|Year : 2018 | Volume
| Issue : 4 | Page : 138-141
Prevalence of vitamin D deficiency among libyan chronic kidney disease patients
Fatimah A Nouh1, Abdalla M Jarari1, Mohamed O Ezwaie2, Omar B Latiwesh1
1 Department of Biochemistry, Faculty of Medicine, University of Benghazi, Benghazi, Libya
2 Department of Medicine, Faculty of Medicine, University of Benghazi, Benghazi, Libya
|Date of Web Publication||17-Jan-2019|
Dr. Mohamed O Ezwaie
Department of Medicine, Faculty of Medicine, University Benghazi, Benghazi
Source of Support: None, Conflict of Interest: None
Background: Vitamin D deficiency is common among patients with chronic kidney disease (CKD). The traditional supplementation of active Vitamin D (1,25–dihydroxyvitamin D (or 1-hydroxyvitamin D to CKD patients has been reported to control the level of secondary hyperparathyroidism but not sufficient to replenish the body store of Vitamin D (25-hydroxyvitamin D). Patients and Methods: We conducted a cross-sectional analysis of two major parameters, namely 25-hydroxyvitamin D and parathyroid hormone (PTH) levels, in 50 female and 30 male CKD patients, compared to a control group of 29 individuals. Aim: The aim of the study was to determine the prevalence of Vitamin D deficiency in different stages of Libyan CKD patients. Moreover, this study aimed to evaluate the prevalence of Vitamin D deficiency in those treated patients compared to untreated ones and also to compare the effect of Vitamin D treatment on Vitamin D and PTH levels. Results: The mean 25(OH) Vitamin D level in CKD patients was 18.45 (±13.6) ng/ml, whereas for the healthy control, it was 19.03 (±11.49) ng/ml. The level of 25(OH) Vitamin D <20 ng/ml was observed in 80.6% of untreated patients and hence classified as deficient, whereas only 69% of the involved healthy controls were found to be Vitamin D deficient. However, on treatment, the prevalence of Vitamin D deficiency in patients had declined to 30.8%. Furthermore, PTH level in Vitamin D-treated patients was 118.56 ± 38 pg/dl, while in untreated, it was 393.77 ± 46 pg/dl; this significant lowering effect on PTH level was not produced on treating patients with 1-hydroxyvitamin D alone, as the mean of PTH was 436.48 ± 62.55 pg/dl in the treated patients and 324.96 ± 67.61 pg/dl in untreated patients. Furthermore, no significant differences in the levels of 25(OH) Vitamin D were detected among patients who representing the different stages of CKD. Nevertheless, gender has no significant effect on 25(OH Vitamin D levels among tested patients (males, 15.34 ± 8.50 ng/ml and females, 16.42 ± 13.55 ng/ml). Conclusion: This study demonstrated significant low Vitamin D stores (low 25-hydroxyvitamin D) in CKD patients (80.6%), who did not receive supplemental doses of Vitamin D (ergocalciferol or cholecalciferol), which was not prevented by the use of microdoses (0.5–1μg/day) of 1-hydroxyvitamin D. Furthermore, there had been significant correlation between the Vitamin D-deficient CKD patients and higher levels of PTH levels. There had been no correlation between Vitamin D deficiency among the different stages of CKD, signifying that deficiency is amenable to correction with the supplemental doses of Vitamin D even in advanced CKD patients. This study, to our knowledge, represents the first biochemical analysis of 25-hydroxyvitamin D deficiency in Libyan CKD patients.
Keywords: 25(OH) Vitamin D, chronic kidney disease, secondary hyperparathyroidism, Vitamin D deficiency
|How to cite this article:|
Nouh FA, Jarari AM, Ezwaie MO, Latiwesh OB. Prevalence of vitamin D deficiency among libyan chronic kidney disease patients. Libyan J Med Sci 2018;2:138-41
|How to cite this URL:|
Nouh FA, Jarari AM, Ezwaie MO, Latiwesh OB. Prevalence of vitamin D deficiency among libyan chronic kidney disease patients. Libyan J Med Sci [serial online] 2018 [cited 2022 May 23];2:138-41. Available from: https://www.ljmsonline.com/text.asp?2018/2/4/138/250303
| Introduction|| |
Normal Vitamin D level is essential for human health. Vitamin D deficiency has been recognized as a risk factor for nearly all causes of mortality in normal individuals and chronic kidney disease (CKD) patients. The prevalence of Vitamin D deficiency around the world in the CKD population has been described to range between 70% and 80%.
Recently, accumulated evidences have shown that the role of Vitamin D is no longer restricted to its classical endocrine function of maintaining calcium and phosphate homeostasis. An additional role of Vitamin D has been described that acts as a cell differentiating and antiproliferative factor with actions in a variety of tissues, including the renal, cardiovascular, and immune systems.
This updated information provided a convincing evidence for the necessity of Vitamin D supplementation to achieve good health welfare. However, administration of both 25 and 1,25 forms of Vitamin D to CKD patients is thought to augment both the classical endocrine and autocrine intracellular pathways through which Vitamin D has now been shown to function. This new finding strongly suggest that the use of Vitamin D in such patients is no longer solely directed for the treatment of secondary hyperparathyroidism (SHPT).
The serum 25-hydroxyvitamin D (25[OH] D) is the main circulating form of Vitamin D, thus its estimation has been adopted to evaluate the body status of Vitamin D. The United States Institute of Medicine defines Vitamin D deficiency as 25(OH)D levels <20 ng/ml. Vitamin D levels between 20 and 30 ng/ml are referred to as Vitamin D insufficient, while the normal level is indicated with >30 ng/ml.
| Patients and Methods|| |
Serum levels of 25(OH) D were analyzed in 80 patients (50 females and 30 males) at advanced CKD stage (estimated creatinine clearance ≤60 ml/min/1.73 m2), specifically Stages 3 and 4 and predialytic Stage 5 of CKD. Their mean age was 62.04 ± 14.40 years, being clinically stable and followed up at Almajory polyclinic in Benghazi and Benghazi Medical Center (BMC) during the period from April to June 2016. A total of 29 (12 females and 17 males) apparently healthy individuals were selected as controls for this study. They were age- and sex-matched individuals recruited from the blood bank and doctors in BMC hospital. All patients presented with stable metabolic conditions. Patients presenting any disease that could affect their Vitamin D level rather than kidney cause as liver disease or malabsorption disease were excluded from the study.
A cross-sectional analysis of serum 25(OH) D and parathyroid hormone (PTH) levels were performed in the four patient subgroups. Only13 out of the 80 analyzed patients had a history of receiving Vitamin D therapy either in the form of oral ergocalciferol or cholecalciferol (50,000 units per week for 12 consecutive weeks), whereas the remaining 67 patients were untreated with Vitamin D.
All samples were processed at medical biotechnology institute laboratory of Benghazi city, Vitamin D was measured by competitive enzyme linked immunosorbent assay (ELISA) using Elisa Reader and Washer (linear; Spain) and an ELISA kit supplied by (Euroimmun, company, Germany) that was based on the immunodiagnostics system enzyme immunoassay, serum bioactive (intact) PTH was estimated using a fully automated Cobas e 411 systems (Roche company, Swiss) by one step sandwich electrochemiluminescence immunoassay that is based on the Elecsys PTH test system. Target PTH level in CKD Stage 3 and 4 is unknown or at the upper limit of normal range, while for CKD Stage 5, it is 2–9 times the upper limit of normal range (150–300 pg/ml).
The data were analyzed using SPSS version 18. Descriptive characteristics of the study participants were calculated as the mean ± standard deviation (SD). Chi-squared test was used to compare categorical variables. The t-test was used to compare continuous variables, and the correlation test was used to determine differences in subject characteristics. Pearson's correlation coefficient determination was done to evaluate the degree of association between the Vitamin D and biochemical parameters. P (two-tailed) <0.05 was considered statistically significant.
| Results|| |
As shown in [Table 1], the mean age and SD of the 80 patients was 62.04 ± 14.40 years (ranging from 18 to 90 years), while that of the 29 healthy controls was 36.28 ± 10.19 years (ranging from 17 to 58 years). [Table 1] also illustrates the insignificant difference (P = 0.83) between the mean ± SD of serum Vitamin D level of control (19.04 ± 11.49 ng/ml) and patients (18.45 ± 13.6 ng/ml). In addition, the result showed that 69% of controls had Vitamin D deficiency in contrast to 80.6% of untreated patients (P = 0.0.21). However, when such patients (13 individuals) were subjected to Vitamin D supplementation, the calculated percentage of Vitamin D deficiency had declined to 30.8%(P = 0.001).
|Table 1: Comparison of means of Vitamin D levels and percent of Vitamin D deficiency in control subjects, and in treated and untreated chronic kidney disease patients with Vitamin D supplementation|
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No significant difference was shown in serum Vitamin D levels of male and female patients [Table 2], as the mean of Vitamin D in both gender was nearly equal (males, 15.34 ± 8.50 ng/ml and females, 16.42 ± 13.55 ng/ml) (P = 0.71).
|Table 2: Means of Vitamin D and parathyroid hormone levels in patients based on the gender and type of Vitamin D treatment|
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However, the results of [Table 2] showed a significant difference (P = 0.000) in means of Vitamin D for patients treated with ergocalciferol or cholecalciferol (31.26 ± 16.25 ng/ml) and untreated patients (15.97 ± 11.64 ng/ml). On the other hand, no significant difference (P = 0.12) was observed between Vitamin D levels in 1-hydroxyvitamin D-treated patients (17.75 ± 13.42 ng/ml) and untreated ones (13.33 ± 7.8 ng/ml). Nevertheless, the results demonstrated a significant difference in PTH levels between Vitamin D treated (118.56 ± 38 pg/dl) and untreated (393.77 ± 46 pg/dl) patients, with P = 0.02. Contrarily, this significant lowering effect on PTH level was not produced on treatment the patients with 1-hydroxyvitamin D, as the mean of PTH was 436.48 ± 62.55 pg/dl in treated patients and 324.96 ± 67.61 pg/dl in untreated patients (P = 0.25). However, there was no significant correlation between Vitamin D treated and untreated CKD patients, in terms of biochemical parameters such as Serum calcium (P = 0.25) and serum phosphorus (P = −0.78), due to concomitant therapy with calcium containing phosphate binders.
No significant difference was indicated in Vitamin D levels of different stages of renal failure [Table 3]. The mean of Vitamin D in Stage 3 was 14.02 ± 7.33 ng/ml, in Stage 4 was 16.41 ± 12.61 ng/ml, and in Stage 5 was 16.69 ± 12.86 ng/ml (P = 0.93).
| Discussion|| |
This case–control study which involved nondialytic CKD patients and matched healthy controls has described a high prevalence of Vitamin D deficiency/insufficiency in 80.6% of the studied patients and 69% of the controls.This finding is in agreement with many reports in Brazil  and in the United States of America.
However, it is important to observe that the high frequency of Vitamin D deficiency shown by our CKD patients (80.6%) is not far off that of healthy controls (69%). Such results of Vitamin D deficiency urge more researches to be conducted on the general population to clarify the causes of such deficiency which can be either of dietary or inadequate sun exposure, or another undiagnosed causes.
In addition, our results demonstrated the lack of correlation between the different stages of renal impairment and the degree of Vitamin D deficiency as the mean of Vitamin D nearly equal in each stage, which is in accordance with previous published studies.
The results of [Table 2] show no influence of gender on Vitamin D levels, which is in contrast to that reported by São Paulo study.
Indeed, the effect of ergocalciferol or cholecalciferol supplementation in patients with CKD and 25(OH) Vitamin D deficiencies has scarcely been described in the literature. However, our results expressed the improving influence of this treatment on the percentage of Vitamin D deficiency, which was shifted from 80.6% to 30.8%; also, the mean of Vitamin D in treated patients was 31.26 ± 16.25 and in untreated patients was 15.97 ± 11. These results are in good agreement with that reported by Al-Aly et al.
In agreement with the above-quoted reference, the present study revealed a statistically significant difference in PTH levels between those of Vitamin D treated and untreated patients.
However, we did not find statistically significant differences between 1-hydroxyvitamin D treated and untreated patients regarding PTH levels. This can be explained by the use of insufficient dose or improper effect of these microdoses of 1-hydroxyvitamin D to control SHPT, which indicates that Vitamin D (ergocalciferol or cholecalciferol) administration is an important adjuvant therapy in the management of SHPT.
These results disagree with that shown by a previous study, which conclude that a single intravenous high dose of 10 mg of 1-hyroxy (OH) D3 or 1,25(OH)2D3 significantly suppressed plasma PTH. The acute suppressive effect of 1, 25(OH)2D3 was three times greater than that of 1-hydroxy (OH) D3. Furthermore, it is in disagreement with that of Kovesdy, et al. which showed that paricalcitol in a dose 1–2 μg/day for 16 weeks is more effective than ergocalciferol 50,000 units to achieve serum levels ≥30 ng/ml and decreasing PTH levels. Interestingly, the same study revealed that serum 25(OH) Vitamin D increased significantly after 16 weeks in only ergocalciferol-treated group but not in the paricalcitol group, which is in agreement with our result that revealed no significant effect of 1-hydroxyvitamin D treatment on Vitamin D level. This indicates that microdoses of Vitamin D treatment are not enough to both correct Vitamin D level and restore the body store of 25(OH) Vitamin D.
Therefore, in clinical practice, it is recommended to start the management of Vitamin D deficiency and insufficiency with Vitamin D (ergocalciferol or cholecalciferol) supplementation throughout different CKD stages to cover the classical (endocrine) and the nonclassical (autocrine and paracrine) actions while continuing to provide the active form of calcitriol or alpha-hydroxylated analogs to patients in Stages 3–5 to achieve a proper control of PTH and thus prevent SHPT.
| Conclusion|| |
This study demonstrated that significant low Vitamin D stores (low 25-hydroxyvitamin D) were found in CKD patients (80.6%), who did not receive supplemental doses of Vitamin D (ergocalciferol or cholecalciferol), and that was not prevented by the use of microdoses (0.5-1ug/day) of 1-hydroxyvitamin D. There had been a significant correlation between Vitamin D-deficient CKD patients and higher levels of PTH levels. There had been no correlation between Vitamin D deficiencies among the different stages of CKD, signifying that deficiency is amenable to correction with supplemental doses of Vitamin D even in advanced CKD patients. Therefore, medical professionals must implement regular measurement of Vitamin D status as an index to start treatment of Vitamin D deficiency or insufficiency and not to wait for symptoms of the deficiency to be apparent. This study, to our knowledge, represents the first biochemical analysis of 25-hydroxyvitamin D deficiency in Libyan CKD patients.
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Conflicts of interest
There are no conflicts of interest.
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[Table 1], [Table 2], [Table 3]