[Renal osteodystrophy in Spain. Multicenter survey. (I). Collaborative Centers of the Multicenter Study on Renal Osteodystrophy]. / Osteodistrofia renal en España. Encuesta multicéntrica. (I). Centros colaboradores del Estudio Multicéntrico sobre Osteodistrofia Renal.

In order to know the current management of renal osteodystrophy in Spain we collected data from 172 centres (10,724 patients) obtained from a 30 questions enquiry designed to show different aspects of the current management of renal osteodystrophy. The levels considered the "goal" for treatment were: Calcium 10-10.5 mg/dL (53% of centres), 9.5-10 mg/dL (28%), 10.5-11 mg/dL (14%) and 9-9.5 mg/dL (5% of centres). Phosphorus: between 4.5 and 5.5 mg/dL (77% of centres), between 5.5 and 6.5 mg/dL (15%) and less than 4.5 mg/dL (8% of centres). Parathormone (PTH): between 120 and 250 pg/mL (75% of centres), between 60 and 120 pg/mL (19% of centres). The calcium concentration used in the dialysis fluids was 2.5 in 44% of centres, 3 in 28%, 3.5 in 26% and 2 mEq/L in the remaining 2% of centres. Pulse therapy was started with PTH higher than 750 in 16% of centres; with PTH higher than 500 pg/mL in 52% and with PTH higher than 250 pg/mL in 28% of the centres. Only 51% of centres decreased the calcium concentration in dialysis fluids when the patients were receiving parenteral calcitriol. Fifty-nine percent of centres considered a positive response to treatment any reduction in PTH levels, 24% of centres considered response a decrease of at least 20%, 78% of centres maintained the treatment with calcitriol 6 months before deciding if the patient was a "responder" or a "non-responder". Parathyroidectomy was performed when PTH was higher than 1,000 pg/mL in 38% of the centres; in 41% when PTH was between 1,000 and 750; in 19% when PTH was between 750 and 500; and when PTH was between 500 and 250 pg/mL in the remaining 2% of the centres. Five percent of the patients had a parathyroidectomy.

[Bone metabolic markers and use of vitamin D in dialysis. Multicenter survey. (II). Collaborative Centers of the Multicenter Study on Renal Osteodystrophy]. / Marcadores metabólicos óseos y uso de vitamina D en diálisis. Encuesta multicéntrica. (II). Centros colaboradores del Estudio Multicéntrico sobre Osteodistrofia Renal.

Renal osteodystrophy has become one of the most important aspects related with morbidity in dialysis patients. The aim of our study was to analyse the main biochemical markers of mineral metabolism in 7,422 dialysis patients from 147 Spanish centres. We present data about serum Ca, P, Ca-P, product, Al and vitamin D. Due to the distribution of the analytical results (not normal), non-parametric tests were used. In this analysis a p < 0.01 was considered as significant. The mean total levels were: Ca 9.7 +/- 0.9 mg/dL; P 5.6 +/- 1.6 mg/dL; Ca-P product 54 +/- 16 mg/dL; PTH 294 +/- 360 pg/mL and Al 27 +/- 23 micrograms/L. There was a great variation particularly on serum Ca and PTH levels. On the contrary, serum P and Ca-P product values were less spread: only a quarter of the patients had P levels higher then 6.5 mg/dL and one third Ca-P product higher than 60. Fifty percent of patients had Al levels lower than 20 micrograms/L. Forty one percent of patients (2,811 out of the 7,422) had a PTH equal or lower than 120 pg/mL and 23% have PTH equal or lower than 60 pg/mL. Patients with PTH equal or lower than 60 have serum Ca levels significantly higher than the remaining patients, on the contrary, serum P, Ca-P product and Al levels were significantly lower. In this group, 21% of patients were receiving vitamin D (in spite of low PTH). On the contrary 32% of patients were not receiving calcitriol (despite PTH higher than 250 pg/mL). Forty four percent of patients were receiving vitamin D (46% on haemodialysis and 31% on peritoneal dialysis). Patients on haemodialysis showed serum Ca, P, PTH and Al levels higher than patients on peritoneal dialysis.

Vitamin D receptor gene polymorphisms, bone mass, bone loss and prevalence of vertebral fracture: differences in postmenopausal women and men.

Bone mineral density (BMD), the major determinant of fracture risk, is under strong genetic control. Although polymorphisms of the vitamin D receptor (VDR) gene have been suggested to account for some of the genetic variation in bone mass, the influence of VDR genotypes on osteoporosis remains controversial. Previous published studies have focused mainly on women, but the pattern of response in men has not been determined. Using the BsmI restriction enzyme, we studied the influence of the different VDR genotypes on bone mass, bone loss and the prevalence of vertebral fractures in a population-based sample of both sexes (n = 326). BMD was measured at the lumbar spine and femoral neck, with a 4-year interval, using dual-energy X-ray absorptiometry. Vertebral fractures were assessed by two lateral radiographs at the beginning and end of the study. The prevalence of the three possible VDR genotypes was similar to those in other Caucasian populations and no differences were found between men and women. Women with the favorable bb genotype showed significantly higher BMD values at the lumbar spine and femoral neck, and a positive rate of BMD change at the femoral neck compared with women with the BB and Bb genotypes. Moreover, women with the bb genotype showed a trend toward a lower prevalence and incidence of vertebral fractures (p = 0.07). We have not found any differences between VDR genotypes in men. In conclusion, VDR gene polymorphisms are related to bone mass and bone loss in women; also a trend in the prevalence of vertebral fractures was observed in postmenopausal women but not in men.

Interaction of aluminium and gallium with human lymphocytes: the role of transferrin.

Aluminium-transferrin (Al-Tf) and gallium-transferrin caused a dose-dependent decrease in proliferation of human peripheral blood lymphocytes cultured for 3 days with phytohaemagglutinin (PHA). Addition of apotransferrin reduced the inhibitory effect. Al added as AlCl3 or aluminium citrate had no effect, and there was no significant difference in the response of cells from renal failure patients with or without high serum Al levels or controls. Lymphocytes cultured in the presence of Al-Tf showed a dose-dependent uptake of Al, whereas uptake from aluminium citrate was low and not dose-dependent. Uptake from AlCl3 was very high but probably involved a nonspecific uptake mechanism. Levels of Al in freshly isolated lymphocytes were approximately 1.6 ng/10(6) cells, there being no difference between cells from patients and controls. It is concluded that Al, when bound to transferrin, may have a detrimental effect on lymphocyte function and might contribute to the decreased immune responsiveness of renal failure patients on haemodialysis. However, lymphocyte Al levels are probably not useful as a marker of Al overload in such patients.

Effect of aluminium on iron uptake and transferrin-receptor expression by human erythroleukaemia K562 cells.

Incubation of human erythroleukaemia K562 cells with Al-transferrin inhibited iron uptake from 59Fe-transferrin by about 80%. The inhibition was greater than that produced by a similar quantity of Fe-transferrin. Preincubation of cells for 6 h with either Al-transferrin or Fe-transferrin diminished the number of surface transferrin receptors by about 40% compared with cells preincubated with apo-transferrin. Al-transferrin did not compete significantly with Fe-transferrin for transferrin receptors and, when cells were preincubated for 15 min instead of 6 h, the inhibitory effect of Al-transferrin on receptor expression was lost. Both forms of transferrin also decreased the level of transferrin receptor mRNA by about 50%, suggesting a common regulatory mechanism. Aluminium citrate had no effect on iron uptake or transferrin-receptor expression. AlCl3 also had no effect on transferrin-receptor expression, but at high concentration it caused an increase in iron uptake by an unknown, possibly non-specific, mechanism. Neither Al-transferrin nor AlCl3 caused a significant change in cell proliferation. It is proposed that aluminium, when bound to transferrin, inhibits iron uptake partly by down-regulating transferrin-receptor expression and partly by interfering with intracellular release of iron from transferrin.