This investigation of 219 hemodialysis patients relates the history and prospective risk of bone fractures to apolipoprotein E (apoE) genotype. A greater percentage of the 41 patients with the E3/4 and E4/4 genotypes than of the 38 patients with the E2/3 and E2/2 genotypes had a history of bone fractures at the time of recruitment (44% versus 16%, P < 0.005). During the 4 years following recruitment, more of the patients with apoE genotypes E3/4 and E4/4 than with apoE genotypes E2/3 and E2/2 suffered bone fractures, but this difference was not statistically significant (17.1 versus 5.3%, P < 0.1). ApoE genotype appears to be an important genetic risk factor for bone fracture, possibly due to its previously reported influence on vitamin K concentrations in blood.

S U M M A R Y1. The metabolism of radioactive vitamin D, has been studied in individuals low or deficient in vitamin D (group I) and in vitamin D treated subjects (group 11).2. In group I there was a smaller serum pool of vitamin D, turning over more rapidly than in group 11. The principal metabolite, peak IV, appeared more rapidly in the serum of group I ; the level of radioactivity attained in this and in the more polar metabolites, peak V and VI, was also higher than in group 11. Peak VI was the major radioactive component in serum after 100 days.3. Vitamin D treatment of individuals in group I converted the pattern of metabolism of radioactive vitamin D, to that characteristic of group 11. This effect was observed in healthy individuals and in patients with vitamin D deficiency or with chronic renal failure.4. The metabolic disposal of vitaminD entering the body appears to be determined by the state of vitamin D nutrition in the individual. Reported changes of vitamin D metabolism in diseases such as renal failure could be determined by the nutritional state of the patients studied rather than by the primary disease.

This investigation of 68 hemodialysis patients (ages 33 to 91) analyzed the association of biochemical indicators of vitamin K nutriture and bone metabolism, and related both to past bone fracture history and prospective bone fracture risk. Phylloquinone concentrations were significantly lower in the 23 patients with previous fractures compared to those without (0.93 vs. 1.50 nmol/liter, P < 0.003) and a smaller percentage of their serum osteocalcin was carboxylated (48.8 vs. 53.6%, P < 0.03). The 41 patients who never had fractures had nearly three times higher phylloquinone concentrations than the nine patients with fractures during a four-year follow-up period (1.59 vs. 0.55 nmol/liter, P < 0.002) and more carboxylated serum osteocalcin (55.2 vs. 42.0%, P < 0.01). None of the patients with phylloquinone concentrations over 2.2 nmol/liter had elevated intact parathyroid hormone (iPTH) concentrations, and only patients with less than 1 nmol/liter phylloquinone had severe hyperparathyroidism (iPTH > 300 ng/liter). Our data thus indicate that suboptimal vitamin K nutriture in hemodialysis patients is associated both with increased bone fracture risk and with a high prevalence of hyperparathyroidism.

SUMMARY In vitamin D deficient rats the influence of diphenylhydantoin (DPH) and phénobarbital (PB) pretreatment on intestinal uptake of 45calcium and on the activity of CaBP was studied. The DPH rats show in contrast to the PB and control rats a significantly reduced intestinal uptake of 45calcium. However, the activity of CaBP was similar in all investigated groups. These results suggest a possibly special effect of DPH on the development of the calcium and bone disorders that have been observed in patients treated with anticonvulsant drugs. RÉSUMÉ On a étudié chez des rats qui manquaient de vitamine D, l'effet d'un pré‐traitement avec de la diphénylhydantoïne (DPH) et du phénobarbital (PB) sur l'absorption intestinale de calcium 45 et sur l'activité du CaPB. Les rats qui avaient du DPH, en opposition aux rats de contrôle et aux rats avec PB, avaient une absorption intestinale de calcium 45 significativement réduite. L'activité du CaPB était cependant semblable chez tous les groupes. Ces résultats suggèrent un effet possible particulier de la DPH sur l'origine des troubles du calcium et du métabolisme des os, qui ont été observés chez des patients en traitement avec des produits anticonvulsivants.

This report is about a 23-year-old man who required hemodialysis in connection with an acute renal failure resulting from uric acid nephropathy without hyperuricemia. After recovering renal function he showed extreme hypouricemia (0.1-0.3 mg/dl) and elevated uric acid clearance (100-300 ml/min). The fractional excretion of uric acid (Cua/Ccr) could be suppressed by oral pyrazinamide and enhanced by probenecid. As no other renal tubular or metabolic abnormalities were detected, it is suggested that a markedly increased renal tubular urate secretion was responsible for the hypouricemia and also for the rare side-effect of an uric acid nephropathy in this patient.