A 61-year-old man admitted with chronic renal failure was known to have been receiving long-term treatment with warfarin for dilated cardiomyopathy, atrial fibrillation and tricuspid regurgitation. During a recent hospital admission, x rays of his legs revealed extensive calcification of his arterial system (fig 1). It is well established that a hypercoagulable state can arise if a patient is given warfarin without adequate heparin cover, because plasma concentrations of natural anticoagulants such as proteins C and S are reduced before the desired fall in coagulation factors II, VII, IX and X.1 The same post-translational mechanism is involved in the synthesis of various other proteins or peptides and it has been suggested that inhibition of γ-carboxylation might play a role in the calcification of arteries and heart valves2 as well as in the development of osteoporosis3 (possible mechanisms already having been discussed by Demer et al4 previously).

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Figure 1

x Ray showing extensive calcification of arterial system.

This patient did not appear to have underlying malignancy or hyperparathyroidism (both of which may have caused hypercalcaemia), and it is suggested that, in addition to reducing his synthesis of coagulation factors, inhibition of γ-carboxylation by warfarin may also have lowered his concentrations of calcification inhibitors (for example matrix Gla protein and α2-Heremans Schmid glycoprotein (Ahsg/fetuin)),5 accelerating the calcification to which renal failure and atherosclerosis had already made him susceptible and giving rise to the dramatic x ray appearance.