Oral vitamin D or calcium carbonate in the prevention of renalbone disease?
Current Opinion in Nephrology and Hypertension It is well known that hyperparathyroidism begins early in renalfailure and progresses, probably not linearly, throughout thenatural course of renal diseases and dialysis therapy. Recentprogress in basic medical science has improved our understandingof the mechanisms by which the classically known stimuli for parathyroidhormone synthesis and secretion may act, including hypocalcaemia, hyperphosphataemia and vitamin D3 metabolism disturbances. Inthe treatment of hyperparathyroidism, although some authors stressthe benefit of treating one of these stimuli, it is probably moreeffective to combine the treatment of them all. There is conclusiverecent work showing the efficacy of using both CaCO3 and vitaminD3, either in chronic renal failure or in dialsis patients atevery stage of hyperparathyroidism. Therefore, the treatment of hyperparathyroidism should start early, long before dialysis, and it should aim to correct any of the causal factors. Both CaCO3and vitamin D3 derivatives may be used in the prevention and treatmentof renal bone disease. The limits of this association are theincreasingly often reported adynamic bone disease, which in our experience has not yet given major clinical problems, and hyperphosphataemia. Uncontrolled serum phosphate levels would counterbalance the beneficialeffect of vitamin D3 derivatives on hyperparathyroidism.
Comparison of effects of calcitriol and calcium carbonateon secretion of interleukin-1beta and tumour necrosis factor-alphaby uraemic peripheral blood mononuclear cells
Nephrology Dialysis Transplantation (United Kingdom), 1996, 11/SUPPL.3 (15-21) We studied 26 non-dialysed patients with chronic renal failure (creatinine clearance (CCr) 32.6 plus or minus 12.7 ml/min). They were divided into three groups according to their CCr and serumintact parathyroid hormone (PTH) and were given 0.5 microg/dayoral calcitriol (calcitriol group, n = 8), 3 g/day calcium carbonate (CaCO3 group, n = 10), or neither (control uraemic group, n =8). Serum intact PTH decreased from 154 plus or minus 75 to 90plus or minus 43 pg/ml in the calcitriol group (P < 0.01) and from 162 plus or minus 97 to 77 plus or minus 62 pg/ml in theCaCO3 group (P < 0.001). Calcium carbonate was also effective in suppressing serum tartrate- resistant acid phosphatase, alkaline phosphatase and intact osteocalcin levels, while calcitriol did not suppress serum osteocalcin. Secretion of interleukin-1beta (IL-1beta) and tumour necrosis factor-alpha (TNF-alpha) by phytohaemagglutinin A (PHA)-activated peripheral bloodmononuclear cells (PBMC) was greater in uraemic patients than in age-matched healthy controls (n = 8). Calcitriol was effective in suppressing secretion of both cytokines, while calcium carbonatewas capable of suppressing only TNF-alpha secretion. CCr decreased from 37.4 plus or minus 15.4 to 33.0 plus or minus 11.8ml/min (P < 0.05) in the CaCO3 group, while it did not decrease in either the calcitriol group or the control uraemic group duringa 6 month period. These results suggest that supplementation with calcitriol is necessary to maintain bone formation and normalize IL-1beta and TNF- alpha secretion by activated PBMC in uraemic patients.
Effect of dietary calcium on urinary oxalate excretion afteroxalate loads
American Journal of Clinical Nutrition (USA), 1997, 65/5 (1453-1459) An experimental model that allowed differentiation between endogenously and exogenously derived urinary oxalate was used to assess the effect of different forms and doses of ingested calcium on oxalate absorption and excretion. In replication 1 (R-1), subjects participated in three oxalate load (OL) tests: baseline (OL alone), calcium carbonate (OL with concomitant calcium carbonate ingestion), and calcium citrate malate (CCM) (OL with concomitant CCM ingestion). The calcium salts each provided 300 mg elemental Ca. OLs consisted of 180 mg unlabeled and 18 mg 1,2(13C2) oxalic acid. In R-2, subjects participated in four OL tests: baseline (OL alone) and OLs administered concomitantly with 100, 200, or 300 mg Ca. Timedurine samples after the OL were collected at 2-h intervalsfor the initial 6 h and samples were pooled into 9-h aliquots for the remaining 18 h of the 24 h period. In R-1, 24-h mean exogenous oxalate decreased (P < 0.05) after the OL from36.2 mg (baseline) to 16.1 mg (after calcium carbonate) and to14.3 mg (after CCM) whereas endogenous oxalate remained relatively constant. Mean 24-h oxalate absorption decreased significantly from that at the time of the baseline treatment (18.3%) afterboth calcium carbonate (8.1%) and CCM (7.2%) treatments. In R-2, mean 24-h oxalate absorption was significantly lower after200 (5.9%) and 300 (7.6%) mg Ca than after 100 mg Ca (9.1%) and the OL alone (11.3%). Concomitant meal ingestion significantly decreased oxalate absorption in the absence of dietary calcium but not in association with the 300-mg Ca treatment. The overall data provided definitive evidence that dietary calcium can reduce oxalate absorption and excretion. Calcium carbonate and CCM were equally effective in this regard and a minimum of 200 mg elemental Ca maximized this effect in conjunction with an oxalic acid intake of 198 mg.
Heated oyster shell-seaweed calcium (AAA Ca) on osteoporosis
Calcified Tissue International (USA), 1996, 58/4 (226-230) A randomized, prospective, double-blind lest was carried out to compare the effects of heated oyster shell-seaweed calcium (AAA Ca), calcium carbonate, and placebo in 58 elderly, hospitalized women with the mean age of 80 divided into three groups. Group A received 900 mg/day Ca as AAA Ca. Group B 900mg/day Ca as CaCO3, and Group C placebo besides regular hospital diet containing approximately 600 mg Ca/day for 24 months. From the 25th to the 30th month, all groups were given AAA Ca. Lumbarspine and radial bone mineral density (BMD) were measured at 3-month intervals. Urinary Ca/Cr and serum alkaline phosphatase, intact and midportion serum parathyroid hormone (PTH), and calcitonin were also measured at intervals. From the 6th to the 24th month of the study, the ratio of lumbar spine BMD (L2-L4 by DPX, Lunar) to the basal pretest value was consistently mid significantly higher in Group A than Group C but not higher in Group B than in Group C. PTH, measured 12 months after the beginning of the study, was lower in Group A than in Group C, but no significant difference was found between Groups B and C. At 3 months after the placebo was switched to AAA Ca in Group C. serum PTH was significantly decreased from the level during placebo supplement. Morning urine Ca/Cr decreased in Groups A after 18 months and in B after 12months, but not in C. Serum alkaline phosphatase decreased in Group A significantly compared with Group C, but not in GroupB. AAA Ca appears to be effective for increasing BMD in elderly subjects.