Hostname: page-component-77c89778f8-n9wrp Total loading time: 0 Render date: 2024-07-19T19:23:30.875Z Has data issue: false hasContentIssue false

The role of vitamin D in the association between tuberculosis and end-stage renal disease

Published online by Cambridge University Press:  30 May 2013

J. PAKPOOR*
Affiliation:
Department of Physiology, Anatomy and Genetics and Medical Research Council Functional Genomics Unit, University of Oxford, Oxford, UK
J. PAKPOOR*
Affiliation:
School of Clinical Medicine, Addenbrooke's Hospital, University of Cambridge, Cambridge, UK
*
*Author for correspondence: Dr J. Pakpoor, Department of Physiology, Anatomy and Genetics, and Medical Research Council Functional Genomics Unit, University of Oxford, Oxford OX1 3PT, UK. (Email: julia.pakpoor@medschool.ox.ac.uk)
*Author for correspondence: Dr J. Pakpoor, Department of Physiology, Anatomy and Genetics, and Medical Research Council Functional Genomics Unit, University of Oxford, Oxford OX1 3PT, UK. (Email: julia.pakpoor@medschool.ox.ac.uk)
Rights & Permissions [Opens in a new window]

Abstract

Type
Correspondence
Copyright
Copyright © Cambridge University Press 2013 

To the Editor:

We read with great interest the study by Hu et al. [Reference Hu1] in which the authors report a significantly increased risk of tuberculosis (TB) within 2 years of onset of end-stage renal disease (ESRD) in their population-based cohort study. The authors suggested that this association is likely to be a consequence of an immunocompromised state and frequent hospital attendance of patients with ESRD. Indeed, whereas these factors plausibly contribute substantially to increased TB risk, vitamin D deficiency may also be an important factor contributing to the observed association between TB and ESRD.

The primary source of vitamin D in the body is endogenous synthesis following UVB exposure to the skin (with a small proportion of vitamin D intake obtained through diet) [Reference Christakos2]. Upon UVB exposure, 7-dehydrocholesterol in the epidermal skin layer is converted to previtamin D3 which rapidly undergoes a thermal reaction to produce cholecalciferol (an inactive form of vitamin D3) [Reference Christakos2]. Subsequently, cholecalciferol is hydroxylated in the liver by 25-hydroxylase to form 25-hydroxyvitamin D3. This molecule is finally hydroxylated in the kidney by the enzyme 1-alpha-hydroxylase to form calcitriol (1,25-dihydroxyvitamin D3), the active form of vitamin D [Reference Christakos2]. Patients with chronic kidney disease including ESRD are thought to have a high incidence of vitamin D insufficiency and deficiency in part as a result of impaired renal function and reduced ability to generate the active form of vitamin D [Reference Al-Badr and Martin3]. An American study of 825 consecutive patients on haemodialysis found that 78% of patients were vitamin D-deficient and 18% classified as severely deficient [Reference Wolf4]. Low vitamin D levels in haemodialysis patients has also been associated with increased mortality [Reference Wolf4, Reference Teng5]. Further, a substantial evidence base of both basic science and clinical research has shown that vitamin D deficiency is significantly associated with active TB (odds ratio 2·9, 95% confidence interval 1·3–6·5) [Reference Wilkinson6]. This is also supported, for example, by the historical use of phototherapy in the treatment of TB.

Vitamin D receptors are found on a variety of human cells including monocytes, macrophages and dendritic cells and both in vivo and in vitro studies have shown that vitamin D has an immune-modulatory role against Mycobacterium tuberculosis [Reference Holick7, Reference Yang8]. Therefore, information on the use of vitamin D supplementation in the reported patients with ESRD would have been highly interesting, but we appreciate that this may not have been available to the authors. Nevertheless, a strong association between chronic kidney disease and vitamin D deficiency suggests that vitamin D supplementation, particularly in individuals with ESRD, may be important in reducing vitamin D-associated comorbidities, including TB. Given that Taiwan has the highest incidence and prevalence of ESRD in the world, this may potentially be an important public health issue for its population.

Declaration of Interest

None.

References

1. Hu, HY, et al. Increased risk of tuberculosis in patients with end-stage renal disease: a population-based cohort study in Taiwan, a country of high incidence of end-stage renal disease. Epidemiology and Infection. Published online: 19 March 2013 . doi:10.1017/S0950268813000551.Google ScholarPubMed
2. Christakos, S, et al. Vitamin D: metabolism. Rheumatic Disease Clinics of North America 2012; 38: 111.CrossRefGoogle ScholarPubMed
3. Al-Badr, W, Martin, KJ. Vitamin D and kidney disease. Clinical Journal of the American Society of Nephrology 2008; 3: 15551560.Google Scholar
4. Wolf, M, et al. Vitamin D levels and early mortality among incident hemodialysis patients. Kidney International 2007; 72: 10041013.CrossRefGoogle ScholarPubMed
5. Teng, M, et al. Activated injectable vitamin D and hemodialysis survival: a historical cohort study. Journal of the American Society of Nephrology 2005; 16: 11151125.CrossRefGoogle ScholarPubMed
6. Wilkinson, RJ, et al. Influence of vitamin D deficiency and vitamin D receptor polymorphisms on tuberculosis among Gujarati Asians in west London: a case-control study. Lancet 2000; 355: 618621.CrossRefGoogle ScholarPubMed
7. Holick, MF. Vitamin D deficiency. New England Journal of Medicine 2007; 357: 266281.Google Scholar
8. Yang, HF, et al. Vitamin D deficiency affects the immunity against Mycobacterium tuberculosis infection in mice. Clinical and Experimental Medicine. Published online: 10 Aug 2012 . doi:10.1007/s10238-012-0204-7.Google Scholar