Short-term effect of vitamin K administration on prednisolone-induced lossof bone mineral density in patients with chronic glomerulonephritis

Glucocorticoid-induced osteoporosis has been reported to be caused by enhan ced bone resorption and suppressed bone formation. To clarify whether admin istration of vitamin K, which enhances bone formation, prevents prednisolon e-induced loss of bone mineral density (BMD), a randomized, prospective, co ntrolled study was conducted on 20 patients with chronic glomerulonephritis scheduled for treatment with prednisolone. All patients were initially tre ated with 0.8 mg/kg body weight/day of prednisolone (maximum of 40 mg) for 4 weeks, tapering to 20 mg/day over approximately 6 weeks. Ten patients rec eived prednisolone alone (Group 1), and the other 10 patients received pred nisolone plus 15 mg of menatetrenone, vitamin K, three times per day (Group 2), BMD of the lumbar spine measured by dual-energy X-ray absorptiometry ( DXA) and biochemical markers of bone metabolism in blood and urine were eva luated before and 10 weeks after administration of prednisolone alone or wi th menatetrenone. In Group 1, treatment with prednisolone significantly red uced BMD of the lumbar spine from 1.14 +/- 0.12 to 1.10 +/- 0.11 g/cm(2) (P = 0.0029). Serum intact osteocalcin and procollagen type I C-peptide (PICP ) concentrations, biochemical markers of bone formation, were markedly redu ced. A biochemical marker of bone resorption, urinary excretion of deoxypyr idinoline, was significantly reduced. In Group 2, prednisolone-induced redu ction of BMD was prevented by menatetrenone administration (1.09 +/- 0.09 t o 1.07 +/- 0.07 g/cm(2), P = 0.153). Menatetrenone prevented reduction of P ICP concentration by prednisolone but not in serum intact osteocalcin conce ntration and urinary excretion of deoxypyridinoline. Thus, treatment with p rednisolone resulted in loss of BMD of the lumbar spine associated with sup pression of both bone formation and bone resorption. Menatetrenone is a use ful agent in preventing prednisolone-induced loss of BMD.