%0 Journal Article
%T Vitamin D and the Immune System from the Nephrologist's Viewpoint
%A Cheng-Lin Lang
%A Min-Hui Wang
%A Chih-Kang Chiang
%A Kuo-Cheng Lu
%J ISRN Endocrinology
%D 2014
%R 10.1155/2014/105456
%X Vitamin D and its analogues are widely used as treatments by clinical nephrologists, especially when treating chronic kidney disease (CKD) patients with secondary hyperparathyroidism. As CKD progresses, the ability to compensate for elevations in parathyroid hormone (PTH) and fibroblast growth factor-23 and for decreases in 1,25(OH)2D3 becomes inadequate, which results in hyperphosphatemia, abnormal bone disorders, and extra-skeletal calcification. In addition to its calciotropic effect on the regulation of calcium, phosphate, and parathyroid hormone, vitamin D has many other noncalciotropic effects, including controlling cell differentiation/proliferation and having immunomodulatory effects. There are several immune dysregulations that can be noted when renal function declines. Physicians need to know well both the classical and nonclassical functions of vitamin D. This review is an analysis from the nephrologist's viewpoint and focuses on the relationship between the vitamin D and the immune system, together with vitamin's clinical use to treat kidney diseases. 1. Introduction Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are diseases that are increasing in the 21st century. Preventing progressive deterioration in renal function and its complications remains the main challenge that nephrology needs to fulfill. CKD is defined according to the glomerular filtration rate (GFR) and/or the presence of pathological damage to the kidneys or the presence of kidney damage markers, such as proteinuria or hematuria, for 3 months [1]. Many complications are found in these patients as the GFR decline; these include fluid overload, anemia, cardiovascular disease, malnutrition, protein energy-wasting, and mineral bone disorders (MBD). In the case of MBD, hyperphosphatemia, hypercalcemia, and hyperparathyroidism contribute to the development of vascular calcification and cardiovascular disease. As CKD progresses, compensation for the elevations in parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23) and for reduced levels of 1,25(OH)2D3 becomes inadequate, resulting in hyperphosphatemia, abnormal bone disorders, and extra-skeletal calcification. In the Kidney Disease Outcomes and Quality Initiative (KDOQI) guideline [2] and the Kidney Disease: Improving Global Outcomes (KDIGO) guideline [3], activated vitamin D or its analogues are frequently used to treat patients with secondary hyperparathyroidism and to prevent the renal osteodystrophy. Therefore, how to use vitamin D and its analogues is an important aspect of clinical nephrology.
%U http://www.hindawi.com/journals/isrn.endocrinology/2014/105456/