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)

53 patients were followed up for an average of 3 years after renal transplantation for evaluation of disturbances in calcium-phosphorus metabolism and skeletal diseases. Postoperative hypercalcemia and hypophosphatemia can be related to persistence of hyperparathyroidism when kidney function is restored. Hypercalcemia was observed in 43% of the patients and lasted less than one year in 80% of cases. Transient hypophosphatemia was present in 15%. These abnormalities did not cause clinical symptoms or deterioration of renal function. However, the skeletal diseases are more impressive and in the first place osteopenia. Bone densitometry revealed decreased bone mineral content in two thirds of the females and one fifth of the males. In females the bone density decreased 3.3% during an average observation period of 7 months, but remained constant in males. Renal osteodystrophy is the main cause of the initial osteopenia. The absence of remineralization or the progression of bone losses is related to the initial persistence of hyperparathyroidism and to corticosteroid treatment. According, 12.5% of the patients presented pathological fractures (spine, hip). In 3 patients (5.7%) with reduced transplant function, osteomalacia without hypophosphatemia was observed. 4 patients (7.5%) had osteonecrosis of the femoral head. There was little progression and surgery was not necessary.
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PMID:[Disturbances of the calcium-phosphorus metabolism and skeletal diseases following kidney transplantation]. 701 May 80

Thirteen patients receiving regular haemodialysis, with biochemical or radiological evidence of renal osteodystrophy, were treated with alfacalcidol (1 alpha hydroxy vitamin D3) for four years. During the first eighteen months of treatment plasma alkaline phosphatase and serum parathyroid hormone concentrations fell and subperiosteal phalangeal erosions improved. Thereafter plasma alkaline phosphatase and serum parathyroid hormone concentrations rose and after four years' treatment only four patients had a normal plasma alkaline phosphatase, only five a normal serum parathyroid hormone level and in only six had the erosions healed completely. Hypercalcaemia occurred in twelve patients, plasma calcium exceeding 3.0 mmol/l in ten. Plasma calcium rose abruptly close to the time when plasma alkaline phosphatase became normal and often remained raised despite reduction in dosage of alfacalcidol. We have reservations about the ultimate value of long-term treatment with alfacalcidol in haemodialysed patients with renal osteodystrophy and urge caution in its use.
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PMID:Long-term experience of alfacalcidol in renal osteodystrophy. 714 11

Growth arrest and renal osteodystrophy are major problems in renal insufficiency of children. The present report describes our experiences in managing renal osteodystrophy in 14 dialyzed children using 1,25-DHCC for 12 months. Values in plasma of Ca, P, Mg, alkaline phosphatase, iPTH, 25-OH-D, and 1,25-DHCC were determined regulary. Skeletal X-rays and analysis of iliac crest biopsies were obtained in each child. In treatment with 1,25-DHCC episodes of severe but reversible hypercalcemia occurred. Alkaline phosphatase and iPTH normalized completely. Radiographic examinations revealed marked improvement. Histological signs of fibro-osteoclasia and resorptive defects disappeared but there was no recovery of osteomalacia. A reduction of osteoblast population and of bone transformation was obvious. 1,25-DHCC failed to normalize growth in uremic children. In short, neither vitamin D nor 1,25-DHCC can guarantee complete recovery of renal osteodystrophy and growth arrest in uremic children.
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PMID:[Renal osteodystrophy in children. Therapy with 1,25-dihydroxy-cholechalciferol (author's transl)]. 739 29

Hypercalcemia and low serum parathyroid hormone (PTH) levels are features of the adynamic lesion (AD) of renal osteodystrophy, but there is little information about parathyroid gland function in this disorder. Therefore, the four parameter model was used to evaluate calcium-regulated PTH release in patients with either adynamic bone or secondary hyperparathyroidism (OF) as documented by bone biopsy and in normal volunteers (NL). Patients had undergone CCPD for 20 +/- 4.2 months, and all received calcium carbonate as the sole phosphate-binding agent. During two hours infusions of sodium citrate, the rate of decline in serum ionized calcium levels did not differ among groups; serum PTH levels rose from 136 +/- 38 to 342 +/- 140 pg/ml in AD and from 691 +/- 99 to 869 +/- 121 pg/ml in OF. Maximum PTH levels were 322 +/- 42% of baseline values in AD but only 146 +/- 9.7% of baseline in OF (P < 0.001), and the increase above baseline levels in AD did not differ from that in NL (300 +/- 25%, NS). During calcium infusions, serum PTH levels fell from 164 +/- 75 to 39 +/- 11 pg/ml in AD and from 622 +/- 76 to 171 +/- 29 pg/ml in OF; minimum serum PTH levels, expressed as a percentage of pre-infusion values, were 25 +/- 2% in AD and 26 +/- 5% in OF (NS).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium-regulated parathyroid hormone secretion in adynamic renal osteodystrophy. 747 73

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.
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PMID:Calcium acetate versus calcium carbonate as phosphate-binding agents in chronic haemodialysis. 780 Feb 11

We report a patient with severe chronic renal failure who developed spontaneous bone fractures. He was found to have hypercalcemia, normal calcitriol levels (probably due to extrarenal production by noncaseating granulomas), and functional hypoparathyroidism. The bone biopsy showed low bone turn-over and the presence of noncaseating granulomas. Treatment with corticosteroids decreased the calcium and calcitriol levels and the parathyroid hormone levels rose. No further fractures occurred. A repeat bone biopsy revealed the presence of osteitis fibrosa. Renal osteodystrophy may be modulated by extrarenal production of calcitriol. In this case, excessive suppression of parathyroid hormone by endogenous calcitriol presumably caused an adynamic bone lesion and spontaneous fractures.
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PMID:Modulation of renal osteodystrophy by extrarenal production of calcitriol. 787 71

Because controlled trials in adults have shown accelerated deterioration of renal function in a small number of patients receiving calcitriol for renal osteodystrophy, we initiated a prospective, randomized, double-blind study of the use of calcitriol versus dihydrotachysterol in children with chronic renal insufficiency. We studied children aged 1 1/2 through 10 years, with a calculated glomerular filtration rate between 20 and 75 ml/min per 1.73 m2, and with elevated serum parathyroid hormone concentrations. Ninety-four patients completed a mean of 8.0 months of control observations and were randomly assigned to a treatment period; 82 completed the treatment period of at least 6 months while receiving a calcitriol dosage (mean +/- SD) of 17.1 +/- 5.9 ng/kg per day or a dihydrotachysterol dosage of 13.8 +/- 3.3 micrograms/kg per day. With treatment the height z scores for both calcitriol- and dihydrotachysterol-treated groups showed no differences between the two groups. In relation to cumulative dose, there was a significant decrease in glomerular filtration rate for both calcitriol and dihydrotachysterol; for calcitriol the rate of decline was significantly steeper (p = 0.0026). The treatment groups did not differ significantly with respect to the incidence of hypercalcemia (serum calcium concentration > 2.7 mmol/L (> 11 mg/dl)). We conclude that careful follow-up of renal function is mandatory during the use of either calcitriol or dihydrotachysterol because both agents were associated with significant declines in renal function. There was no significant difference between calcitriol and dihydrotachysterol in promoting linear growth or causing hypercalcemia in children with chronic renal insufficiency. Dihydrotachysterol, the less costly agent, can be used with equal efficacy.
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PMID:A prospective, double-blind study of growth failure in children with chronic renal insufficiency and the effectiveness of treatment with calcitriol versus dihydrotachysterol. The Growth Failure in Children with Renal Diseases Investigators. 815 64

The mechanism of crystal deposition in joints varies with the chemical nature of the crystal. Crystallisation of monosodium urate, characteristic of gout, requires a neutral pH and supersatured tissues, which is the basis for the clinical definition of the upper limit of normal blood uric acid level. The appearance of crystals also is dependent on time since crystallisation of monosodium urate is very slow. Inhibitory or promoting factors could intervene and explain rare cases of gout without hyperuricemia or the rapid crystallisation which seems to characterise some types of drug-induced gout. Crystal deposits of calcium pyrophosphate dihydrate form mainly in the cartilage where they seem favoured by ageing or by trauma, which could deplete cartilage of crystallisation inhibitors, notably proteoglycans. High pyrophosphate levels within cartilage also play an important role. The appearance of these pyrophosphates in the interstitial cartilagenous medium would be in large part due to the activity of an ectoenzyme, nucleoside triphosphate pyrophosphatase; increased activity of this ectoenzyme could be responsible for some chondrocalcinosis. Chronic hypercalcaemia can also be involved in the pathogenesis of cartilage deposition of calcium pyrophosphate dihydrate by raising the calcium-pyrophosphate product, or by decreasing the activity of alkaline phosphatase, an enzyme responsible for breakdown of extracellular pyrophosphates. The pathophysiology of calcium phosphate deposits is poorly understood. For some authors, these deposits occur within matrix vesicles, but for others, within collagen fibres. Increase in the calcium-phosphate product can also be a cause, for example, during renal osteodystrophy or vitamin D intoxication.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Mechanism of crystal deposition in the joints]. 817 67

We evaluated 259 dialysis patients using serum parathyroid hormone (PTH, IRMA; normal range 1 to 5.5 pM or 10 to 55 pg/ml), the deferoxamine infusion test and iliac crest bone biopsy to determine the various forms of renal osteodystrophy and their risk factors. Although half of the biopsied patients had low turnover osteodystrophy, evidence of aluminum toxicity was present in only 1/3 of them. Additional risk factors for this bone lesion included treatment with peritoneal dialysis, ingestion of calcium carbonate, diabetes mellitus and advanced age. The PTH levels in patients with the aplastic lesion were significantly lower than in patients with normal or high bone turnover lesions [7.7 +/- 6.1 vs. 36.9 +/- 3.2 pM (77 +/- 61 vs. 369 +/- 32 pg/ml), P < 0.0001]. Aside from hypercalcemia, these patients were relatively asymptomatic. In a second study, 10 patients on peritoneal dialysis with the aplastic lesion had their dialysate calcium lowered from 1.62 to 1.0 mM. This resulted in a significant increase in PTH levels, from [3.7 +/- 0.8 to 10.6 +/- 1.9 pM (37 +/- 8 to 106 +/- 19 pg/ml), P < 0.001] which persisted over the nine-month observation period. In conclusion, the aplastic lesion is the most common form of renal osteodystrophy, with aluminum intoxication implicated in only 1/3 of the cases. In the remainder, factors identified include therapy with peritoneal dialysis using supraphysiological dialysate calcium, oral CaCO3 intake and diabetes mellitus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aplastic osteodystrophy without aluminum: the role of "suppressed" parathyroid function. 825 62

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.
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PMID:Transperitoneal calcium mass transfer using dialysate with a low calcium concentration (1.0 mM). 839 41


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