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Saudi Journal of Kidney Diseases and Transplantation
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Table of Contents   
ORIGINAL ARTICLE  
Year : 2019  |  Volume : 30  |  Issue : 6  |  Page : 1389-1397
Vitamin-D deficiency is encountered in almost all egyptian stage 3-5 chronic kidney disease patients in spite of the sunny weather


1 Department of Internal Medicine, Nephrology Unit, School of Medicine, Cairo University, Cairo, Egypt
2 Department of Rheumatology and Rehabilitation, School of Medicine, Cairo University, Cairo, Egypt
3 Department of Internal Medicine, Endocrinology Unit, School of Medicine, Cairo University, Cairo, Egypt

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Date of Submission08-Jul-2018
Date of Decision20-Aug-2018
Date of Acceptance25-Aug-2018
Date of Web Publication9-Jan-2020
 

   Abstract 


Currently, there is no available data about Vitamin D status among Egyptian chronic kidney disease (CKD) patients. This cross-sectional study is looking for the prevalence of Vitamin D deficiency among Stage 3a-5 CKD Egyptian patients and its possible associations. We studied 1624 Stage 3a-5 CKD adults (689 males and 935 females) together with 200 normal control persons. All the recruited candidates were tested for body mass index (BMI); serum levels of blood urea nitrogen, creatinine, calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25 hydroxy vitamin D (25(OH)D), albumin, and uric acid (UA); urine albumin/creatinine ratio (ACR), and estimated glomerular filtration rate. The optimal level of Vitamin D was encountered in only 1.4% of CKD patients versus 52% of the normal controls. A total of 1107 (68.2%) CKD patients versus 23 (11.5%) controls had serum 25(OH)D <20 ng/mL (mean ± standard deviation = 16.8 ± 5.8 versus 37.3±7.6 ng/mL for CKD versus control group, respectively, P <0.001). There was a highly statistically significant positive correlation between serum 25(OH)D and serum Ca (r = 0.299, P <0.001) and a highly statistically significant negative correlation between serum 25(OH)D on the one hand and serum P, serum PTH, serum UA, and urine ACR on the other hand (r = -0.46, -0.69, -0.73, and -0.8, respectively, P <0.001). Vitamin D deficiency is very common among Egyptian CKD patients. Serum P, UA, and urine ACR ratio are the most important variables which are found to be negatively associated with serum 25(OH)D.

How to cite this article:
El Din US, Fayed A, El Nokeety MM, Abdulazim DO, Salem MM, on behalf of the Vascular Calcification Group. Vitamin-D deficiency is encountered in almost all egyptian stage 3-5 chronic kidney disease patients in spite of the sunny weather. Saudi J Kidney Dis Transpl 2019;30:1389-97

How to cite this URL:
El Din US, Fayed A, El Nokeety MM, Abdulazim DO, Salem MM, on behalf of the Vascular Calcification Group. Vitamin-D deficiency is encountered in almost all egyptian stage 3-5 chronic kidney disease patients in spite of the sunny weather. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2020 Jan 18];30:1389-97. Available from: http://www.sjkdt.org/text.asp?2019/30/6/1389/275483



   Introduction Top


The role of Vitamin D in bone and mineral metabolism is pivotal. Beside its central role in calcium (Ca) and phosphate metabolism, it is very essential for musculoskeletal development and health.[1] Vitamin D deficiency may have an additional impact on different body organs. The hepatic 25-hydroxylase enzyme (CYP2R1) converts Vitamin D into 25 hydroxy vitamin D (25(OH)D). Serum 25(OH)D level reflects Vitamin D status in humans. The normal level is above 30 ng/mL, whereas a level below 20 ng/mL is considered as Vitamin D deficiency.[2] Vitamin D deficiency may predispose to cardiovascular, neoplastic, infectious, metabolic, and autoimmune diseases. The rate of progression of chronic kidney disease (CKD) might accelerate in Vitamin D-deficient cases.[3],[4] CKD patients have impaired renal 1-α hydroxylase (CYP27B1) activity with consequent decrease in the rate of conversion of 25(OH)D to calcitriol.[2] This can lead to secondary hyperparathyroidism. Superimposed deficiency of 25(OH)D may aggravate secondary hyper-parathyroidism both directly and indirectly. Calcitriol level should not be used to diagnose Vitamin D deficiency as it can lead to erroneous interpretations of Vitamin D status. Calcitriol levels are usually normal or even elevated in Vitamin D-deficient patients as a result of elevated parathyroid hormone (PTH) levels.[2]

Egypt has sunny weather allover the four seasons of the year. In spite of the sunny weather, restricted exposure to sunlight is very common mainly due to religious and cultural rules.[5],[6] Food fortification with Vitamin D is optional in Egypt. CKD patients have additional factors that can increase the prevalence and severity of Vitamin D deficiency. These factors include anorexia, dietary restriction, diabetes, and increased body mass index (BMI).[7] To date, the status of Vitamin D among the Egyptian predialysis CKD patients has not been evaluated.


   Patients and Methods Top


This study has recruited 1624 (688 males and 936 females) CKD patients. Their ages ranged between 18 and 55 years. The etiology of their renal disease is summarized in [Table 1]. A total of 271 (16.7%) patients were in Stage 3, 1290 (79.4%) were in Stage 4, and 63 (3.9%) were in Stage 5. Two hundred normal persons were included as control group. All the recruited candidates were individually interviewed for history taking and clinical examination and to obtain a written consent after discussing the mission of the study. Blood and urine samples were then collected for laboratory assessment of the different planned parameters. Intact PTH level was determined by enzyme-amplified sensiti-vity immunoassay (Roche Diagnostics, IN, USA), 25(OH)D was assessed using highperformance liquid chromatography,[8] and estimated glomerular filtration rate (eGFR) was measured using the Modification of Diet in Renal Disease equation.[9]
Table 1: Etiology of chronic kidney disease.

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The IBM SPSS Statistics for Windows version 24.0 (IBM Corp., Armonk, NY, USA) was used for data analysis. Data were summarized as mean and standard deviation. Comparison between groups was evaluated using Student’s /-test. Correlation coefficient between different parameters of mineral metabolism and kidney function tests was also performed.


   Results Top


The results are summarized in [Table 1],[Table 2],[Table 3],[Table 4],[Table 5],[Table 6],[Table 7],[Table 8],[Table 9] and [Figure 1],[Figure 2],[Figure 3],[Figure 4]. Nearly 98.6% of the CKD patients (1602) had suboptimal 25(OH)D levels (<30 ng/mL). There was no statistically significant difference in serum 25(OH)D level among CKD group based on gender [Table 3], BMI [Table 4], or on the presence or absence of diabetes mellitus [Table 5]. The ratio of CKD patients with serum level of 25(OH)D less than 10 ng/mL, between 10 and 19.9 ng/mL, between 20 and 29.9 ng/mL, or 30 ng/mL or more was not statistically different based on gender [Table 3], BMI [Table 4], or diabetic status [Table 5].
Table 2: Patient versus control groups.

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Table 3: Comparative analysis of different studied quantitative parameters according to gender.

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Table 4: Comparative analysis of different studied quantitative parameters according to body mass index.

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Table 5: Comparative analysis of different studied quantitative parameters according to diabetic status.

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Table 6: Comparative analysis of different studied quantitative parameters according to urine albumin excretion.

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Table 7: Comparative analysis of different studied quantitative parameters according to serum uric acid.

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Table 8: Correlation between different parameters and serum 25 hydroxy vitamin D.

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Table 9: Multivariate linear regression for predictors of Vitamin D level.

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Figure 1: Correlation between serum phosphorus and serum 25 hydroxy vitamin D.

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Figure 2: Correlation between serum uric acid and serum 25 hydroxy vitamin D.

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Figure 3: Correlation between serum PTH and serum 25 hydroxy vitamin D, PTH: Parathyroid hormone.

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Figure 4: Correlation between urine albumin creatinine ratio and serum 25 hydroxy vitamin D.

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On the other hand, there was a statistically significant difference in serum 25(OH)D based on urine albumin excretion (10.7 ± 2.08 vs.

20.6 ± 4.15 ng/mL) in patients with increased versus normal urine albumin, respectively, P <0.001, [Table 6]. A similar finding was observed in patients with serum UA >5 mg/dL versus patients with lower levels (10.9 ± 2.94 vs. 21 ± 4.35 ng/mL, respectively, P <0.001, [Table 7].

A statistically significant positive correlation (two-tailed P ≥0.001 if r >0.082) was encountered between serum 25(OH)D and serum Ca (r = 0.3) and significant negative correlations between serum 25(OH)D and serum P (r = -0.46), serum PTH (r = -0.69), serum UA (r = -0.73), and urine albumin/creatinine ratio (ACR) (r = -0.8). Age, BMI, and eGFR failed to have a significant asso-ciation with serum 25(OH)D [Table 8].


   Discussion Top


The central role of Vitamin D in Ca homeostasis and bone welfare is well established. To maximize the beneficial effects of Vitamin D, the serum level of 25(OH)D should be kept above 30 ng/mL.[10],[11] In the current study, 98.6% of the CKD patients have serum level below this target. We failed to encounter similar alarming figure in the literature. In Louisiana, 77% of CKD patients had suboptimal levels of 25(OH)D,[12] whereas in Italy, a more sunny country compared to Louisiana, only 39.6% of the studied CKD patients were considered Vitamin D insuf-ficient.[13] Among healthy controls, Vitamin D insufficiency is connected to inadequate sun exposure and poor food fortification.[14] For CKD patients, additional factors are accused as causes of increased prevalence and severity of Vitamin D insufficiency. Decreased food intake, dietary restriction,[7] old age,[15],[16],[17] increased body weight,[17],[18] and diabetic status[12],[17],[19],[20] were incriminated in different studies. However, the association between these different factors and serum level of 25(OH)D lacks consistency. Many studies failed to find an association between Vitamin D status on the one hand and age, BMI, urine albumin excretion, and eGFR on the other hand. In the current study, we failed to encounter significant association between Vitamin D status and any of these variables.

It seems that air pollution might interfere with sun effect. Most of the Egyptian adult females lack adequate exposure to sun thanks to culture and religious reasons. However, there was no appreciable difference in the prevalence and severity of Vitamin D deficiency between male and female Egyptian CKD patients. In addition, in Brazil, which possesses sunny weather comparable to Egypt, Vitamin D deficiency is dramatically much lower compared to Egypt (20% vs. 68.2%, respectively).[18] It is worth mentioning that a significant difference has been also observed among healthy control persons of the current study and elsewhere with similar sunny weather.[21]

The current study demonstrates a highly significant association between Vitamin D status and serum Ca, serum phosphorus, serum PTH, serum UA, and urine ACR. These results might suggest that different variables can have an impact on Vitamin D status in CKD. These variables are metabolic and functional consequences of CKD.

In addition, this study raised suggestions for future studies to explain the marked discrepancy in the prevalence and severity of Vitamin D deficiency that cannot be explained by the environmental and nutritional factors, the inconsistency in the association between Vitamin D deficiency, and the different factors accused in different studies beside the negative association between 25(OH)D on the one hand and serum P and serum UA on the other hand.


   Ethical Committee Approval Top


The local ethical committee of the Internal Medicine department, School of Medicine, Cairo University, approved this work.


   Human and Animal Rights Top


All procedures performed in this study involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards.


   Informed consent Top


Informed consent was obtained from all the individual participants included in the study.

Conflict of interest: None declared.



 
   References Top

1.
Holick M. Medical progress: Vitamin D deficiency. N Engl J Med 2007;357:266-81.  Back to cited text no. 1
    
2.
Kennel KA, Drake MT, Hurley DL. Vitamin D deficiency in adults: When to test and how to treat. Mayo Clin Proc 2010;85:752-7.  Back to cited text no. 2
    
3.
Plum LA, DeLuca HF. Vitamin D, disease and therapeutic opportunities. Nat Rev Drug Discov 2010;9:941-55.  Back to cited text no. 3
    
4.
DeLuca HF. Overview of general physiologic features and functions of Vitamin D. Am J Clin Nutr 2004;80:1689S-96S.  Back to cited text no. 4
    
5.
El Rifai NM, Abdel Moety GA, Gaafar HM, Hamed DA. Vitamin D deficiency in Egyptian mothers and their neonates and possible related factors. J Matern Fetal Neonatal Med 2014; 27:1064-8.  Back to cited text no. 5
    
6.
Amr N, Hamid A, Sheta M, Elsedfy H. Vitamin D status in healthy Egyptian adolescent girls. Georgian Med News 2012;210:65-71.  Back to cited text no. 6
    
7.
Echida Y, Mochizuki T, Uchida K, Tsuchiya K, Nitta K. Risk factors for Vitamin D deficiency in patients with chronic kidney disease. Intern Med 2012;51:845-50.  Back to cited text no. 7
    
8.
Neyestani TR, Gharavi A, Kalayi A. Determination of serum 25-hydroxy cholecal-ciferol using high-performance liquid chromatography: A reliable tool for assessment of vitamin D status. Int J Vitam Nutr Res 2007;77:341-6.  Back to cited text no. 8
    
9.
Levey AS, Bosch JP, Lewis JB, Greene T, Rogers N, Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: A new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med 1999;130:461-70.  Back to cited text no. 9
    
10.
Zhu JG, Ochalek JT, Kaufmann M, Jones G, Deluca HF. CYP2R1 is a major, but not exclusive, contributor to 25-hydroxyvitamin D production in vivo. Proc Natl Acad Sci U S A 2013;110:15650-5.  Back to cited text no. 10
    
11.
Holick MF, Chen TC. Vitamin D deficiency: A worldwide problem with health consequences. Am J Clin Nutr 2008;87:1080S-6S.  Back to cited text no. 11
    
12.
Yaturu S, Davis J. Prevalence of decreased Vitamin D levels is high among veterans with Diabetes AND/or CKD. ISRN Endocrinol 2011:2011:109458.  Back to cited text no. 12
    
13.
Cuppari L, Carvalho AB, Draibe SA. Vitamin D status of chronic kidney disease patients living in a sunny country. J Ren Nutr 2008:18:408-14.  Back to cited text no. 13
    
14.
Holick MF. Vitamin D deficiency. N Engl J Med 2007:357:266-81.  Back to cited text no. 14
    
15.
Ureña-Torres P, Metzger M, Haymann JP, et al. Association of kidney function, Vitamin D deficiency, and circulating markers of mineral and bone disorders in CKD. Am J Kidney Dis 2011:58:544-53.  Back to cited text no. 15
    
16.
Cupisti A, Vigo V, Baronti ME, D’Alessandro C, Ghiadoni L, Egidi MF. Vitamin D status and cholecalciferol supplementation in chronic kidney disease patients: An Italian cohort report. Int J Nephrol Renovasc Dis 2015:8:151-7.  Back to cited text no. 16
    
17.
Rodríguez Villarreal I, Ortega O, Gallar P, et al. Clinical and biochemical characteristics of predialysis patients in terms of 25 hydroxy vitamin D levels. Nefrologia 2011:31:185-91.  Back to cited text no. 17
    
18.
Barreto Silva MI, Cavalieri VV, Lemos CC, Klein MR, Bregman R. Body adiposity predictors of Vitamin D status in nondialyzed patients with chronic kidney disease: A cross-sectional analysis in a tropical climate city. Nutrition 2017:33:240-7.  Back to cited text no. 18
    
19.
Rozita M, Noorul Afidza M, Ruslinda M, et al. Serum Vitamin D levels in patients with chronic kidney disease. EXCLI J 2013:12:511-20.  Back to cited text no. 19
    
20.
Yuste C, García De Vinuesa S, Goicoechea M, et al. Vitamin D deficiency in a Spanish cohort of patients with chronic kidney disease. Med Clin (Barc) 2013:141:338-42.  Back to cited text no. 20
    
21.
Alsuwadia AO, Farag YM, Al Sayyari AA, et al. Prevalence of Vitamin D deficiency in Saudi adults. Saudi Med J 2013:34:814-8.  Back to cited text no. 21
    

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Correspondence Address:
Ahmed Fayed
Department of Internal Medicine, Nephrology Unit, School of Medicine, Cairo University
Egypt
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DOI: 10.4103/1319-2442.275483

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