The Effect of Vitamin K on Bone Homeostasis in Experimental Renal Failure

Original article


Abdussalam E1-Shakmak 1, Balلzs Gyorffy1, Erika Heninger 1, Andrلs Gyorffy 2, Helmut Reichel 2, Andrلs Szabَ 1

1- Semmeiweis University, Department of Pediatrics Research Laboratory for Pediatrics and Nephrology, Hungarian Academy of Sciences and Semmeiweis University, Budapest, Hungary. 2-Nephrology Center, Villingen-hwenningen, Germany

Garyounis Medical Journal Vol. 21, No.1. 2004:64-71


Recent studies indicated that vitamin K influences bone mineralization. Objectives: Our aim was to investigate the effect of exogenous vitamin K on bone metabolism an experimental renal failure. Materials and Methods: Three groups of rats (10 per each group) were studied: (Or. I) sham-operated intact animals (Intact); (Gr.1I) sub totally nephrectomized animals (sNX÷V); (Gr.ffl) sub totally nephrectomized animals treated with vitamin K (Konakion MM®) at a dose of 1 mg/kg body weight (bw)/day subcutaneously for 2 weeks (sNX÷K). The animals were sacrificed 8 weeks after the second operation. Results and Discussion:
Hyperparathyroidism was present in sNX + V and sNX + K animals. Urinary pyridinoline, deoxypyndinoline and calcium excretion were elevated in sNX + V as compared to intact documenting increased bone turnover. In contrast, these parameters were comparable in sNX + K and Intact, suggesting that vitamin K treatment prevented the uremia-associated increase in bone turnover. Calcium and phosphorus content of bone were lower in sNX + V as compared to Intact. In sNX + K, vitamin K treatment prevented the decrease of calcium and phosphorus content of bone found in sNX + V. Bone mineral density decreased significantly in sNX + V vs. Intact, but not in sNX + K. Conclusion: Our results indicate that vitamin K treatment may modify bone mineral metabolism in experimental hyperparathyroid renal bone disease by attenuating the increase in bone turnover by an as yet unidentified mechanism.

Keywords: vitamin K, bone homeostasis, chronic renal failure, renal osteodystrophy, rat.