Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calcitonin-secreting cells, 'C cells', have specific receptors for calcitriol, thus the calcitriol deficiency in uraemia may affect calcitonin secretion and/or production. The aim of the present study was to evaluate in CAPD patients the effect of calcitriol replacement (4 weeks of oral calcitriol, 0.5 micrograms/day) on both, basal calcitonin concentration and calcitonin response to calcium infusion (calcium gluconate, 3 mg/kg/h). Calcitriol replacement produced a normalization of serum calcitriol level without a significant change in serum calcium concentration. After calcitriol replacement, basal calcitonin increased from 78 +/- 15 to 101 +/- 13 pg/ml, P < 0.05. The increment in calcitonin induced by a calcium infusion was lower after (15 +/- 4 pg/ml) than before (29 +/- 4 pg/ml) calcitriol replacement. In addition, calcitriol administration induced a decrease in serum PTH level. Replacement of calcitriol in CAPD patients produced an increase in serum calcitonin concentration and a decrease in the calcitonin response to hypercalcaemia.
Nephrol Dial Transplant 1995
PMID:Effect of calcitriol replacement on serum calcitonin and parathyroid hormone levels in CAPD patients. 772 33

We studied 43 CAPD patients for 4 months during the change from a high-calcium dialysis fluid (Baxter PD1) to a low-calcium fluid (Baxter PD4), which also contained low magnesium (0.25 mmol/l) and high lactate concentrations (40 mmol/l). Serum calcium fell significantly as did the incidence of hypercalcaemia, whilst the proportion of patients taking calcium-containing phosphate binders increased. There was a non-significant increase in serum i-PTH levels but the proportion with i-PTH > 150 pg/ml (normal range 10-65 pg/ml) increased significantly. There was a significant fall in serum magnesium level and seven patients developed hypomagnesaemia. Serum bicarbonate increased significantly and progressively and 17 patients were alkalotic at 4 months, five severely (bicarbonate 35-40 mmol/l). One patient developed recurrent episodes of painful subcutaneous and periarticular calcification, which may have been related to the alkalosis. Initial serum bicarbonate levels correlated significantly with dialysis adequacy assessed by daily Kt/V (r = 0.458, P = 0.002). The relationship to adequacy was abolished during the period of use of the high-lactate dialysis fluid. Use of low-magnesium CAPD fluids must be supported by regular monitoring of serum magnesium levels. The high lactate concentration in such fluids may not be appropriate and is potentially hazardous when individualization of dialysis dose demands the use of relatively high exchange volumes. Low serum bicarbonate levels in CAPD patients reflect inadequate dialysis, which use of these fluids serves to mask.
Nephrol Dial Transplant 1995
PMID:Alkalosis and hypomagnesaemia: unwanted effects of a low-calcium CAPD solution. 775 61

Hyperphosphataemia plays a key role in the pathogenesis of renal osteodystrophy, and phosphate-binding agents are required in many chronic dialysis patients. Aluminium hydroxide and calcium carbonate are well-established phosphate binders, but their use is associated with toxicity or poor efficacy. Calcium acetate is known to be a potent phosphate binder, and has recently been used successfully in chronic dialysis patients. In this randomized cross-over trial in 31 chronic haemodialysis patients, equimolar doses of calcium acetate and calcium carbonate were administered for 6 weeks each. Compliance was estimated from tablet counts, and biochemical parameters were measured at the end of each treatment period. Of the 31 patients 23 completed both treatment arms; of the remainder, three withdrew due to adverse symptoms, hypercalcaemia necessitated treatment withdrawal in two, and three died. Non-compliance was significantly higher with acetate (18.3% tablets not taken) than with carbonate (8.7%). Serum phosphate was significantly lower after treatment with acetate (1.51 mmol/l) than with carbonate (1.80), as was the Ca x PO4 product (3.59 vs 4.18 respectively) and PTH (17.8 vs 25.4 pmol/l respectively). Serum calcium was significantly higher after acetate therapy (2.40 vs 2.32 mmol/l). No significant difference was found for sodium, potassium, bicarbonate, urea, creatinine, and haemoglobin. This study confirms that the treatment of hyperphosphataemia is more effective with calcium acetate than with calcium carbonate. For the first time an associated beneficial effect on secondary hyperparathyroidism has also been demonstrated. Patient tolerability of calcium acetate was considerably poorer, probably due in part to tablet formulation and bulkiness, as well as possible direct gastrointestinal effects of the acetate salt.
Nephrol Dial Transplant 1994
PMID:Calcium acetate versus calcium carbonate as phosphate-binding agents in chronic haemodialysis. 780 Feb 11

To further study the effect of pulse oral calcitriol on the level of intact parathyroid hormone (iPTH), we have studied the response of 43 patients treated with 5.0 mcg calcitriol bi-weekly for one year. Mean iPTH decreased from 603 pg/mL +/- 262 (+/- SD) to 222 pg/mL +/- 185 (p < 0.001). Thirty-six patients responded showing a decrease in iPTH from baseline; 7 patients showed no decrease in iPTH. Transient hypercalcemia (calcium > 10.5 mg/dL) was noted in 6 patients of the responder group which corrected with temporary discontinuation of pulse therapy. Pulse oral calcitriol is an effective therapy to decrease elevated iPTH levels in continuous ambulatory peritoneal dialysis (CAPD) patients with hyperparathyroidism.
Adv Perit Dial 1994
PMID:Pulse oral calcitriol to treat hyperparathyroidism in 43 CAPD patients. 799 40

This study was undertaken to evaluate the long-term effect of single weekly oral pulse calcitriol therapy (0.05 mcg/kg) in 16 uremic patients. Eight (5 female, 3 male; aged 51.6 +/- 8.5 years) were on continuous ambulatory peritoneal dialysis (CAPD) for 28.8 +/- 12.7 months with basal intact parathyroid hormone (iPTH) 247 +/- 60 pg/mL. Eight (6 female, 2 male; aged 53 +/- 17.9 years) were on hemodialysis (HD) for 76.3 +/- 55 months with basal iPTH 270.9 +/- 92. Calcium dialysate was 1.75 mmol/L in all patients and serum phosphorus was controlled with CaCO3 2-4 g/day. Ca and P were measured weekly; iPTH and alkaline phosphatase were measured monthly. After two months, iPTH decreased to 132.4 +/- 89 (p < 0.05 vs basal values) in the HD patients and to 158.2 +/- 61 (p < 0.05) in the CAPD group. After six months, iPTH decreased to 108.6 +/- 73.2 (p < 0.01) in the HD patients and to 126.5 +/- 48 (p < 0.01) in the CAPD patients. Two patients (1 HD and 1 CAPD) who were not compliant with phosphate binder therapy were dropped. To control hyperphosphatemia in 1 HD patient we reduced bolus to 0.03 mcg/kg. Two CAPD patients presented hypercalcemia and required calcium dialysate of 1.25 mmol/L. In conclusion, single weekly oral pulse of calcitriol appears to be effective in suppressing mild hyperparathyroidism both in CAPD and in HD patients, even though some variations in the protocols may be required.
Adv Perit Dial 1994
PMID:Long-term effect of oral calcitriol single weekly pulse in CAPD and in HD. 799 42

Peritoneal dialysate containing 2.5 mEq/L of calcium has been used to prevent hypercalcemia when calcium-containing phosphate binders are given. However, worsening of hyperparathyroidism may result. Calcitriol used in conjunction with 2.5 mEq/L calcium dialysate is an attractive alternative, but has not been examined in a controlled trial. Eighteen patients were randomly assigned to either a control group (3.5 mEq/L calcium dialysate without calcitriol) or a study group (conversion to 2.5 mEq/L calcium dialysate with oral calcitriol, median dose 0.25 microgram/day). The initial mean serum calcium (9.9 vs 9.6 mg/dL), phosphate (5.4 vs 5.6 mg/dL), median n-terminal parathyroid hormone (PTH) levels (71 vs 55 pg/mL, normal < 25), and median 1,25 (OH)2 vitamin D levels (4 vs 5 pg/mL, normal 15-60 pg/mL) were not different in the two groups. After 8 weeks the serum calcium and phosphate were unchanged from baseline in both groups. The 9 patients who converted to 2.5 mEq/L calcium dialysate had an insignificant fall in the PTH level, not different from the control group. The median 1,25 (OH)2 vitamin D level rose from 4 to 23 pg/mL (p = 0.003) on calcitriol, but remained unchanged in the control group (5 pg/mL). The median doses of oral calcium (0.9 vs 1.1 g/day) and the frequency of serum calcium levels greater than 11 mg/dL (4/9 vs 3/9 patients, 10% vs 8% of all values) were similar in the study and control groups. Aluminum hydroxide was required intermittently for serum phosphate control in 3 patients on 2.5 mEq/L calcium dialysate and 4 on 3.5 mEq/L calcium dialysate.(ABSTRACT TRUNCATED AT 250 WORDS)
Adv Perit Dial 1993
PMID:A randomized trial comparing 2.5 mEq/L calcium dialysate and calcitriol to 3.5 mEq/L calcium dialysate in patients on peritoneal dialysis. 810 43

A 42-year-old female patient on hemodialysis (HD) developed S. aureus endocarditis of her aortic and mitral valves following the unsuccessful antibiotic treatment of an infected vascular access. She required aortic valve replacement and repair of her mitral valve. She had been receiving HD 2-3 times per week using a standard dialysate bath. Three and one-half weeks postoperatively she developed hypercalcemia with the following peak values: total calcium (t-Ca), 13.7 mg/dL; ionized calcium (i-Ca), 1.76 mmol/L. Hemodynamic instability necessitated switching from HD to peritoneal dialysis (PD). Following 48 hours of unsuccessful treatment of hypercalcemia using Baxter 2.5 mEq/L Dianeal, zero calcium dialysate prepared by our in-hospital pharmacy was used for cycler PD. Four days later the t-Ca was 10.6 mg/dL, and i-Ca was 1.32 mmol/L. Thereafter, 2.5 mEq/L calcium Dianeal was resumed. When hypercalcemia recurred (t-Ca 12.0 mg/dL and i-Ca 1.76 mmol/L), repeat use of zero calcium dialysate returned the patient's calcium values to within normal limits (t-Ca 9.0 mg/dL, i-Ca 1.20 mmol/L) by 7 days posttreatment. The results in this patient demonstrate that in-hospital pharmacies can conveniently prepare prescription-ordered dialysate and that zero calcium dialysate is yet an additional modality available to correct hypercalcemia in PD patients.
Adv Perit Dial 1993
PMID:Successful use of zero calcium dialysate to treat hypercalcemia in a postsurgical peritoneal dialysis patient. 810 44

Acute pancreatitis in patients on CAPD treatment is an infrequent, but serious complication. We studied the records of all CAPD patients with acute pancreatitis in the Netherlands from 1979 until May 1992. The incidence of acute pancreatitis during CAPD treatment was 0.46 per 100 treatment-years. In all patients at least one risk factor was present. Hypercalcaemia was the most frequently observed risk factor in our patients. The clinical picture consisted of abdominal pain and vomiting, with normal temperature and normal peristalsis. Plasma amylase was elevated in 18 episodes. Dialysate amylase concentrations exceeded 100 U/l in seven of ten episodes. The dialysate could either be clear, haemorrhagic, or cloudy. Positive dialysate cultures were found in five patients, in most cases with skin flora. No direct correlation with the pancreatitis could be established. Mortality was 58%. Continuation of CAPD or transfer to haemodialysis had no apparent effect on the outcome, but the best prognosis was found in patients with a persistently clear dialysate.
Nephrol Dial Transplant 1993
PMID:Acute pancreatitis during CAPD in The Netherlands. 815 8

Lower dialysate calcium concentrations were recently proposed to overcome the risk of hypercalcemia in continuous ambulatory peritoneal dialysis (CAPD) patients on calcium-containing phosphate binders and/or vitamin D metabolites using the standard dialysate calcium concentration (SCa) of 1.75 mM. To assess transperitoneal calcium mass transfer (CaMT) in CAPD patients using a dialysate with a low calcium concentration (LCa, 1.00 mM), 18 stable patients were randomly allocated to receive either LCa or SCa. CaMT was assessed over 4 hours using 2L dialysate bags with three different dialysate glucose concentrations (1.5%, 2.3%, 4.25%). Total serum calcium (tCa), ionized calcium (iCa), and the exact dialysate volume were measured before and after the 4-hour dwell. A sample of the drained dialysate was obtained to measure the dialysate calcium concentration. The tCa and iCa levels were not significantly different in both groups prior to and did not change throughout the test. CaMT (median/range) was -0.64 mmol/exchange (-0.35(-)-1.29 mmol/exchange) using LCa with 1.5% glucose compared to 0.23 mmol (-0.18-0.87 mmol) with SCa (p < 0.0001). CaMT was negatively correlated to iCa and ultrafiltration volume [4.25%: LCa-1.22 (-0.84(-)-1.9); SCa -0.43 (-1.35-0.13); p < 0.001]. In summary, LCa results in a loss of calcium into the dialysate even at low ultrafiltration volumes and serum iCa levels. This might facilitate the prevention and therapy of renal osteodystrophy with calcium-containing phosphate binders and calcitriol. However, patients using LCa must be carefully monitored for calcium homeostasis and bone turnover.
Perit Dial Int 1993
PMID:Transperitoneal calcium mass transfer using dialysate with a low calcium concentration (1.0 mM). 839 41

Calcium carbonate (CaCO3) is an effective phosphate (PO4) binder in uremics, and its use reduces aluminum (Al) intake. By maintaining high serum Ca2+, it decreases serum parathyroid hormone (PTH) levels. Hypercalcemia, however, often limits the dosage. In order to evaluate the effects of a low-Ca peritoneal dialysis solution (PDS) (1.25 mmol/L) on Ca metabolism, we studied the following in 12 continuous ambulatory peritoneal dialysis (CAPD) patients with hypercalcemia (6 with low PTH levels, low-turnover bone disease, group 1, and 6 with high PTH levels, high-turnover bone disease, group 2, documented by bone biopsies): serum Ca2+; serum PTH; bone morphology. The follow-up was 12 months. Results show that in both groups within the third month there was a decrease in serum Ca2+. In group 1 serum PTH increased, reaching the norm, and in group 2 it further increased exceeding the norm. Because in both groups serum Ca2+ was normal, it was possible to increase oral CaCO3 (10.5 +/- 2.5 g/day) to control PO4 levels and to stop Al gels. In group 2, in order to avoid the further rise of serum PTH, the low-Ca PDS was supplemented with 2 micrograms/day of 1,25(OH)2D3 (vitamin D3); this was followed by a reduction in serum PTH with no increase in Ca2+ and PO4. The use of low-Ca PDS may be useful in preventing hypercalcemia in CAPD patients treated with high oral doses of CaCO3 and in improving low-turnover bone disease, while low-Ca PDS supplemented with vitamin D3 improves high-turnover bone disease.
Perit Dial Int 1993
PMID:Low- and high-turnover bone disease in continuous ambulatory peritoneal dialysis: effects of low-Ca2+ peritoneal dialysis solution. 839 44


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