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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

3 Ongoing Clinical Trials Aiming at Studying the Effects of Vitamin D3 on Extra-Osseous Criteria After Renal Transplantation, Including Graft Function and Rejection

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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 [57] (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.


1. Palmer SC, McGregor DO, Strippoli GF. Interventions for preventing bone disease in kidney

transplant recipients. Cochrane Database Syst Rev. 2007;(18):CD005015.

2. De Sevaux RG, Hoitsma AJ, Corstens FH, Wetzels JF. Treatment with vitamin D and calcium

reduces bone loss after renal transplantation: a randomized study. J Am Soc Nephrol.


3. El-Agroudy AE, El-Husseini AA, El-Sayed M, Mohsen T, Ghoneim MA. A prospective randomized study for prevention of postrenal transplantation bone loss. Kidney Int. 2005;67:2039–45.


M. Courbebaisse

4. Torres A, Garcia S, Gomez A, Gonzalez A, Barrios Y, Concepcion MT, Hernandez D, Garcia

JJ, Checa MD, Lorenzo V, Salido E. Treatment with intermittent calcitriol and calcium reduces

bone loss after renal transplantation. Kidney Int. 2004;65:705–12.

5. Dawson-Hughes B, Heaney RP, Holick MF, Lips P, Meunier PJ, Vieth R. Estimates of optimal

vitamin D status. Osteoporos Int. 2005;16:713–6.

6. Heaney RP. Vitamin D, depletion and effective calcium absorption. J Bone Miner Res.


7. Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation

of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am

J Clin Nutr. 2006;84:18–28.

8. Courbebaisse M, Souberbielle JC, Thervet E. Potential nonclassical effects of vitamin D in

transplant recipients. Transplantation. 2010;89:131–7.

9. Pascussi JM, Robert A, Nguyen M, Walrant-Debray O, Garabedian M, Martin P, Pineau T,

Saric J, Navarro F, Maurel P, Vilarem MJ. Possible involvement of pregnane X receptorenhanced CYP24 expression in drug-induced osteomalacia. J Clin Invest. 2005;115:177–86.

10. Bhan I, Shah A, Holmes J, Isakova T, Gutierrez O, Burnett SM, Juppner H, Wolf M. Posttransplant hypophosphatemia: tertiary ‘hyper-phosphatoninism’? Kidney Int. 2006;70:1486–94.

11. Reichrath J. Dermatologic management, sun avoidance and vitamin D status in organ transplant recipients (OTR). J Photochem Photobiol B. 2012;101:150–9.

12. Courbebaisse M, Thervet E, Souberbielle JC, Zuber J, Eladari D, Martinez F, Mamzer-Bruneel

MF, Urena P, Legendre C, Friedlander G, Prie D. Effects of vitamin D supplementation on the

calcium-phosphate balance in renal transplant patients. Kidney Int. 2009;75:646–51.

13. Wissing KM, Broeders N, Moreno-Reyes R, Gervy C, Stallenberg B, Abramowicz D. A controlled study of vitamin D3 to prevent bone loss in renal-transplant patients receiving low

doses of steroids. Transplantation. 2005;79:108–15.

14. Benaboud S, Urien S, Thervet E, Prié D, Legendre C, Souberbielle JC, Hirt D, Friedlander G,

Treluyer JM, Courbebaisse M. Determination of optimal cholecalciferol treatment in renal

transplant recipients using a population pharmacokinetic approach. Eur J Clin Pharmacol.


15. Tanaci N, Karakose H, Guvener N, Tutuncu NB, Colak T, Haberal M. Influence of

1,25-dihydroxyvitamin D3 as an immunomodulator in renal transplant recipients: a retrospective cohort study. Transplant Proc. 2003;35:2885–7.

16. Sezer S, Uyar M, Arat Z, Ozdemir FN, Haberal M. Potential effects of 1,25-dihydroxyvitamin

D3 in renal transplant recipients. Transplant Proc. 2005;37:3109.

17. Lee JR, Dadhania D, August P, Lee JB, Suthanthiran M, Muthukumar T. Circulating levels of

25-hydroxyvitamin D and acute cellular rejection in kidney allograft recipients. Transplantation.


18. Obi Y, Hamano T, Ichimaru N, Tomida K, Matsui I, Fujii N, Okumi M, Kaimori JY, Yazawa K,

Kokado Y, Nonomura N, Rakugi H, Takahara S, Isaka Y, Tsubakihara Y. Vitamin D deficiency

predicts decline in kidney allograft function: a prospective cohort study. J Clin Endocrinol

Metab. 2014;99(2):527–35.

19. Lemire JM, Adams JS, Kermani-Arab V, Bakke AC, Sakai R, Jordan SC. 1,25-Dihydroxyvitamin

D3 suppresses human T helper/inducer lymphocyte activity in vitro. J Immunol. 1985;134:


20. Reichel H, Koeffler HP, Tobler A, Norman AW. 1 alpha, 25-Dihydroxyvitamin D3 inhibits

gamma-interferon synthesis by normal human peripheral blood lymphocytes. Proc Natl Acad

Sci U S A. 1987;84:3385–9.

21. Rigby WF, Yirinec B, Oldershaw RL, Fanger MW. Comparison of the effects of

1,25-dihydroxyvitamin D3 on T lymphocyte subpopulations. Eur J Immunol. 1987;17:563.

22. Veldman CM, Cantorna MT, DeLuca HF. Expression of 1, 25-dihydroxyvitamin D(3) receptor

in the immune system. Arch Biochem Biophys. 2000;374:334.

23. Chen S, Sims GP, Chen XX, Gu YY, Chen S, Lipsky PE. Modulatory effects of 1,

25-dihydroxyvitamin D3 on human B cell differentiation. J Immunol. 2007;179:1634–47.


Vitamin D in Acute and Chronic Rejection of Transplanted Kidney


24. Fritsche J, Mondal K, Ehrnsperger A, Andreesen R, Kreutz M. Regulation of 25-hydroxyvitamin

D3–1 alpha-hydroxylase and production of 1 alpha,25-dihydroxyvitamin D3 by human dendritic cells. Blood. 2003;102:3314–6.

25. Penna G, Adorini L. 1 Alpha,25-dihydroxyvitamin D3 inhibits differentiation, maturation,

activation, and survival of dendritic cells leading to impaired alloreactive T cell activation.

J Immunol. 2000;164:2405–11.

26. Griffin MD, Lutz W, Phan VA, Bachman LA, McKean DJ, Kumar R. Dendritic cell modulation

by 1alpha,25 dihydroxyvitamin D3 and its analogs: a vitamin D receptor-dependent pathway

that promotes a persistent state of immaturity in vitro and in vivo. Proc Natl Acad Sci U S A.


27. Chen W. The role of plasmacytoid dendritic cells in immunity and tolerance. Curr Opin Organ

Transplant. 2005;10:181.

28. Mora JR, Iwata M, von Andrian UH. Vitamin effects on the immune system: vitamins A and D

take centre stage. Nat Rev Immunol. 2008;8:685.

29. Lemire JM, Archer DC, Khulkarni A, Ince A, Uskokovic MR, Stepkowski S. Prolongation of

the survival of murine cardiac allografts by the vitamin D3 analogue 1,25-dihydroxy-delta

16-cholecalciferol. Transplantation. 1992;54:762–3.

30. Zhang AB, Zheng SS, Jia CK, Wang Y. Effect of 1,25-dihydroxyvitamin D3 on preventing

allograft from acute rejection following rat orthotopic liver transplantation. World

J Gastroenterol. 2003;9:1067.

31. Casteels K, Waer M, Laureys J, Valckx D, Depovere J, Bouillon R, Mathieu C. Prevention of autoimmune destruction of syngeneic islet grafts in spontaneously diabetic nonobese diabetic mice by

a combination of a vitamin D3 analog and cyclosporine. Transplantation. 1998;65:1225–32.

32. Kallio E, Häyry P, Pakkala S. MC1288, a vitamin D analogue, reduces short- and long-term

renal allograft rejection in the rat. Transplant Proc. 1996;28(6):3113.

33. Cantorna MT, Hullett DA, Redaelli C, Brandt CR, Humpal-Winter J, Sollinger HW, Deluca

HF. 1,25-Dihydroxyvitamin D3 prolongs graft survival without compromising host resistance

to infection or bone mineral density. Transplantation. 1998;66:828.

34. Ardalan MR, Maljaei H, Shoja MM, Piri AR, Khosroshahi HT, Noshad H, Argani H. Calcitriol

started in the donor, expands the population of CD4+CD25+ T cells in renal transplant recipients. Transplant Proc. 2007;39:951–3.

35. Ahmadpoor P, Ilkhanizadeh B, Ghasemmahdi L, Makhdoomi K, Ghafari A. Effect of active

vitamin D on expression of co-stimulatory molecules and HLA-DR in renal transplant recipients. Exp Clin Transplant. 2009;7:99–103.

36. van Etten E, Mathieu C. Immunoregulation by 1, 25-dihydroxyvitamin D3: basic concepts.

J Steroid Biochem Mol Biol. 2005;97:93.

37. Agarwal R, Acharya M, Tian J, Hippensteel RL, Melnick JZ, Qiu P, Williams L, Batlle D.

Antiproteinuric effect of oral paricalcitol in chronic kidney disease. Kidney Int. 2005;68:


38. Lee DR, Kong JM, Cho KI, Chan L. Impact of vitamin D on proteinuria, insulin resistance, and

cardiovascular parameters in kidney transplant recipients. Transplant Proc. 2011;43(10):


39. de Boer IH, Ioannou GN, Kestenbaum B, Brunzell JD, Weiss NS. 25-Hydroxyvitamin D levels

and albuminuria in the Third National Health and Nutrition Examination Survey (NHANES

III). Am J Kidney Dis. 2007;50:69–77.

40. Ravani P, Malberti F, Tripepi G, Pecchini P, Cutrupi S, Pizzini P, Mallamaci F, Zoccali

C. Vitamin D levels and patient outcome in chronic kidney disease. Kidney Int. 2009;75:88.

41. O’Herrin JK, Hullett DA, Heisey DM, Sollinger HW, Becker BN. A retrospective evaluation

of 1,25-dihydroxyvitamin D(3) and its potential effects on renal allograft function. Am

J Nephrol. 2002;22:515–20.

42. Vu D, Sakharkar P, Tellez-Corrales E, Shah T, Hutchinson I, Min DI. Association of vitamin D

binding protein polymorphism with long-term kidney allograft survival in hispanic kidney

transplant recipients. Mol Biol Rep. 2013;40(2):933–9.


M. Courbebaisse

43. Lavin PJ, Laing ME, O’Kelly P, Moloney FJ, Gopinathan D, Aradi AA, Shields DC, Murphy

GM, Conlon PJ. Improved renal allograft survival with vitamin D receptor polymorphism. Ren

Fail. 2007;29(7):785–9.

44. Adorini L, Amuchastegui S, Daniel KC. Prevention of chronic allograft rejection by vitamin D

receptor agonists. Immunol Lett. 2005;100:34–41.

45. Brewster UC, Perazella MA. The renin-angiotensin-aldosterone system and the kidney: effects

on kidney disease. Am J Med. 2004;116:263.

46. Sun J, Kong J, Duan Y, Szeto FL, Liao A, Madara JL, Li YC. Increased NF-kappaB activity in

fibroblasts lacking the vitamin D receptor. Am J Physiol Endocrinol Metab. 2006;291:E315.

47. Tan X, Li Y, Liu Y. Paricalcitol attenuates renal interstitial fibrosis in obstructive nephropathy.

J Am Soc Nephrol. 2006;17:3382.

48. Schwarz U, Amann K, Orth SR, Simonaviciene A, Wessels S, Ritz E. Effect of 1,25 (OH)2

vitamin D3 on glomerulosclerosis in subtotally nephrectomized rats. Kidney Int. 1998;53:1696.

49. Kuhlmann A, Haas CS, Gross ML, Reulbach U, Holzinger M, Schwarz U, Ritz E, Amann K.

1,25-Dihydroxyvitamin D3 decreases podocyte loss and podocyte hypertrophy in the subtotally nephrectomized rat. Am J Physiol Renal Physiol. 2004;286:F526.

50. Freundlich M, Quiroz Y, Zhang Z, Zhang Y, Bravo Y, Weisinger JR, Li YC, Rodriguez-Iturbe B.

Suppression of renin-angiotensin gene expression in the kidney by paricalcitol. Kidney Int.


51. Zhang Z, Sun L, Wang Y, Ning G, Minto AW, Kong J, Quigg RJ, Li YC. Renoprotective role

of the vitamin D receptor in diabetic nephropathy. Kidney Int. 2008;73:163.

52. Park JW, Bae EH, Kim IJ, Ma SK, Choi C, Lee J, Kim SW. Paricalcitol attenuates cyclosporineinduced kidney injury in rats. Kidney Int. 2010;77(12):1076–85.

53. Hullett DA, Laeseke PF, Malin G, Nessel R, Sollinger HW, Becker BN. Prevention of chronic

allograft nephropathy with vitamin D. Transpl Int. 2005;18:1175–86.

54. de Zeeuw D, Agarwal R, Amdahl M, Audhya P, Coyne D, Garimella T, Parving HH, Pritchett

Y, Remuzzi G, Ritz E, Andress D. Selective vitamin D receptor activation with paricalcitol for

reduction of albuminuria in patients with type 2 diabetes (VITAL study): a randomised controlled trial. Lancet. 2010;376(9752):1543–51.

55. Courbebaisse M, Xu-Dubois YC, Thervet E, Prié D, Zuber J, Kreis H, Legendre C, Rondeau

E, Pallet N. Cholecalciferol supplementation does not protect against renal allograft structural

and functional deterioration: a retrospective study. Transplantation. 2011;91(2):207–12.

56. Courbebaisse M, Alberti C, Colas S, Prié D, Souberbielle JC, Treluyer JM, Thervet E. VITamin

D supplementation in renAL transplant recipients (VITALE): a prospective, multicentre,

double-blind, randomized trial of vitamin D estimating the benefit and safety of vitamin D3

treatment at a dose of 100,000 UI compared with a dose of 12,000 UI in renal transplant recipients: study protocol for a double-blind, randomized, controlled trial. Trials. 2014;15:430.

57. Thiem U, Heinze G, Segel R, Perkmann T, Kainberger F, Mühlbacher F, Hörl W, Borchhardt K.

VITA-D: cholecalciferol substitution in vitamin D deficient kidney transplant recipients: a randomized, placebo-controlled study to evaluate the post-transplant outcome. Trials. 2009;10:36.

Chapter 27

Nutrition and Dietary Vitamin D in Chronic

Kidney Disease

Jean-Claude Souberbielle

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

e-mail: jean-claude.souberbielle@nck.aphp.fr

© Springer International Publishing Switzerland 2016

P.A. Ureña Torres et al. (eds.), Vitamin D in Chronic Kidney Disease,

DOI 10.1007/978-3-319-32507-1_27



J.-C. Souberbielle

Fig. 27.1 Simplified

representation of vitamin

D, 25-hydroxyvitamin D

molecules, and

1,25-dihydroxyvitamin 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 [3], whether the

animal lived indoor or outdoor, and, for those living outdoor, on the season the animal has been sacrificed [4], 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 [6]).

Having said that, it is clear that fatty fish liver oil such as cod liver oil [7] (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) [1].

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


J.-C. Souberbielle

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 [10]. 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 [11]. 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 [12]. 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 [10].


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 [16]. 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 [19]), 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 [20], it is now

accepted that this metabolite contributes significantly to the 25(OH)D serum concentration of certain persons [21]. 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) [22]. 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

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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

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