UMLS:C0020437 - FACTA Search

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

1. The best way to prevent early growth failure in children with renal disease is by the use of specified nutrition and appropriate buffer, activated vitamin D, and calcium-containing phosphate binders as needed. With prenatal diagnosis of anatomically abnormal kidneys available, this type of early intervention may be much more feasible in the 1990s. 2. Supplemental sodium and water in children with polyuria and intravascular volume depletion may prevent growth failure. Cow milk is detrimental in this group of individuals because of high solute and protein load, often causing intravascular volume depletion, hyperphosphatemia, and acidosis. 3. Children with acquired glomerular disease may need sodium restriction and, if treated with steroids, a diet low in saturated fat. 4. Children with nephrotic syndrome and severe edema should be evaluated for malabsorption and subsequent malnutrition. Protein intake should be supplemented only at the RDA and to replace ongoing losses. Long-term sodium restriction is appropriate. Hyperlipidemia should be monitored: if nephrosis is chronic, a low saturated fat diet should be instituted. Angiotensin-converting enzyme inhibitors can decrease urinary protein loss and may ameliorate hyperlipidemia. Children resistant to therapy can have very high morbidity. 5. Children with <50 % of normal creatinine clearance should have PTH measured and activated vitamin D therapy should be started if PTH is elevated more than two to three times normal. Thereafter careful monitoring of calcium, phosphorus, and PTH is crucial to prevent renal osteodystrophy, low turnover bone disease, and hypercalcemia with hypercalciuria and nephrocalcinosis. 6. Children with tubular defects with severe polyuria also may benefit from low-solute, high-volume feedings. 7. All physicians caring for children with renal disease should have pediatric nephrology consultation available. Prevention of growth failure is much more cost effective than pharmacologic therapy. Before initiating growth hormone treatment for growth retardation, assiduous treatment of co-existing renal osteodystrophy and provision of optimal nutritional intake should be accomplished.
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PMID:Nutritional management of the child with mild to moderate chronic renal failure. 876 44

A quality assessment (QA) activity revealed that the percentage of parathyroid hormone (PTH) levels above 300 micrograms/dL was higher in the peritoneal dialysis (PD) unit than in the hemodialysis (HD) unit (44% vs 27%). To reduce the proportion of patients with a target PTH above 200 micrograms/dL, a protocol that emphasized control of the serum phosphate level, standard pulsed doses of calcitriol, and increased patient education was created for the management of renal osteodystrophy. Serum calcium, phosphate, and PTH levels were obtained according to the protocol from July 1994 through June 1996. The percentage of patients achieving a PTH level below 200 micrograms/dL increased from 40% in June 1994 to 57% in June 1996. Significant differences were found in PTH levels at baseline and at test times 1, 2, and 3. Hypercalcemia (Ca > 12) occurred in 4% of the 532 Ca levels drawn during the study period and were due to breaches of protocol. In conclusion, we have confirmed previous work indicating that pulsed calcitriol can control elevated PTH levels in PD patients. Furthermore, we have developed a protocol that can be used as a QA tool to reduce the prevalence of hyperparathyroidism in the outpatient PD setting without inducing excess hypercalcemia.
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PMID:Oral pulsed calcitriol protocol reduces the prevalence of hyperparathyroidism in a PD unit. 936 Jun 91

This article reviews the clinical, biological, radiological, and pathological procedures and their respective indications for the practical diagnosis of the following various histological patterns of renal osteodystrophy: osteitis fibrosa due to parathyroid hormone (PTH) hypersecretion: osteomalacia or rickets due to native vitamin D deficiency and/or aluminum overload; and adynamic bone disease (ABD) due to aluminum overload and/or PTH secretion oversuppression. Our advice regarding bone biopsy is to restrict it to patients with symptoms and hypercalcemia, especially those who have been previously exposed to aluminum. In other cases, we propose relying merely on the determination of the plasma concentrations of calcium, protide, phosphate, bicarbonate, intact PTH, aluminum, 25(OH)D3, and alkaline phosphatase (total and bony if hepatic disease is associated) to choose the appropriate treatment. Because of the danger of the desferrioxamine treatment necessary to chelate and remove aluminum, the suspicion of aluminic bone disease (osteomalacia or ABD) will always be confirmed by a bone biopsy. In the case of nonaluminic osteomalacia, correction of the vitamin D deficiency by native vitamin D or 25(OH)D3, and of the calcium deficiency and acidosis by alkaline salts of calcium and if necessary sodium bicarbonate are sufficient to cure the disease. In the case of nonaluminic ABD, the stimulation of PTH secretion by the discontinuation of 1alpha hydroxylated vitamin D and the induction of a negative calcium balance during dialysis by decreasing the calcium concentration in the dialysate will allow an increase of the CaCO3 dose to correct for hyperphosphatemia without inducing hypercalcemia. For hyperparathyroidism, i.e., plasma intact PTH levels greater than two- or four-fold the upper limit of normal levels (according to the absence or presence of previous aluminum exposure), the treatment will consist in increasing the CaCO3 dose to correct for hyperphosphatemia together with a decrease of the calcium concentration in the dialysate if the dose of CaCO3 is so high that it induces hypercalcemia. When the hyperphosphatemia has been corrected and there is still a low or normal corrected plasma calcium level, 1alpha(OH)D3 in an oral bolus 2 or 3 times a week should be given at the minimal dose of 1 microg. When the PTH level stays above 400 pg while hypercalcemia occurs and hyperphosphatemia persists, surgical subtotal parathyroidectomy is recommended or the injection of calcitriol into the big nodular hyperplastic parathyroid glands under sonography control in high surgical risk patients. Special recommendations are given for children.
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PMID:Renal osteodystrophy in dialysis patients: diagnosis and treatment. 968 90

In patients with chronic renal insufficiency, phosphate retention is a major factor in the development of secondary hyperparathyroidism, renal osteodystrophy, and soft tissue calcification, and may contribute to progression of renal failure. Prevention of phosphate retention with dietary and pharmacological means, along with the administration of calcitriol, may prevent or reverse secondary hyperparathyroidism. With more-advanced renal failure, phosphate binders become necessary to maintain phosphate balance and to prevent hyperphosphatemia. Because of toxicity, aluminum-containing phosphate binders are no longer used. Currently, calcium-containing phosphate binders, such as calcium carbonate and calcium acetate, are the most widely prescribed. Although calcium salts eliminate the problems associated with aluminum toxicity, they often result in transient hypercalcemia, requiring discontinuation of calcitriol and the use of low-calcium dialysate. Several new non- aluminum- and non-calcium-containing phosphate binders are currently at various stages of development, and may provide an alternative to the currently used binders. It is unlikely, however, that the newer compounds will completely replace calcium salts, since mild hypercalcemia may be necessary in chronic renal failure patients to suppress parathyroid hormone production. Other areas of investigation must include the development of drugs to inhibit soft tissue and renal calcifications, and to enhance urinary phosphate excretion.
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PMID:Phosphate binders for control of phosphate retention in chronic renal failure. 1050 31

The past 30 years have seen substantial advances in our understanding of the pathogenesis of the mineral, hormonal and skeletal disorders that comprise renal osteodystrophy. The introduction of calcitriol and alfacalcidol as treatments for this disorder in the early 1970s represented an enormous step forward in clinical practice, but unfortunately, the subsequent refinement of these therapies still leaves us well short of the ideal: hyperphosphatemia and hypercalcemia induced by the vitamin D metabolites, and failure to control parathyroid hyperplasia, all remain problematic. Novel pulsed regimens using alfacalcidol and calcitriol, while clearly effective, have not fulfilled initial high expectations of superiority in the context of comparative studies. New vitamin D metabolites, some of which have exhibited desirable selectivity in experimental settings with reduced tendency to raise phosphate and/or calcium while maintaining good control of the parathyroid glands, are now being evaluated. Of these, 22-oxacalcitriol, paricalcitol (19 nor-1,25 dihydroxyvitamin D2) and doxercalciferol (1 alpha-hydroxyvitamin D2) have all shown high efficacy when compared with placebo, but so also did alfacalcidol and calcitriol in similar studies in the 1970s and 1980s. The results of randomized studies comparing the new vitamin D metabolites with current standard therapy (alfacalcidol or calcitriol) are either not yet available or show uncertain benefits in relation to hypercalcemia, hyperphosphatemia and hyperparathyroidism. The impact of these new metabolites on the increasing prevalence of low turnover bone disease is unknown, although experimentally there is evidence of potentially important differences at the level of the skeleton.
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PMID:What is the optimal regimen for vitamin D? 1063 66

Control of serum phosphorus continues to be of utmost importance in renal replacement therapy, due to the high prevalence of hyperphosphatemia in the dialysis population. Hyperphosphatemia has traditionally been associated with secondary hyperparathyroidism, soft tissue calcification, and renal osteodystrophy. Recent evidence implicates poor phosphorus control as an important factor in the development of cardiovascular calcification, cardiac disease, and death in patients with chronic renal failure. Dietary restriction of phosphorus, while an important factor in the control of serum phosphorus, has practical problems that limit its success in most patients. Aluminum was used in the past to inhibit phosphorus absorption, but its accumulation has serious, toxic effects on bone. Calcium-based binders have largely replaced aluminum; however, these binders are limited by the excessive amounts of calcium absorbed, which can frequently lead to positive calcium balance, suppression of bone turnover, and hypercalcemia. Calcium overloading is also associated with soft tissue and cardiovascular calcification. More recent strategies for managing hyperphosphatemia and renal bone disease include the use of nonabsorbed phosphate binders that are aluminum- and calcium-free and the development of vitamin D analogs that control parathyroid hormone activity with less calcemic effects. Future goals include defining optimal target levels of phosphorus, calcium, and parathyroid hormone and developing clinical approaches that will promote parathyroid glands, bone, and cardiac health.
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PMID:Hyperphosphatemia: pharmacologic intervention yesterday, today and tomorrow. 1107 7

The prevalence and the clinical gravity of the various histopathological varieties of renal osteodystrophy in dialysis patients depends on the severity of both the aluminium intoxication and that of hyperparathyroidism. The prevalence of bone pains, fractures and hypercalcemias are the highest in adynamic bone diseases (ABD) with severe aluminium intoxication, then in osteitis fibrosa and mixed osteopathy, in the ABD with moderate aluminium intoxication and rare in the mild lesion in spite of similar moderate aluminium intoxication. In the absence of aluminium intoxication, hypercalcemia and hyperphosphatemia prevalence is higher only when intact PTH is more that 4 times the upper limit of normal. When PTH is between 1 and 2 folds the ULN this prevalence is null and bone mineral density is the highest. 2. The low turnover aluminic bone diseases (osteomalacic or adynamic) will be cured by long term deferoxamine treatment. The hazards of such treatment justify the performance of a bone biopsy to ensure the diagnosis. Their prevention relies on adequate treatment of tapwater and definitive exclusion of long term administration of aluminum phosphate binders. 3. Non aluminic osteomalacia will be treated according to the same guidelines given for the uremic patients before dialysis. 4. Non aluminic adynamic bone disease will be cured by means aiming at stimulating PTH secretion as discontinuing 1 alpha hydroxylated vitamin D derivatives, and, if there is no hyperphosphatemia by discontinuation of calcium supplement. In case of hyperphosphatemia in dialysis patients CaCO3 doses have to be nevertheless increased after the dialysate calcium concentration (DCa) has been decreased in order to induce a negative perdialytic calcium balance for PTH secretion stimulation. In the near future substitution of CaCO3 by non calcemic non aluminic phosphate binders will suffice. 5. Osteitis fibrosa due to hyperparathyroidism will be treated first by securing an optimal vitamin D repletion (bringing plasma 25OH vitamin D around 30 and 60 ng/ml or 75-150 nmol/l) and by correcting hypocalcemia and hyperphosphatemia by CaCO3 at high doses (3-12 g/day) taken with the meals. In case of hypercalcemia dialysate calcium concentration will be decreased to correct it or, in a near future, CaCO3 will be decreased to 3 g/day and hyperphosphatemia will be controlled by non calcemic, non aluminic phosphate binders. When hyperphosphatemia is controlled whereas plasma calcium is normal or low, 1 alpha hydroxylated vitamin D derivatives can be administered. 6. Instrumental parathyroidectomy should be considered when plasma levels of intact PTH remain above 7 folds the upper limit of normal whereas hyperphosphatemia persists and hypercalcemia occurs in order to prevent thining of the corticals and subsequent fracture risk. In case of previous exposition to aluminum, a deferoxamine test and/or a bone biopsy will be performed to decide a long term DFO treatment before the parathyroidectomy in order to prevent the transformation of a mixed osteopathy into an aluminic adynamic bone disease. 7. The difficulty of hyperparathyroidism control in dialysis patients is due to poor compliance to phosphate binders and to irreversible parathyroid hyperplasia with occured before the dialysis stage. This stress the primary importance if its early prevention without iatrogenia by first CaCO3 and vitamin D repletion, as soon as the creatinine clearance decreases below 60 ml/min/1.73 m2.
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PMID:[Renal osteodystrophy (3); its treatment in dialysis patients]. 1121 85

The methods for preventing hyperparathyroid bone disease, the major variety of renal osteodystrophy, from developing in patients with renal impairment are reviewed. With far-advanced chronic renal failure (creatinine clearance [CCr] < 15 to 20 ml/min), when many of these patients are seen by nephrologists, the use of diets very low in protein, and hence also very low in phosphorus content, combined with calcium-containing phosphate binders, have been shown to lower serum intact PTH levels and improve the osseous pathology. However, the degree of dietary restriction required to achieve success may be quite difficult to follow by most patients encountered in clinical practice. In less-advanced renal insufficiency (CCr, 25 to 60 ml/min), the active vitamin D sterols calcitriol or alfacalcidol [1 alpha-hydroxyvitamin D3] have been shown to ameliorate the skeletal lesions of renal osteodystrophy. The results of six double-blind, placebo-controlled studies and five major open-labeled studies with calcitriol or alfacalcidol are reviewed. Skeletal biopsies were improved and sometimes normalized by using calcitriol or alfacalcidol in daily doses of 0.25 to 0.5 microgram/d, and the incidence of hypercalcemia was quite low with these doses. When the dosage was increased in one study, there was a higher incidence of hypercalcemia. Improved bone mineral density of the spine and hip was reported after 1 yr in calcitriol-treated patients compared with results in the placebo group. Another report documented more favorable intact PTH suppression with intermittent dosing of 2.0 micrograms given either once or three times weekly compared with daily dosing (0.5 microgram/d); there was no rise of serum Ca over the 3-mo trial with any protcol. Other data support the greater likelihood of having normal bone if treatment is initiated when CCr exceeds 25 ml/min. There was no risk of more rapid progression of renal insufficiency in any of the studies reviewed, which include 242 patients who were given an active vitamin D sterol. One trial that used a calcitriol dose of 0.5 microgram/d noted a fall in CCr and a rise in serum creatinine, but true GFR (inulin clearance) did not change. A calcitriol-induced reduction of tubular creatinine secretion is suggested. The risk of inducing low bone turnover (adynamic bone) seems to be quite low with 10.4% of alfacalcidol-treated patients versus 6.5% of placebo developing this "lesion" after 2 yr. Despite the lack of Food and Drug Administration approval for use of these sterols in the predialysis state, evidence is compelling that: there are benefits in retarding the development or progression of metabolic bone disease; there is minimal risk, providing that low doses are used; and there is close monitoring of serum Ca, P, and creatinine. The optimal benefits may be obtained if this treatment is started early in the course of renal insufficiency (CCr in the range of 25 to 60 ml/min).
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PMID:Prevention of metabolic bone disease in the pre-end-stage renal disease setting. 1144 72

Hyperparathyroidism is a common problem for patients on renal replacement therapy programs. Many long-term dialysis patients require parathyroidectomy while on dialysis. Some patients, however, despite severe renal osteodystrophy, are transplanted, and in these a large proportion show a slow resolution of bony problems, in the context of the removal of the uremic stimulus to abnormal bone metabolism. A proportion of these patients become hypercalcaemic after renal transplantation, sometimes with symptoms. There is not a consensus on how these patients should be managed, with opinions varying from early parathyroidectomy to later parathyroidectomy and to conservative treatment. We present the case of a lady who underwent 23 years of conservative management of her post-transplant hyperparathyroidism. She was hypercalcaemic for almost all of that period, despite excellent renal transplant function. Finally, after 23 years she underwent surgical parathyroidectomy with autografting with prompt sustained resolution of her symptomatic hypercalcaemia.
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PMID:Persistent post-transplant autonomous hyperparathyroidism despite 23 years of excellent renal allograft function. 1152 40

End-Stage Renal Disease Network 11 initiated a renal osteodystrophy quality improvement activity in 1999. One component was the collection and assessment of dialysis facility renal osteodystrophy protocols, whereas another component was the analysis of bone disease-related medication use. Two hundred eighty-eight facilities were invited to submit protocols. A model bone disease and mineral metabolism protocol was developed as the standard for comparison. From the model protocol, an instrument was created to evaluate eight key areas (baseline screening of key laboratory data, dietary intervention, phosphate-binder use, vitamin D use, monitoring of key laboratory indicators, management of hypercalcemia, oversuppression of parathyroid hormone [PTH], and guidelines for both hemodialysis and peritoneal dialysis patients). A bone disease-related prescription survey was completed for 749 randomly selected patients. Survey information included vitamin D and phosphate-binder use and related laboratory values (calcium, phosphorus, intact PTH [iPTH], and calcium x phosphorus product). Although 45% of facilities had six or more points on the evaluation tool, protocols were still incomplete compared with the model. Mean facility-specific scores among the five states in the Network ranged from 1.0 to 5.9 (possible scores, 0 to 8). Most patients were prescribed a phosphate binder; however, 31.8% had average phosphorus levels greater than 6.0 mg/dL during the 3-month period. Only 58% of patients with average iPTH concentrations greater than 260 pg/mL were prescribed vitamin D. Of patients treated with vitamin D, 39% had iPTH concentrations less than 130 pg/mL. There is opportunity to improve renal osteodystrophy protocols in Network 11 and reinforce potential hazards of sustained hyperphosphatemia and hyperparathyroidism.
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PMID:Analysis of renal bone disease treatment in dialysis patients. 1204 41

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