vitamin D deficiency may need more. Check with your health care provider about how much you need.
What causes vitamin D deficiency?
You can become deficient in vitamin D for different reasons:
- You don't get enough vitamin D in your diet
- You don't absorb enough vitamin D from food (a malabsorption problem)
- You don't get enough exposure to sunlight.
- Your liver or kidneys cannot convert vitamin D to its active form in the body.
- You take medicines that interfere with your body's ability to convert or absorb vitamin D
Who is at risk of vitamin D deficiency?
Some people are at higher risk of vitamin D deficiency:
- Breastfed infants, because human milk is a poor source of vitamin D. If you are breastfeeding, give your infant a supplement of 400 IU of vitamin D every day.
- Older adults, because your skin doesn't make vitamin D when exposed to sunlight as efficiently as when you were young, and your kidneys are less able to convert vitamin D to its active form.
- People with dark skin, which has less ability to produce vitamin D from the sun.
- People with disorders such as Crohn's disease or celiac disease who don't handle fat properly, because vitamin D needs fat to be absorbed.
- People who have obesity, because their body fat binds to some vitamin D and prevents it from getting into the blood.
- People who have had gastric bypass surgery
- People with osteoporosis
- People with chronic kidney or liver disease.
- People with hyperparathyroidism (too much of a hormone that controls the body's calcium level)
- People with sarcoidosis, tuberculosis, histoplasmosis, or other granulomatous disease (disease with granulomas, collections of cells caused by chronic inflammation)
- People with some lymphomas, a type of cancer.
- People who take medicines that affect vitamin D metabolism, such as cholestyramine (a cholesterol drug), anti-seizure drugs, glucocorticoids, antifungal drugs, and HIV/AIDS medicines.
Talk with your health care provider if you are at risk for vitamin D deficiency. There is a blood test which can measure how much vitamin D is in your body.
What problems does vitamin D deficiency cause?
Vitamin D deficiency can lead to a loss of bone density, which can contribute to osteoporosis and fractures (broken bones).
Severe vitamin D deficiency can also lead to other diseases. In children, it can cause rickets. Rickets is a rare disease that causes the bones to become soft and bend. African American infants and children are at higher risk of getting rickets. In adults, severe vitamin D deficiency leads to osteomalacia. Osteomalacia causes weak bones, bone pain, and muscle weakness.
Researchers are studying vitamin D for its possible connections to several medical conditions, including diabetes, high blood pressure, cancer, and autoimmune conditions such as multiple sclerosis. They need to do more research before they can understand the effects of vitamin D on these conditions.
How can I get more vitamin D?
There are a few foods that naturally have some vitamin D:
- Fatty fish such as salmon, tuna, and mackerel
- Beef liver
- Egg yolks
You can also get vitamin D from fortified foods. You can check the food labels to find out whether a food has vitamin D. Foods that often have added vitamin D include
- Breakfast cereals
- Orange juice
- Other dairy products, such as yogurt
- Soy drinks
Vitamin D is in many multivitamins. There are also vitamin D supplements, both in pills and a liquid for babies.
If you have vitamin D deficiency, the treatment is with supplements. Check with your health care provider about how much you need to take, how often you need to take it, and how long you need to take it.
Can too much vitamin D be harmful?
Getting too much vitamin D (known as vitamin D toxicity) can be harmful. Signs of toxicity include nausea, vomiting, poor appetite, constipation, weakness, and weight loss.
Excess vitamin D can also damage the kidneys. Too much vitamin D also raises the level of calcium in your blood.
High levels of blood calcium (hypercalcemia) can cause confusion, disorientation, and problems with heart rhythm.
Most cases of vitamin D toxicity happen when someone overuses vitamin D supplements. Excessive sun exposure doesn't cause vitamin D poisoning because the body limits the amount of this vitamin it produces.
- Vitamin D and Health (Harvard School of Public Health)
Excess Vitamin D Linked to Kidney Damage
Vitamin D has been reported to have a wide range of benefits. However, a recent case study indicates that excessive use of vitamin D can cause kidney damage in people who are not deficient in the vitamin.
The article was published online April 8 in the Canadian Medical Association Journal.
“The aim of this case study is to inform a wider audience that vitamin D at large doses [10,000 IU daily] in patients with normal serum vitamin D levels can lead to toxicity,” first author Bourne Auguste, MD, University of Toronto, Ontario, Canada, told Medscape Medical News.
“The public should know that taking more vitamin D than is recommended does not necessarily lead to added benefit. Rather, it can lead to increased harm and specifically kidney failure,” he added.
2010 guidelines from Osteoporosis Canada recommend 400–1000 IU of vitamin D daily for most adults, and 800–2000 IU daily for older adults and those at increased risk for osteoporosis. The US recommended daily intake of vitamin D for males and females between the ages of 1 and 70 years is 600 IU daily and 800 IU for those older than 70 years.
Because vitamin D has a wide therapeutic range, toxicity is rare, Auguste and colleagues note. However, as a fat-soluble vitamin, high doses of it taken for extended periods can lead to buildup.
“Many patients think of vitamin D as a simple supplement with no harm and perhaps historically overstated benefits,” Auguste said. “Given that it is so readily available in various over-the-counter formulations and the perception that it has many benefits with no harm, other patients [besides the one in this case study] may be at risk for vitamin D toxicity and potentially kidney failure.”
Vitamin D toxicity has a wide range of symptoms, which can delay diagnosis. Those symptoms include, among others, fatigue, high blood pressure, frequent urination, confusion, and itchiness. Early recognition of vitamin D toxicity may prevent chronic kidney damage.
“Vitamin D toxicity may go unrecognized for a long period of time, given the nonspecific symptoms patients may have on presentation. Patients may be taking over-the-counter supplements without full disclosure,” Auguste explained.
Management includes careful review of prescription and over-the-counter medications, limiting exposure to sunlight, decreasing dietary and supplemental sources of vitamin D, and monitoring vitamin D levels in asymptomatic patients. Because it is fat soluble, it can take several months for levels to return to normal. In addition, after stopping vitamin D supplements, calcium levels may continue to increase before reversing.
“Clinicians should also consider adjunctive therapies beyond cessation of vitamin D and calcium supplements, such as hydroxychloroquine, glucocorticoids, and ketoconazole in those patients who are symptomatic to decrease the active form of vitamin D in the body,” Auguste advised.
Supplements and Sunlight Triggered Toxicity
The reported case concerns a 54-year-old man who had recently returned from a trip to Southeast Asia, where he had spent an extended time sunbathing (6–8 hours per day for 2 weeks).
Upon returning to Canada, a family physician found that his creatinine level was elevated (132 μmol/L from a baseline of 100 μmol/L).
Four weeks later, despite discontinuing antihypertensive medication and diuretics, which could have caused dehydration and elevations in creatinine, the patient's creatinine level was even higher (376 μmol/L), and he was referred to a kidney specialist.
Further questioning revealed that the man had seen a naturopath who had prescribed high doses of vitamin D. Despite no known history of bone loss or vitamin D deficiency, the man took 8000–12000 IU of vitamin D daily for 2.5 years.
Workup disclosed hypercalcemia (ionized calcium, 1.48 mmol/L) and elevated levels of vitamin D (1,25-dihydroxyvitamin D3 level, 274 pmol/L; 25-hydroxyvitamin D3, 241 nmol/L). Renal biopsy results showed kidney damage (nephrosclerosis and microcalcifications without sarcoidosis or light chain deposition).
The nephrologist advised him to stop taking vitamin D supplements and to stop eating calcium-rich foods. His diuretics remained on hold, and the patient resumed taking one antihypertensive medication.
At the second visit, physicians found that his levels of 1,25-dihydroxyvitamin D3 (the biologically active form of vitamin D) and calcium had continued to increase.
The patient also described new-onset skin itchiness, ly due to his high calcium levels.
The patient declined to receive glucocorticoids because of concerns about weight gain. Upon starting hydroxychloroquine 400 mg daily, his calcium and vitamin D levels decreased. Almost 1 year later, his calcium and vitamin D levels returned to normal, but he has stage 3B chronic kidney disease.
The authors have disclosed no relevant financial relationships.
CMAJ. Published online April 8, 2019. Full text
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How Vitamin D Improves Bone & Kidney Health
Vitamin D is required for healthy, strong bones and calcium absorption. Limited research suggests that vitamin D might also protect the kidneys. Continue reading to learn about its role in bone and kidney health.
Vitamin D for Bone & Kidney Health Snapshot
- Required for bone health and calcium absorption
- May prevent osteoporosis in older adults, along with calcium
- Supplementation ly improves bone health in the elderly who are at a higher risk of deficiency
- Insufficient evidence for kidney protection
Vitamin D is a fat-soluble vitamin the body needs to build and maintain strong bones. It helps absorb calcium in the gut, keeping calcium and phosphorus in balance to mineralize bones .
Without enough vitamin D, bones can become thin, weak, brittle, or misshapen. Getting enough vitamin D prevents rickets in children and osteomalacia in adults. Along with calcium, vitamin D also helps protect older adults from osteoporosis .
The body naturally makes vitamin D when exposed to sunlight. Getting regular, moderate sun exposure is a safe way to maintain normal vitamin D levels during the summer months.
Vitamin D is also found in certain foods, such as fatty fish salmon and sardines. Additionally, many vitamin D supplements are available on the market.
Many older adults don’t get enough vitamin D from sunlight. The elderly also tend to have poor vitamin D absorption, which puts them at a higher risk of deficiency. Taking a supplement with vitamin D may be beneficial for bone health in such cases .
There is insufficient evidence to recommend vitamin D for kidney health, though early research findings are promising.
Taken at the recommended doses, vitamin D supplements are considered safe. However, taking too much can be harmful. Vitamin D supplements may also interact with prescription medications. Remember to talk to your doctor before supplementing!
Vitamin D Improves Bone Health
Vitamin D maintains calcium and phosphorus balance in the body. Specifically, it promotes calcium and phosphorus absorption from the gut, calcium reabsorption in the kidney, and calcium mobilization in bone [2, 3, 4].
Additionally, vitamin D suppresses parathyroid hormone and reduces bone degradation, thus indirectly increasing bone mass [5, 6].
Bone cells also use vitamin D to grow and remodel bones. In turn, vitamin D regulates the growth and function of bone-building cells (osteoblasts) [7, 8].
However, in cell-based studies, higher doses of this vitamin stimulate cells that degrade bones (osteoclasts) due to its narrow therapeutic range. This further emphasizes the importance of taking vitamin D at the recommended doses [6, 9].
Vitamin D Prevents Rickets and Osteomalacia
Vitamin D deficiency causes rickets in infants, young children, and adolescents and osteomalacia in adults [10, 11].
Rickets is characterized by a delay in the mineralization of growth cartilage. Bones soften over time and become deformed, leading to growth retardation, enlargement of the epiphyses of the long bones, and leg deformities [11, 12].
Maternal vitamin D deficiency can affect the skeletal development of fetuses. In a study of 424 pregnant women, mothers with a deficiency were more ly to have fetuses with femoral bones that had rachitic features .
Osteomalacia is an absence or delay in the mineralization of newly-formed bone collagen. Adults with osteomalacia may experience global bone discomfort, and muscle aches and weakness [12, 14, 12].
Osteomalacia and rickets attributable to vitamin deficiency are preventable with an adequate nutritional intake of this vitamin. Varying doses and treatment regimes have been described with the aim is to achieve a blood level between 20 and 50 ng/mL .
Vitamin D Prevents Osteoporosis and Fractures
Low blood levels of vitamin D are associated with lower bone mineral density, mineralization defects, and an increased risk of bone loss or fracture in both men and women [16, 17, 18, 19].
This vitamin should be considered for the therapy of osteoporosis, alone or in a combination with other therapeutic bone agents [20, 21].
Studies show that in adults aged 50 years or older, vitamin D supplementation in combination with calcium has beneficial effects on bone mineral density, osteoporotic fractures and falls without evidence of harm [22, 23, 24].
In elderly women that were given 1,200 mg of calcium and 800 IU of vitamin D3 daily for 3 years, the risk of hip fracture was reduced by 43% and the risk of fractures, in general, was reduced by 32% .
Populations that shield themselves from the sun or who have dark skin, African American and Hispanic men, may be at elevated risk of vitamin deficiency and fractures [26, 19].
However, the annual administration of high doses of vitamin D (500,000 IU) resulted in an increased risk of falls and fractures in older community-dwelling women .
Vitamin D & Kidney Health
Chronic kidney disease patients have a higher prevalence of vitamin D deficiency compared to the general population .
Supplementation decreases elevated calcium levels in chronic kidney disease patients thus preventing multiple organ dysfunction [29, 30].
Studies suggest that vitamin D deficiency or insufficiency is frequent after renal transplantation .
The VITALE study (VITamin D supplementation in renal transplant recipients) showed that high doses of vitamin D prevent posttransplant bone loss without causing adverse events .
According to other studies, vitamin D prevents kidney damage in sepsis-induced acute kidney injury [33, 34].
In one study, it protected patients with diabetic kidney disease from kidney injuries .
Despite these promising findings, more large-scale studies are needed before vitamin D can be routinely recommended for people with kidney disease.