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| Year : 2014 | Volume
: 25
| Issue : 5 | Page : 981-985 |
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| Prevalence of vitamin D deficiency in peritoneal dialysis patients |
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Jamal S Alwakeel Professor 1, Saira Usama1, Ahmad H Mitwalli1, Abdulkareem Alsuwaida1, Mohammed Alghonaim2
1 Nephrology Division, Department of Medicine, King Khalid University Hospital, King Saud University, Riyadh, Saudi Arabia
2 Nephrology Division, Department of Medicine, King Khalid University Hospital, King Saud University; Prince Salman bin Abdulaziz Chair for Kidney Research, Riyadh, Saudi Arabia
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| Date of Web Publication | 2-Sep-2014 |
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 Abstract | | |
Peritoneal dialysis (PD) patients have a high risk of developing vitamin D deficiency as 25(OH) vitamin D, the precursor of active vitamin D, is lost during dialysis. This crosssectional study was conducted to investigate the prevalence of vitamin D deficiency among adult Saudi patients on regular PD The data was collected in the summer of 2010 from patients who were on PD for more than six months at the King Khalid University Hospital, Riyadh. We recorded the demographic and clinical parameters for all patients. Blood samples were taken for serum vitamin D level (25 OH), serum parathyroid hormone (PTH) levels and other necessary biochemical parameters. There were 27 patients (11 males and 16 females) with a mean age of 46 (15-78 ± 21) years. Five patients were on continuous ambulatory PD and 22 patients were using automated PD. The average time on PD was 27.5 (6-84 ± 18.5) months. The mean serum vitamin D 25 (OH) level was 16.1 (4.9-41.5 ± 8.23) nmol/L. Sixteen (59.2%) of the patients had levels below 15 nmol/L, while another eight patients (29.6%) had vitamin D levels between 15 and 25 nmol/L, indicating a marked deficiency. The mean serum calcium was 2.2 (1.7-2.6 ± 0.2) mmol/L and the mean serum phosphorous was 1.48 (0.64-2.22 ± 0.37) mmol/L. Fifteen patients (55.5%) had significant hyperparathyroidism (serum PTH levels above 30 pmol/L). Majority of the PD patients in our center had vitamin D deficiency. The possible reasons include chronic renal failure, dietary restrictions, loss of vitamin D and decreased exposure to sunlight.
How to cite this article:
Alwakeel JS, Usama S, Mitwalli AH, Alsuwaida A, Alghonaim M. Prevalence of vitamin D deficiency in peritoneal dialysis patients. Saudi J Kidney Dis Transpl 2014;25:981-5 |
How to cite this URL:
Alwakeel JS, Usama S, Mitwalli AH, Alsuwaida A, Alghonaim M. Prevalence of vitamin D deficiency in peritoneal dialysis patients. Saudi J Kidney Dis Transpl [serial online] 2014 [cited 2022 May 18];25:981-5. Available from: https://www.sjkdt.org/text.asp?2014/25/5/981/139873 |
| Introduction | |  |
Vitamin D deficiency is common in patients with chronic kidney disease (CKD) and occurs due to multiple factors such as progressive hyperparathyroidism and hyperphosphatemia. [1] The vitamin D endocrine system is essential for calcium homeostasis, bone metabolism and immunomodulation. [2] Vitamin D deficiency is linked with increased cardiovascular morbidity in dialysis patients.
Patients on peritoneal dialysis (PD) have lower levels of vitamin D due to dietary inadequacy, decreased sunlight exposure and loss of vitamin D (1,25(OH)2 vitamin D) in the peritoneal effluent. [3] Low levels in dialysis patients are associated with hyperparathyroidism. [4] The
K/DOQI guidelines recommend measuring 25 (OH) D levels in stages three and four CKD patients with elevated parathyroid hormone (PTH) levels. [5]
| Subjects and Methods | | |
This cross-sectional study was conducted in the PD unit at the KKUH, supported by the Deanship of Scientific Research in King Saud University, in the summer of 2010. All patients included in the study signed a formal informed consent. All patients in the PD program were considered for the study, but patients less than 15 years, on PD for less than six months, with active malignancy, hemato-logical disorders, post parathyroidectomy or active bone pathology, were excluded.
Based on these criteria, 27 patients undergoing regular PD were included in the study. Patients' age, race, cause of renal failure, presence of diabetes and drugs, including calcium supplements, phosphate binders, calcimimetics and any vitamin D supplements, were recorded. Blood samples were taken for serum vitamin D level (25 OH), blood urea nitrogen (BUN), serum creatinine, serum-corrected calcium, serum inorganic phosphorous and serum parathyroid hormone (PTH) levels.
The total Kt/V and total creatinine clearance was derived from urea and creatinine levels in 24-h urine collection, dialysate effluent and serum samples. The total Kt/V and total creatinine clearance were calculated using Adequest software program from Baxter Ltd.
Definition of vitamin D deficiency
The results of serum vitamin D level (25 OH) were interpreted as: Levels above 75 nmol/L (30 ng/mL) were considered as normal, levels between 25 and 75 nmol/L (10-30 ng/mL) were considered as vitamin D insufficiency, and patients with serum levels below 25 nmol/ L (6 ng/mL) were considered severe vitamin D sufficiency. [5]
| Statistical Analysis | | |
We analyzed the data using IBM SPSS for Windows, version 18.0. Descriptive data were expressed as the mean ± standard deviation and percentage. We used Student's t test to compare the various variables and a P <0.05 was considered significant.
| Results | | |
The mean age of the patients was 46 ± 21 years. The M:F ratio was 11:16, the mean body mass index was 32 ± 9.45 and the mean urine volume was 353 ± 365 mL/24 h. Ten patients were anuric. Five patients were on continuous ambulatory PD and 22 were on automated PD. The average time on PD was 27.5 months. The etiology of end-stage renal disease was diabetes mellitus in 11 (40.7%) patients, glomerulonephritis in nine (33.3%) patients and hypertension in three (11.1%) patients. Three patients were suffering from other causes including Systemic Lupus Erythematosis and for one (3.7%) patient, the primary cause was not known.
The mean serum vitamin D 25 (OH) level was 16.1 ± 8.23 nmol/L. None of our patients had 25 OH levels within the normal range [i.e., above 75 nmol/L (30 ng/mL)]. Sixteen (60%) patients had 25 OH <15 nmol/L (severe deficiency) while eight (30%) patients had levels between 15 and 25 nmol/L (vitamin D insufficiency).
The average serum creatinine was 701 ± 347.54 μmol/L, the mean serum urea was 17.8 ± 7.09 mmol/L, the mean total Kt/V was 2.15 ± 1/week and the mean total creatinine clearance was 78.74 ± 54.5/week. The serum-corrected calcium was 2.2 ± 0.2 mmol/L, the serum inorganic phosphorous was 1.47 ± 0.37 mmol/ L and the PTH level was 45 ± 39 pmol/ L. Fifteen patients (53.5%) had hyperpara-thyroidism (serum PTH level above 30 pmol/L as per the KDOQI guidelines). [5] Twenty-one patients (77.8%) were using calcitriol and 24 (85.7%) patients were on calcium carbonate. Five patients (18.56%) were using Cinacalcet.
| Discussion | | |
The serum 25(OH) D levels reflect the status of vitamin D storage. The K/DOQI guidelines recommend measuring 25(OH) D levels in stages three and four CKD if PTH is elevated. [5] A serum 25(OH) D level >75 nmol/L is recommended for the general population and CKD stage three and four patients. Replacement with ergocalciferol is recommended if levels are low. No guidelines are given for therapeutic approaches toward replacement of 25 (OH)D in stage five and dialysis populations. There is limited research available for the prevalence of 25(OH) D deficiency and replacement in patients with stage 5 CKD. Production of 1, 25(OH) D appears to be more dependent on 25(OH) D levels in CKD patients. [6],[7] Studies have shown loss of vitamin D in the PD dialysate, leading to severe and persistent deficiency. [8] Results of a study on PD and hemodialysis (HD) patients by Martensen, [9] Renee et al suggest a higher frequency of 25(OH) D inadequacy/deficiency in PD compared with HD patients. The prevalence of inadequate/insufficient vitamin D differed between dialysis modality [31% and 43% insufficient (<50 nmol/L); 4% and 34% deficient (<25 nmol/L) in HD and PD patients, respectively (P = 0.002)].
A study by Taskapan et al [8] reported 273 PD patients from 20 centers in Greece and Turkey. The results showed that 92% (251 patients) had vitamin D deficiency, i.e. serum 25 (OH) D3 levels less than 15 ng/mL and 119 (43.6%) had severe vitamin D deficiency, i.e. serum 25 (OH) D3 levels less than 5 ng/mL. A study by Nirav Shah et al [10] at the University of Pittsburgh USA in 2005 showed a high prevalence (100%) of inadequate 25(OH) D levels in PD patients at a single center, similar to the results seen in our study. Replacement with oral ergocalciferol once weekly for four weeks showed an increase in the 25(OH)D levels as well as symptomatic improvement. Furthermore, studies with ergocalciferol, or 25 (OH) D therapies, have shown improved serum calcitriol. [11]
Despite ample sunshine, the Middle East and Africa register high rates of vitamin D deficiency. [12] A study by Sadat-Ali Mir et al [13] reported prevalence of vitamin D deficiency among 28-37% of the healthy Saudi population. This is partially explained by limited sun exposure due to climate and cultural practices, and skin color. Another study by Elshafie et al [14] showed that vitamin D deficiency is very high among Saudi married couples, especially wives. Female gender is an independent predictor of lower vitamin D level, in addition to sedentary life-style and low milk consumption. There is a need to revise the levels set for the diagnosis of vitamin D deficiency or insufficiency in the study region.
Another study by El-Menyar et al [15] in 547 patients in Qatar reported a high prevalence of low vitamin D (498 patients (91%) with a low vitamin D level <30 ng/mL) in Qatar and countries similar to Qatar in regard with traditional, cultural and environment characteristics. Low vitamin D was also associated with a high prevalence of DM, dyslipidemia and coronary artery disease in males compared with females.
A study from Jordan in healthy non-pregnant females [16] showed 60.3% (95% CI: 57.1-63.4%) deficiency (<12 ng/mL) and 95.7% (95% CI: 94.4-96.8%) insufficiency (<20 ng/mL) among women.
PD has been used as renal replacement therapy in the Kingdom of Saudi Arabia since the 1980s. [17],[18] However, the status of vitamin D deficiency has not been well studied for this population.
In CKD stage three, vitamin D supplementation can be a valuable treatment for preventing secondary hyperparathyroidism (SHPT), [11] but is less useful in CKD stage four, probably due to insufficient renal one-alfa hydroxyl-lation. In HD patients, monthly ergocalciferol supplementation was efficient in achieving serum 25(OH) D level >75 nmol/L. [19] A meta-analysis of prospective trials [20] showed that higher 25(OH)D levels were associated with significantly improved survival in patients with CKD. Vitamin D replacement with active derivates can be associated with adverse events including extra-skeletal calcification. [21] In a systematic review by Lu Wang et al, [22] the investigators independently selected 17 prospective studies and randomized trials published in England that examined vitamin D supplementation, calcium supplementation or both and subsequent cardiovascular events. Vitamin D supplements at moderate to high doses may reduce CVD risk, whereas calcium supplements seem to have minimal cardiovascular effects.
| Conclusion | | |
All of the PD patients in our center are suffering from vitamin D deficiency. This can be due to renal disease, dietary restrictions, decreased exposure to sunlight and loss of vitamin D through PD as well as a reflection of low vitamin D levels seen in the local non-CKD population. Evidence-based clinical guidelines are needed for optimal management, including vitamin D 2 supplements and oral vitamin D receptor agonists.
Conflict of Interest: None.
| References | | |
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Correspondence Address:
Jamal S Alwakeel
Department of Medicine (38), King Saud University, P. O. Box 2925, Riyadh 11461
Saudi Arabia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/1319-2442.139873
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