Prevalence of vitamin D deficiency among libyan chronic kidney disease patients

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.