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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oral calcium carbonate is an effective phosphate binder in dialysis patients. Its use minimizes aluminium intake, and by maintaining a high-normal serum ionized calcium, suppresses serum parathyroid hormone levels. However, the dose required to control hyperphosphataemia may cause hypercalcaemia. We performed prospective studies in 50 previously undialysed patients starting CAPD (28 study group, 22 control group). Calcium carbonate was the only phosphate binder used in the study group which utilized a low calcium PD fluid (calcium 1.25 mmol/l), whilst the control group used standard PD solution (calcium 1.75 mmol/l) with calcium carbonate plus aluminium hydroxide phosphate binders as clinically indicated. The study group was able to take larger doses of oral calcium carbonate with no increase in episodes of hypercalcaemia compared to the control group. There were no instances of hypocalcaemia in any patient using the low-calcium dialysis fluid. Phosphate control was better in the study group, despite the additional use of aluminium-containing phosphate binders by some patients in the control group. Serum aluminium levels in the study group were maintained at < 11.5 mumol/l, but increased significantly in the control group from 3 months onward. Mean serum parathyroid hormone in the study group declined significantly from baseline values over the first 6 months, and remained at the lower level. Bone histology showed a tendency towards improvement over the 12 months, in terms of osteoclast numbers and activity. We conclude that using dialysis fluid with a reduced calcium concentration in compliant, well-monitored patients is safe.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephrol Dial Transplant 1992
PMID:Low-calcium dialysis fluid and oral calcium carbonate in CAPD. A method of controlling hyperphosphataemia whilst minimizing aluminium exposure and hypercalcaemia. 133 63

Twelve patients (median age 44.5 years) on CAPD, who had previously used a dialysate calcium concentration of 1.75 mmol/l (for a median time of 11.5 months) were started on a low calcium dialysate (LCD) with a calcium concentration of 1.25 mmol/l and followed up for 24 weeks. During the first eight weeks, no changes in the doses of oral phosphate binders were made and serum ionized calcium decreased from 1.30 +/- 0.02 (mean +/- SE) mmol/l to 1.17 +/- 0.02 (p < 0.0001) and serum PTH (1-84) rose from 68 (median, range 16-397) ng/l to 147 (70-449, p = 0.005). After week 8, increasing doses of calcium carbonate were used to achieve target calcium levels of 1.20-1.30 mmol/l. No aluminum-containing binders were used. Calcium carbonate doses were increased from 2.3 (median, range 0.75-12) g/d to 6.8 (3.8-15.0, p = 0.0004) and serum phosphorus concentrations decreased from 2.00 mmol/l (median, range 1.25-2.67) at 8 weeks to 1.61 (1.18-2.39) at 24 weeks (p = 0.023). Serum intact PTH(1-84) values remained elevated despite the gradually increasing serum calcium concentrations. Hypercalcemia was recorded in 20/36 (56%) of blood samples during a period of four weeks before the start of LCD, and such episodes were observed in 15/89 (17%) of samples (p < 0.001) on LCD during the period when calcium carbonate doses were increased. It is concluded that on LCD 1) the number of episodes of hypercalcemia was markedly reduced, 2) higher calcium carbonate doses could be used, and thus 3) the control of serum phosphorus improved.(ABSTRACT TRUNCATED AT 250 WORDS)
Adv Perit Dial 1992
PMID:CAPD with low calcium dialysate and calcium carbonate: results of a 24-week study. 136 22

We studied calcium (Ca), magnesium (Mg) mass transfer (MT) in 10 and lactate balance in 5 CAPD patients using standard dialysis solution [(ST) (Ca 1.75 mmol/l; Mg 0.75 mmol/l; lactate 35 mmol/l)] and with reduced Ca/Mg, high lactate solution [(LC) (1.25 mmol/l; 0.25 mmol/l; 40 mmol/l respectively)]. Exchanges were performed with 1.36% and 3.86% glucose solutions. MT was calculated as mmol/exchange. Ca MT was +0.96 and +0.39 with ST 1.36% and 3.86% glucose respectively. Serum ionised Ca (iCa++) levels were less than fluid Ca during these exchanges. With LC 1.36% glucose it was -0.66 when ICa++ was more than dialysate Ca, but +0.66 when iCa++ was less than dialysate Ca. Ca MT was negative with LC 3.86% glucose irrespective of iCa++ levels. All patients were hypermagnesaemic (mean 1.24 mmol/l. Mg MT was +0.21 and -0.04 with ST 1.36% and 3.86% glucose respectively and -0.62 and -1.13 with LC 1.36% and 3.86% glucose respectively. The difference between mean lactate gain and bicarbonate loss was less (-0.4) during exchange with LC 1.36% glucose. Mean plasma TCo2 and plasma pH did not differ between ST and LC solutions. We conclude that reduced Ca/Mg, high lactate solutions should reduce hypercalcaemia/magnesaemia and maintain a better acid base balance in CAPD patients who may require Ca/Mg containing phosphate binders.
Adv Perit Dial 1992
PMID:Calcium, magnesium mass transfer and lactate balance study in CAPD patients with reduced calcium/magnesium and high lactate dialysis fluid. 136 24

Due to toxic side effects of aluminum-containing agents for treatment of uremic hypophosphatemia, much interest has been focused upon aluminum-free phosphate binder alternatives. From results of experimental studies with calcium acetate, this salt has been suggested as a possible effective and safe phosphate binder. In the present study, calcium acetate was used during a mean of 11 months for serum phosphate control in 30 uremic patients previously treated with aluminum and/or calcium carbonate. Satisfactory control of serum phosphate was achieved during the study (mean phosphate concentration +/- SE: 2.15 +/- 0.12 mmol/l compared to prestudy 2.23 +/- 0.19 mmol/l). Mean serum concentrations of calcium, alkaline phosphatase and parathyroid hormone did not change significantly during the study. Serum aluminum decreased significantly (p less than 0.01). Moderate hypercalcemia was observed in 6 patients. Calcium acetate treatment was withdrawn in 2 patients due to gastrointestinal discomfort. It is concluded that calcium acetate seems to be an effective phosphate binder alternative with relatively few side effects.
Adv Perit Dial 1991
PMID:Calcium acetate used as phosphate binding treatment in uremic hyperphosphatemia. 168 Apr 30

At start of dialysis most patients have histological bone abnormalities. These can be divided into two groups--high turnover and low turnover bone disease. Low turnover aplastic disease was previously attributed to aluminum accumulation but is now known to occur even in patients with less than 5% surface stainable aluminium. It is characterised by a mineralisation defect, thin osteoid seams, decreased numbers of osteoclasts and osteoblasts and absent aluminium staining. We have avoided aluminium containing phosphate binders (ACPBs) completely, with a combination of oral calcium carbonate and "low calcium" (1.25 mMol/l) dialysis fluid. Phosphate control has been good (mean less than 1.6 mMol/l) and over the first twelve months serum PTH levels have fallen significantly. Transient asymptomatic episodes of hypercalcaemia have occurred but no patient required ACPBs. Bone biopsies at the start of CAPD in 34 patients showed over 50% to have osteitis fibrosa (OF) but in five cases (15.6%) the aplastic lesion was found without aluminium staining. In seven follow-up biopsies OF improved in 3 cases, osteomalacia improved in 1, became aplastic in 1, while aplastic bone worsened in 1 and changed to mild OF in 1. We conclude that the predominant bone lesion in our patients at start of CAPD is OF, but 15% already have aplastic bone. "Low calcium" dialysis fluid enables ACPBs to be avoided in the majority of CAPD patients.
Adv Perit Dial 1991
PMID:Renal osteodystrophy in CAPD. 168 Apr 34

Patients on CAPD using calcium carbonate (CaCO3) as phosphate binder might benefit from low-calcium (Ca) concentration dialysis solutions; however, no data are available for the effects of this regimen on Ca metabolism. We studied 10 patients on stable CAPD regimens with standard dialysis solutions (Ca 7 mg/dL) who were taking CaCO3 to control hyperphosphatemia (mean daily doses 4.5 +/- 2.4 g). Hypercalcemic episodes had been recorded in 6 patients. Standard dialysis solutions were replaced with solutions containing 5 mg/dL of Ca. Calcium and phosphate peritoneal mass transfer (MT), serum concentrations of total Ca, ionized Ca (Ca++), phosphate, intact PTH, and mid-molecular PTH, were evaluated before and 48 hours after change of dialysate. The switch to low-Ca solutions was accompanied by significant changes in calcium mass transfer (Ca MT) (+9.84 +/- 48.22 versus -96.74 +/- 48.32 mg/day, p less than .001). Ca MT was significantly (p less than .05) correlated with the serum/dialysate Ca gradient. There was no difference in phosphate MT. Serum Ca++ significantly (p less than .05) decreased from 5.20 +/- 0.32 to 4.88 +/- 0.36 mg/dL, and intact PTH significantly increased (81.5 +/- 139 versus 112.4 +/- 168 pg/mL, p less than .05). It is concluded that dialysis solutions with Ca 5 mg/dL result in a negative peritoneal Ca MT and can be useful to prevent and treat hypercalcemia in CAPD patients taking CaCO3 as phosphate binder. A careful monitoring of ionized calcium, PTH, and phosphate is suggested when an extensive and long-term use of this solution is considered.
Perit Dial Int 1991
PMID:Short-term effects of low-calcium dialysis solutions on calcium mass transfer, ionized calcium, and parathyroid hormone in CAPD patients. 175 98

Progression of hyperparathyroidism and bone disease on CAPD has been noted by several authors. In our CAPD patients we observed that aluminium-containing phosphate binders were often required because administration of CaCO3 was limited by the development of hypercalcaemia particularly in patients concomitantly requiring calcitriol. We propose that CAPD fluids with lower calcium concentration should be evaluated to facilitate control of plasma phosphate and secondary hyperparathyroidism.
Nephrol Dial Transplant 1991
PMID:Is control of secondary hyperparathyroidism optimal with the currently used calcium concentration in the CAPD fluid? 132 80

A comparative study of long-term haemodialysis patients investigated the effects of calcium acetate and calcium carbonate on concentrations of serum phosphate, calcium, and parathyroid hormone. It was demonstrated that both substances led to a significant decrease in phosphate and serum parathyroid hormone. Administration of calcium acetate reduced the serum phosphate concentration in 7 weeks from an initial value of 2.08 +/- 0.53 mmol/l to 1.51 +/- 0.39 mmol/l (P less than 0.01). Following a 1-week wash-out period, calcium carbonate reduced the serum phosphate concentration in the same patients from 1.99 +/- 0.62 mmol/l to 1.34 +/- 0.40 mmol/l (P less than 0.01). Of particular significance, however, is the fact that in relation to daily elementary calcium intake, calcium acetate was a considerably more effective binder of intestinal phosphate than calcium carbonate. During administration of calcium acetate only 1.02 g of elementary calcium were required daily in order to reduce the serum phosphate concentration. The same patients, however, required 1.88 g of elementary calcium during calcium carbonate therapy. Complementary studies investigated the influence of an accompanying calcitriol medication. In this instance, too, calcium acetate was shown to be more effective; although the patients developed hypercalcaemia with calcium acetate, this happened more often with calcium carbonate. In summary it can be said that daily calcium loading of the uraemic organism under calcium acetate therapy is reduced by nearly half as compared to calcium carbonate therapy, and that this can be achieved with the same effective decrease of the serum phosphate concentration.
Nephrol Dial Transplant 1991
PMID:The treatment of uraemic hyperphosphataemia with calcium acetate and calcium carbonate: a comparative study. 186 45

Secondary hyperparathyroidism (HP) is well known complication of long-term uremia. CAPD patients show a peculiar behaviour due to loss of vitamin D metabolites through peritoneum. Severe degrees of hyperparathyroidism may require parathyroidectomy in order to achieve appropriate control. Recently, the possibility of controlling this situation with high oral doses of calcitriol has been communicated. The purpose of this study is to evaluate the effect of this agent on hyperparathyroidism in CAPD patients. Two different groups were constituted according to the length of time on dialysis when HP was detected. All of the patients had i-PTH serum levels five times higher than the normal values (50 pg/ml). During a six month period the daily dose of oral calcitriol was increased in order to achieve a reduction in i-PTH level. The results after this period showed a significant reduction in i-PTH levels (614 +/- 378 to 241 +/- 80 pg/ml) with an average increase in oral calcitriol from 0.16 +/- 0.1 to 0.67 +/- 0.4 with no significant changes in serum calcium or phosphorus. The group with HP at start of dialysis achieved these effects easier and with lower doses of calcitriol. We conclude that moderately high doses of oral calcitriol control secondary hyperparathyroidism in CAPD patients without hypercalcemia.
Adv Perit Dial 1990
PMID:Secondary hyperparathyroidism in CAPD patients: its suppressibility with high doses of calcitriol. 198 16

We treated nineteen haemodialysis patients with secondary hyperparathyroidism with increasing oral doses of 1,25 dihydroxycholecalciferol (calcitriol) over a 12-week period and used low calcium dialysate (1.0 mmol/l) to prevent hypercalcaemia. Nine patients received daily calcitriol and ten received calcitriol thrice weekly, and at the end of the study the mean doses were 2.0 micrograms daily and 2.6 micrograms thrice weekly respectively. The regimen was well tolerated with nine episodes of mild hypercalcaemia, none of which were symptomatic. Mean PTH and alkaline phosphatase concentrations decreased from 62.0 pmol/l (15-125) to 22.0 pmol/l(1-70) (P less than 0.01), and 144 IU/l (48-461) to 123 IU/l (61-346) (P less than 0.05) respectively. Mean serum calcium increased from 2.33 mmol/l (2.05-2.55) to 2.52 mmol/l (2.26-2.67) (P less than 0.01). There were no significant changes in serum phosphate, magnesium, or aluminium concentrations and there were no significant differences in outcome between patients receiving daily therapy compared to those receiving it thrice weekly. A combination of high-dose oral calcitriol and low calcium dialysate can reverse secondary hyperparathyroidism without causing hypercalcaemia and these results suggest a benefit over conventional low-dose calcitriol.
Nephrol Dial Transplant 1990
PMID:Low calcium dialysate and high-dose oral calcitriol in the treatment of secondary hyperparathyroidism in haemodialysis patients. 212 83


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