Abstract
It is well known that vitamin D deficiency and associated elevation of parathyroid hormone (PTH) are common in general population. This fact also applies to chronic kidney disease (CKD) patients. The risk factors for 25-hydroxyvitamin D [25 (OH) D] deficiency are malnutrition, nephrotic syndrome, and low sunlight exposure. Low serum 25 (OH) D leads to low calcitriol level in CKD patients, because compensative elevation in PTH cannot activate 1-alpha hydroxylase in proximal tubules efficiently due to reduced viable nephron numbers and elevated fibroblast growth factor-23 (FGF-23) . Given that vitamin D is associated with renin-angiotensin-aldosterone system and insulin resistance, intervention on vitamin D metabolism in CKD patients may have impact on clinical outcomes besides bone metabolism.
