Vitamin K Status in Relation to Bone Metabolism in Patients with Renal Failure

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Abstract
Vitamin K abnormalities may be involved in the pathogenesis of bone disease in patients with advanced renal failure since vitamin K plays a role in the synthesis of osteocalcin, a marker of bone formation. Vitamin K may also indirectly suppress parathyroid function. The aim of this study was to evaluate vitamin K status in patients with renal failure and in healthy volunteers in relation to some biochemical markers of bone turnover. The studies were performed on: patients with chronic renal failure (CRF) on conservative treatment; hemodialyzed patients treated with continuous ambulatory peritoneal dialysis (CAPD); kidney transplant patients, and a control group. Intact PTH, osteocalcin, vitamin 1,25-(OH)2D3, 25-OH-D3, bone-specific alkaline phosphatase, procollagen type-I cross-linked carboxyterminal telopeptide, deoxypyridinoline, and osteonectin were assayed using commercially available kits, and the vitamin K concentration by HPLC. We found that vitamin K concentrations did not differ significantly between all the groups studied. Only in CRF patients was the vitamin K concentation low, almost reaching statistical significance when compared to the healthy volunteers (p = 0.05) and correlated positively with age, serum calcium and osteonectin. No statistically significant correlations were found between vitamin K and osteocalcin, PTH or other biochemical parameters of bone metabolism studied in patients with CRF and renal replacement therapy. In patients after renal replacement therapy, the only significant positive correlation was found between phylloquinone and osteonectin (r = 0.027, p = 0.004). The same applied when we also included healthy volunteers. The correlations of osteonectin and vitamin K are of unknown clinical relevance. Our study does not support the hypotheses of a possible role of vitamin K deficiency in patients with CRF and the influence of vitamin K on bone metabolism.

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