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3 Ongoing Clinical Trials Aiming at Studying the Effects of Vitamin D3 on Extra-Osseous Criteria After Renal Transplantation, Including Graft Function and Rejection
Vitamin D in Acute and Chronic Rejection of Transplanted Kidney
allograft function using estimated glomerular filtration rate; proteinuria; graft
survival; blood pressure control; the incidence of infection; echocardiography findings; bone mineral density; the incidence of fractures; and biological relevant
parameters of mineral metabolism. The VITA-D study  (Vitamin D3 Substitution
in Vitamin D Deficient Kidney Transplant Recipients; ClinicalTrials.gov Identifier:
NCT00752401) is a double-blind, randomized, placebo-controlled study of RTR
deficient in vitamin D, focusing on the impact of cholecalciferol substitution on
graft function (MDRD eGFR), incidence of acute rejection episodes, and posttransplant infections within the first year after renal transplantation. In total, 200
RTR with serum 25(OH)D level of less than 20 ng/ml at time of transplantation will
be randomized to receive either cholecalciferol (6,800 IU/day during 1 year) or
placebo. The CANDLE-KIT study (Correcting Anemia and Native Vitamin D
Supplementation in Kidney Transplant Recipients; ClinicalTrials.gov Identifier:
NCT01817699) is an open-label randomized controlled trial with four arms: (1) no
intervention: low haemoglobin (Hb) target (Hb level: ≥9.5 and <10.5 g/dL) without
cholecalciferol; (2) low Hb target with cholecalciferol 1,000 IU/day; (3) high Hb
target (Hb level: ≥12.5 and <13.5 g/dL) without cholecalciferol, and (4) the experimental arm: high Hb target with cholecalciferol 1,000 IU/day. This study will recruit
324 RTR, who are at least 1 year post-transplantation. The primary endpoint will be
the change in allograft kidney function using MDRD estimated GFR. Among the
secondary endpoints are urinary markers of kidney injury, the dose of methoxypolyethylene glycol epoetin β required to maintain the target Hb level, blood pressure, cardiac biomarkers, left ventricular mass index, acute cellular rejection,
bone-turnover markers, intact PTH, bone mineral density, cardiovascular events,
all-cause death, and cancer development or recurrence.
Further studies in RTR will help to elucidate if VDR activation, directly through
administration of active vitamin D compounds or indirectly via administration of
native vitamin D, might protect long-term graft function by reducing acute rejection
episodes, proteinuria and renal fibrosis. We are awaiting the results of ongoing interventional clinical trials, which should help us answer this question.
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Nutrition and Dietary Vitamin D in Chronic
Abstract Although the main source of vitamin D is not nutritional, some foods
contain significant amounts of vitamin D. Fatty fish liver oil such as cod liver and
fatty fish are the main natural source of dietary vitamin D3. White fish, offal (liver,
kidney), egg yolk, and to a lesser extent meat (muscle) also contain significant
amounts of vitamin D3, while dairy products (non fortified) contain very small
amounts of vitamin D3 with the exception of butter that has significant amounts of
vitamin D3 due to its high fat content. Mushrooms seem to be the only significant
source of vitamin D2, and are the only non-animal-based foods containing vitamin
D. As it has been demonstrated that some animal foods (meat, offal, egg yolk) contain 25(OH)D, and that 25(OH)D is better and more quickly absorbed than native
vitamin D, it is now accepted that this metabolite contributes significantly to the
vitamin D status. Food fortification is a good way to eradicate severe vitamin D deficiency (i.e. 25(OH)D <12 ng/mL) in the general population assuming staple foods
are supplemented taking into account the nutritional habits and the diversity of consumption. In CKD patients however, the higher target serum 25(OH)D concentration
makes that individualized pharmacological supplementation (i.e. adapting the dosage with the help of serum 25(OH)D measurement) should probably be preferred.
Keywords Vitamin D • Cholecalciferol • Ergocalciferol • 25-hydroxyvitamin D •
Calcitriol • Food sources • Food fortification • Biofortification • Chronic kidney
The term vitamin D refers to two different molecules, ergocalciferol, or vitamin D2,
of plant origin, and cholecalciferol, or vitamin D3, of animal/human origin. These
two secosteroids are chemically close from each other, vitamin D2 differing from
J.-C. Souberbielle, MD
Laboratoire d’explorations fonctionnelles, Hôpital Necker-Enfants Malades, Paris, France
© Springer International Publishing Switzerland 2016
P.A. Ureña Torres et al. (eds.), Vitamin D in Chronic Kidney Disease,
Fig. 27.1 Simplified
representation of vitamin
D, 25-hydroxyvitamin D
Vitamine D3 (D2)
25(OH) Vitamine D3 (D2)
1,25(OH)2 Vitamine D3 (D2)
vitamin D3 only by having a double bond between C22 and C23, and a methyl residue in C24 as represented in Fig. 27.1. To become fully active, vitamin D, either D2
or D3, needs to be hydroxylated twice. A first hydroxylation occurs in the liver to
Nutrition and Dietary Vitamin D in Chronic Kidney Disease
form 25-hydroxyvitamin D [25(OH)D], which has a long half-life and whose serum
concentration is the consensual marker of the vitamin D status. A second hydroxylation occurs in the proximal tubule of the kidney as well as in many other tissues to
form 1,25-dihydroxyvitamin D [1,25(OH)2D], also called calcitriol, the active
metabolite. The renal production of 1,25(OH)2D is tightly regulated, mainly stimulated by parathyroid hormone (PTH) and inhibited by Fibroblast Growth Factor 23
(FGF23). 1,25(OH)2D produced by the proximal tubular cells is released into the
bloodstream and binds, in distant target tissues, to a specific receptor, the VDR, to
exert genomic effects. It can thus be considered as a hormone.
Vitamin D is not a vitamin stricto sensu (i.e. a “vital” compound that the body is not
able to produce), as its main source comes from the synthesis by the skin when we
expose ourselves to UVB-rays. However, vitamin D (D2 or D3) is also a vitamin in some
way as a few natural dietary sources exist, and as pharmacological supplementation and/
or food fortification with vitamin D are commonly available, at least in some countries.
The aim of this chapter is to present the various dietary sources of vitamin D, and
to discuss their capacity to improve the vitamin D status of the general population
as well as of CKD patients.
Dietary Sources of Vitamin D2 and Vitamin D3
In the following paragraphs, vitamin D intakes/contents are expressed in μg. To
convert into international units (IU), multiply the μg by 40 (1 μg = 40 IU).
Reviewing the relevant literature leads to the remark that evaluating the exact
vitamin D content of a given natural food is far from an easy task. First, the analytical
methods that have been used to measure vitamin D in foods, mostly HPLC or mass
spectrometry, are not standardized (i.e. do not use the same calibrator) and differ
sometimes greatly in their extraction step [1, 2]. Second, for a given mass (say 100 g)
of a given animal species, the vitamin D content varied greatly in the published
reports, depending on the fat content of the studied piece of food , whether the
animal lived indoor or outdoor, and, for those living outdoor, on the season the animal has been sacrificed , and whether the animal has been supplemented with
vitamin D [4, 5] or has a diet rich in vitamin D (a good example is the twice higher
vitamin D content in wild salmon compared to farmed salmon ).
Having said that, it is clear that fatty fish liver oil such as cod liver oil  (seldom
consumed outside the high latitude countries such as Norway, Iceland, or Greenland),
and fatty fish are the main natural source of dietary vitamin D3 [8, 9]. White fish,
offal (liver, kidney), egg yolk, and to a lesser extent meat (muscle) also contain
significant amounts of vitamin D3, while dairy products (non fortified) contain very
small amounts of vitamin D3 (with the exception of butter that has significant
amounts of vitamin D3 due to its high fat content) .
Concerning vitamin D2, only mushrooms seem to be a significant source, and are
the only non-animal-based food containing vitamin D. Vitamin D2 contents
are large in many wild mushrooms such as the chanterelle, and in mushrooms that are
cultivated outdoors, while the total content of vitamin D2 in mushrooms that are
cultivated indoors depends whether the mushrooms have been irradiated by UVB
rays . While it has been suggested that vitamin D2 is insignificant in the human
diet, it was calculated from a recent nutrition survey that the median vitamin D2
intake of the Irish general population was close to 2 μg/day . Interestingly, it
was recently shown that some mushrooms such as the shiitake mushroom are able
to produce vitamin D4, a form of vitamin D, produced from the irradiation of
22,23-dihydroergocalciferol, that is similar to vitamin D3, but with a methyl group
on carbon 24 of the vitamin D3 side chain . Although the exact potency of vitamin D4 in humans is unknown, it has been shown to be approximately 60 % as
active as vitamin D3 in healing rickets in the rat .
25(OH)D as a Dietary a Source of Vitamin D
While the mean vitamin D intake that is usually calculated from food frequency
questionnaires (FFQs) in the general population during various nutrition surveys is in
the range of 3–4 μg [13–15], it has been recently hypothesized that the food inputs of
vitamin D3 are in fact probably larger . Indeed, despite discrepancies in the evaluation of the increase in serum 25(OH)D concentration for each μg of ingested vitamin
D 3 (considered to be of approximately 1 nmol/L in mean with a huge inter-individual
variability by some authors [17, 18], and approximately 2 nmol/L by others ), this
apparent intake of 3–4 μg seems too low to explain the mean measured 25(OH)D
concentration of approximately 50 nmol/L that is observed in winter in some populations living at latitude higher than 40° (i.e. when vitamin D3 skin synthesis is absent),
who do not consume vitamin D-fortified foodstuffs or pharmacological supplements.
As it has been demonstrated that some animal foods contain 25(OH)D, and that
25(OH)D is better and more quickly absorbed than native vitamin D , it is now
accepted that this metabolite contributes significantly to the 25(OH)D serum concentration of certain persons . Indeed, while 25(OH)D contents are very low in dairy
and fish, it has been reported to be between 0.15 and 0.5 μg/100 g in meat and offal and
between 0 and 4 μg/100 g in egg yolk depending on the supply of dietary vitamin D3
or 25(OH)D3 to the laying hen, with a mean content of 1 μg/100 g [2, 20]. Furthermore,
intervention studies showed that 25(OH)D3 is about five times more effective in raising serum 25(OH)D levels than an equivalent amount of vitamin D3, 1 μg 25(OH)D
corresponding thus to approximately 5 μg vitamin D (200 IU) . According to these
data, it may thus be assumed that consuming one egg may correspond to ingesting
approximately 1 μg vitamin D3 and 0.2 μg 25(OH)D3 (one egg yolk weights approximately 20 g) corresponding thus to approximately 2 μg vitamin D3 equivalents, while
consuming one 150 g beefsteak would correspond to approximately 2–2.5 μg vitamin
D3 equivalents essentially through the ingestion of 25(OH)D3. In addition to the
vitamin D content of some foods, the 25(OH)D content has now been taken into
account in some food composition tables but not in all.
A summary of the content in vitamin D and 25(OH)D of different foods is
presented in Table 27.1