The absorption of a pharmacological dose of vitamin D, from two different lipid vehicles, peanut oil, containing long chain fatty acids, and a medium chain triglyceride was compared. Serial measurements of the serum concentration of vitamin D, after dosage were made. The serum levels of 25-hydroxyvitamin D,, the major circulating vitamin D3 metabolite, were also determined. The analytical methods used were based on HPLC. In the fasting state, the serum levels of vitamin D, were significantly higher after administration in peanut oil than after administration in the medium chain triglyceride. When the vitamin D3 dose was ingested together with food no difference between the two formulations was observed. Only small inter-formulation differences in serum 25-hydroxyvitamin D, levels were detected. The results indicate that the presence of long chain fatty acids facilitates the absorption of vitamin D, KEY WORDS Vitamin D3 Lipid vehicle Absorption

Crystals of calcium phosphate (CaP) added to solutions with a composition corresponding to that at different levels of the collecting duct (CD) and with different pH were rapidly dissolved at pH 5.0, 5.25 and 5.5. Only minor or no dissolution was observed at higher pH levels. Despite this effect, CaP crystals induced nucleation or heterogeneous crystallization of CaOx up to a pH of 6.1, whereas CaP was the type of crystalline material that precipitated at higher pH. Accordingly, small crystal volumes were recorded at pH 5.5 and great volumes at pH 6.7 4 h after the addition of CaP crystals to the solutions. Dialyzed urine appeared to counteract the dissolution of CaP and to reduce the rate of secondary crystallization. The CaP induced crystallization of CaOx was confirmed by a reduction of (14)C-labeled oxalate in solution. The AP(CaOx) required for a nucleation or heterogeneous crystallization of CaOx in the presence of CaP was around 1.5 x 10(-8) (mol/l)(2). For CaP crystal formation on CaP, an AP(CaP) ((a)Ca(2+) x (a)PO(4)(3-)) of approximately 50 x 10(-14) (mol/l)(2) appeared to be necessary. The CaOx crystals formed were microscopically found in association with the CaP crystalline material and were most frequently of CaOx dihydrate type. Step-wise crystallization experiments comprising supersaturation with CaP (Step A), supersaturation with CaOx (Step B) and subsequently acidification (Step C) showed that CaOx crystal formation occurred when CaP crystals were dissolved and thereby served as a source of calcium. The ensuing formation of CaOx crystals is most likely the result from high local levels of supersaturation with CaOx caused by the increased concentration of calcium. These experimental studies give support to the hypothesis that crystallization of CaOx at lower nephron levels or in caliceal urine might be induced by dissolution of CaP formed at nephron levels above the CD, and that a low pH is prerequisite for the precipitation of CaOx. The observations accordingly provide additional evidence for the important role of calcium phosphate in the crystallization of calcium oxalate, that might occur both at the surface of Randall's plaques and intratubularly at the papillary tip.

We evaluated a new, simple, enzymatic kinetic method from Wako Chemicals GmbH in comparison with a kinetic Jaffé method by using isotope dilution-mass spectrometry (ID-MS) as a reference method. An ID-MS-calibrated serum standard was used. Both the enzymatic and the Jaffé method correlated well with ID-MS, except for sera with high concentrations of bilirubin. Ethyl acetoacetate, acetone, and glucose in serum interfered somewhat with the Jaffé method but not with the enzymatic method. We conclude that the present enzymatic method has merit as compared with a Jaffé method for routine work, but is more expensive.

Using a standardised procedure, we assessed the crystallisation properties of calcium phosphate in urine with a composition matching that in the distal part of the distal tubules (DTd) and of calcium oxalate in urine with a composition matching that in the mid-collecting duct (CDm). We used 8-h urine samples collected between 2200 h and 0600 h with sodium azide as preservative. Urine from ten patients with recurrent CaOx stone formation and from ten normal subjects was used for the measurements. The DTd and CDm samples were obtained by diluting the voided 8-h urine to 3000 ml and 1750 ml per 1.73 m2 body surface area, respectively. The nucleation was studied in DTd urine following supersaturation with CaP. The crystal size distribution was assessed with a Coulter counter both following supersaturation of DTd urine with CaP and of CDm urine with CaOx. The crystallisation of CaP in DTd urine as well as that of CaOx in CDm urine, in the presence of CaP crystals that had been precipitated in DTd urine, was measured with the isotope technique. The inhibition of CaOx and brushite crystal aggregation in standardised diluted aliquots of DTd and CDm urine was assessed spectrophotometrically as the rate of sedimentation. There was a slightly increased sedimentation rate and a lower initial absorbance in DTd urine from stone formers supersaturated with CaP. Although these findings might reflect a state of increased crystal aggregation in stone formers' urine, this could not be confirmed by crystal size measurements in the Coulter counter. The inhibition of brushite crystal aggregation in DTd urine was significantly in stone formers' urine than in normal subjects' urine (P < 0.001). Moreover, all inhibition values in DTd samples from stone formers were negative, suggesting a promoter effect on crystal aggregation. The inhibition of CaOx crystal aggregation in CDm urine also was significantly higher in CDm urine from normal subjects than in CDm urine from stone formers (P < 0.05). For all other variables the level was similar when urine samples from the two groups were compared. Although this series of crystallisation assessments was carried out on a small number of standardised diluted urine samples only, the results nevertheless emphasise a defect in aggregation inhibition as one important determinant for an abnormal calcium salt crystallisation in patients with recurrent stone formations. This difference obviously includes aggregation of both CaP crystals in DTd urine and CaOx crystals in CDm urine. The results also show that assessment of crystallisation properties of this kind can be carried out in standardised, diluted 8-h night urine samples, which accordingly can be used in the routine work-up of patients with calcium stone disease. Such an approach might prove useful in order to get information on the combined effects of the driving force of supersaturation and crystallisation modifying properties accomplished by urinary macromolecules and other modifying agents.