ORIGINAL PAPER
The prevalence of vitamin D deficiency in pre-dialysis patients with chronic kidney disease
More details
Hide details
Submission date: 2015-04-17
Final revision date: 2015-05-26
Acceptance date: 2015-06-01
Publication date: 2015-07-13
Medical Studies 2015;31(2):75-81
KEYWORDS
TOPICS
ABSTRACT
Introduction: Reduced vitamin D levels were seen early in the course of chronic kidney disease (CKD). Its prevalence increased and severity worsened with the progression of CKD.
Aim: To assess the prevalence of vitamin D deficiency in pre-dialysis CKD patients.
Material and methods: In the study 100 adult patients were divided into three groups depending on estimated glomerular filtration rate (eGFR). Group A consisted of 30 patients with eGFR between 30–49 ml/min, group B consisted of 33 patients with eGFR between 15–29 ml/min, and group C had 37 patients with eGFR less than 15 ml/min. Renal functions, intact parathyroid hormone, 25 hydroxy vitamin D, and 1,25 dihydroxy vitamin D were measured at baseline.
Results: The mean serum phosphate and iPTH levels increased steadily as CKD progressed. On the other hand, mean corrected serum calcium levels, 25 hydroxy vitamin D, and 1,25 dihydroxy vitamin D decreased progressively in group A, B, and C. There was a significant increase in mean serum iPTH level from group A to group C (p < 0.05). The mean level of 25 hydroxy vitamin D and 1,25 dihydroxy vitamin D showed a trend of declination from group A to C (p < 0.05). Both 25 hydroxy vitamin D and 1,25 dihydroxy vitamin D positively correlated with eGFR. There was negative correlation of 25 hydroxy vitamin D and 1,25 dihydroxy vitamin D with iPTH and proteinuria.
Conclusions: The study concluded that both prevalence and severity of low 25 hydroxy and 1,25 dihydroxy vitamin D increases with progression of CKD. Their levels were negatively correlated to factors like parathyroid hormone levels and proteinuria.
REFERENCES (21)
1.
Block GA, Cunningham J. Morbidity and mortality associated with abnormalities in bone and mineral metabolism in CKD. In: Clinical guide to the basics of bone and mineral metabolism in CKD. Chapter 4. Olgaard K (ed). National Kidney Foundation, New York 2006; 77-92.
2.
St-Arnaud, Arabian A, Travers R, et al. Deficient mineralization of intramemranous bone in vitamin D-24- hydroxylase-ablated mice is due to elevated l1,25 dihydroxy vitamin D and not to the absence of 24,25 dihydroxy vitamin D. Endocrinology 2000; 141: 2658-66.
3.
Jones G, Strugnell SA, DeLuca HF. Current understanding of the molecular actions of vitamin D. Physiol Rev 1998; 78: 1193-23.
4.
Jacob AI, Sallaman A, Santiz Z, Hollis BW. Defective photoproduction of cholecalciferol in normal and uremic humans. J Nutr 1984; 114: 1313-9.
5.
Pitts TO, Piraino BH, Mitro R, et al. Hyperparathyroidism and 1,25 dihydroxyvitamin D deficiency in mild, moderate and severe renal failure. J Clin Endocrinol Metabol 1988; 67: 876-81.
6.
Ibrahim S, Rashed L. Serum fibroblast growth factor-23 levels in chronic hemodialysis patients. Int Urol Nephrol 2009; 41: 163-9.
7.
Gonzalez EA, Sachdev A, Oliver DA, Martin KJ. Vitamin D insufficiency and deficiency in chronic kidney disease. A single centre observational study. Am J Nephrol 2004; 24: 503-10.
8.
Martin KJ, Gonazalez EA. Metabolic bone disease in chronic kidney disease. J Am Soc Nephrol 2007; 18: 875-85.
9.
Coen G, Ballanti P, Bonucci E, et al. Renal osteodystrophy in predialysis and hemodialysis patients: comparison of histologic patterns and diagnostic predictivity of intact PTH. Nephron 2002; 91: 103-11.
10.
Bringhurst FR, Demay MB, Krane SM, et al. Harrison’s principles of internal medicine. Vol 2 18th edn., McGraw Hill, New York 2008; 3092-95.
11.
Willnow TE, Nykjaer A. Pathways for kidney-specific uptake of the steroid hormone 25-hydroxyvitamin D3. Curr Opin Lipidol 2002; 13: 255-60.
12.
Farrow EG, Davis SI, Summers LJ, White KE. Initial FGF23-mediated signalling occurs in the distal convoluted tubule. J Am Soc Nephrol 2009; 20: 955-60.
13.
Gattineni J, Bates C, Twombley K, et al. FGF23 decreases renal NaPi-2a and NaPi-2c expression and induces hypophosphatemia in vivo predominantly via FGF receptor 1. Am J Physiol Renal Physiol 2009; 297: F282-91.
14.
Stavroulopoulos A, Porter CJ, Roe SD, et al. Relationship between vitamin D status, parathyroid hormone levels and bone mineral density in patients with chronic kidney disease stages 3 and 4. Nephrology 2008; 13: 63-7.
15.
Zendher D, Landray MJ, Wheeler DC, et al. Cross sectional analysis of abnormality of mineral homeostasis, vitamin D and parathyroid hormone in cohort of predialysis patients. Nephron Clin Pract 2007; 103: 109-16.
16.
Satirapoj B, Limwannata P, Chaiprasert A, et al. Vitamin D insufficiency and deficiency with stages of chronic kidney disease in an Asian population. BMC Nephrol 2013; 14: 206.
17.
Levin A, Bakris G, Motich M, Smulders M. Prevalence of abnormal vitamin D calcium PTH and phosphorus in patients with CKD: results of the study to evaluate early kidney disease. Kidney Int 2007; 71: 31-8.
18.
Jabbar Z, Aggarwal PK, Chandel N, et al. Noninvasive assessment of bone health in Indian patients with chronic kidney disease. Indian J Nephrol 2013; 23: 161-7.
19.
Kawahra M, Iwassaki Y, Sakaguchi K, et al. Predominant role of 25(OH) in the negative regulation of PTH expression: clinical relevance of hypovitaminosis D. Life Sci 2008; 82: 677-83.
20.
Healy KD, Vanhooke JL, Prahl JM, Deluca HF. Parathyroid hormone decreases renal vitamin D receptor expression in vivo. Proc Natl Acad Sci USA 2005; 102: 4724-8.
21.
Isakova T. Vitamin D deficiency inflammation and albuminuria in CKD: complex interaction. J Ren Nutr 2011; 21: 295-302.