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PubMed1980

The interrelationship between phosphate and magnesium metabolism.

a) It appears that the interrelationship between phosphate and magnesium metabolism is complicated and the mechanisms involved are not fully understood, b) the interaction between the homeostasis of these two ions is species dependent and its full expression is most evident in the rat, c) body depletion of either of these ions may result in marked changes in the blood levels, intestinal absorption, renal handling and body content of the other, d) hypermagnesemia causes hyperphosphatemia and decreased urinary excretion of phosphate, and e) the effects of hyperphosphatemia on magnesium are not elucidated as yet.

Animals↗

PubMed1977

Bicarbonate-induced phosphaturia: Dependence upon the magnitude of phosphate reabsorption.

The acute effect of bicarbonate infusion on inorganic phsophate (Pi) reabsorption was determined in thyroparathyroidectomized (TPTX) rats stabilized on a high phsophorus diet. In the normophosphatemic state, bicarbonate did not affect Pi reabsorption significantly. On the other hand, after hyperphosphatemia was induced by phosphate loading, bicarbonate inhibited Pi reabsorption. In order to determin if eht aboslute level of plasma or filtered Pi was an improtant determinant of this phosphaturic action of bicarbonate during hyperphosphatemia, equivalent rates of Pi reabsorption were achieved after phosphate infusion in TPTX rats previously stabilized on a low dietary phosphorus intake, but at significantly lower plasma Pi concentrations and filtered Pi loads than in their high dietary phosphorus counterparts. Bicarbonate inhibited Pi reabsorption equivalently in both hyperphosphatemic groups, indicating that the magnitude of Pi transport itself was of importance in determining the inhibitory response to bicarbonate. In addition, the results suggest that transport mechanisms for bicarbonate and Pi may interact competitively.

Animals↗

PubMed1995

Tumor lysis syndrome: pathogenesis and management.

Tumor lysis syndrome refers to the metabolic disturbances (hyperuricemia, hyperphosphatemia, hyperkalemia, and hypocalcemia) associated with lymphoproliferative malignancies which occur secondary to cell lysis. In some patients, tumor lysis results in acute renal failure. The nature and severity of the metabolic alterations are variable and may be influenced by the timing and intensity of chemotherapy, the magnitude of cell lysis, and the general condition of the patient with respect to hydration and glomerular filtration rate. Not only do hyperuricemia and hyperphosphatemia result from tumor lysis syndrome, they also contribute to oliguric acute renal failure in patients with tumor lysis. The pathogenesis of tumor lysis syndrome and current therapeutic strategies are discussed.

Acute Kidney Injury↗

PubMed1994

Prospective, randomized, endoscopic-blinded trial comparing precolonoscopy bowel cleansing methods.

PURPOSE: Recent reports have suggested that precolonoscopy bowel preparation is easier to tolerate if a small volume solution is used. Therefore, the aim of this study was to compare three oral solutions for colonoscopy to determine any changes in either patient compliance or cleansing ability. METHODS: Four hundred fifty patients were prospectively randomized to receive either a standard 4-liter polyethylene glycol solution, a newer sulfate-free 4-liter polyethylene glycol solution, or a 90-ml oral sodium phosphate preparation. Before and after bowel preparation all patients were weighed, and serum electrolytes as well as phosphate, magnesium, calcium, and osmolarity were measured. In addition, a detailed questionnaire was used to assess side effects and patient satisfaction. Endoscopists blinded to the type and quantity of preparation used scored the type of residual stool and the percentage of bowel wall visualized for each segment of colon and for the overall examination. Nurses recorded all procedure times as well as the quantity of irrigation and aspiration. RESULTS: Four hundred twenty-two age-matched and sex-matched patients completed all phases of the trial. There were no clinically significant changes in weight or in any biochemical parameters. There was, however, asymptomatic hyperphosphatemia in the sodium phosphate group (P < 0.01). The length of time to the cecum was similar for all three groups, with a higher volume of fluid suctioned for sodium phosphate (P < 0.01). Overall, endoscopists scored sodium phosphate as "excellent" or "good" in 90 percent vs. 70 percent and 73 percent after the polyethylene glycol or sulfate-free lavage, respectively (P < 0.01). Particulate or solid stool was found in all segments of the colon more frequently after both large volume preparations than after sodium phosphate (P < 0.05). There were no significant differences in the frequency or intensity of any of the 11 side effects questioned. Eighty-three percent of the patients who received the sodium phosphate preparation stated they would take this same preparation again, vs. only 19 percent and 33 percent for polyethylene glycol and the sulfate-free lavage, respectively (P < 0.01). CONCLUSION: The smaller volume oral sodium phosphate was not associated with any clinically significant problem, caused no increase in the incidence of side effects, was preferred by patients, and was more effective in colonic cleansing. However, the hyperphosphatemia seen may limit its use in patients with impaired renal function.

Adolescent↗

PubMed1981

Increased 1,25-dihydroxyvitamin D3 synthesis in rats fed a high-phosphorus diet.

Rats fed vitamin D-deficient diets containing 0.6% Ca and 0.3%, 0.6%, 1.2%, or 1.8% P exhibited progressive increments of hypocalcemia and hyperphosphatemia. In vitro assay of 25-hydroxyvitamin D3-1-alpha-hydroxylase (1-alpha-hydroxylase) activity in isolated kidney cortical mitochondria showed that hyperphosphatemia in the presence of hypocalcemia was associated with an increase in enzyme activity. The results indicate that the stimulation of 1-alpha-hydroxylase associated with depressed plasma Ca in rats fed a high-P diet overrides any inhibition of the enzyme that may be caused by excess plasma phosphate.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMedDate not supplied

Multiple intracranial calcifications and spinal compressions: rare complications of type la pseudohypoparathyroidism.

Type la pseudohypoparathyroidism (PHP la) is an unusual inherited disease. PHP la often causes extraskeletal calcifications and even soft tissue ossifications. Patients may present neurologic symptoms and signs related to hypocalcemia and hyperphosphatemia. We report here a 38-yr-old woman with PHP la who had two uncommon neurologic complications. One was involuntary movements related to basal ganglia calcification, and the other was myelopathy owing to ossifications of the posterior longitudinal ligament and multiple herniated intervertebral disks. Aggressive body weight control and corrections of hypocalcemia, hyperphosphatemia, and elevated PTH may be important to prevent these unusual neurologic complications. Regular and careful neurologic examinations should be performed for early diagnosis and treatments of these spinal lesions.

Adult↗

PubMed2003

Cardiovascular calcifications in pediatric patients receiving maintenance dialysis.

Cardiovascular disease is a major cause of morbidity and mortality in adult patients with end-stage renal disease receiving maintenance dialysis. Coronary artery calcifications (CAC) contribute to the high prevalence of cardiac disease and are associated with hyperphosphatemia, an elevated calcium-phosphorus product (CaxP), and prolonged time on dialysis. Chronic inflammation and malnutrition are also associated with an increased risk for development of cardiac calcifications. Young adults receiving maintenance dialysis develop cardiac calcifications at a degree out of proportion to healthy adults of the same age and gender. Many of these young adults initiated dialysis as children or teenagers. Risk factors associated with the development of CAC are also seen in the pediatric dialysis population. To date, reports of cardiac calcifications in pediatric patients receiving maintenance dialysis are limited to post-mortem studies. We present two pediatric patients with ANCA-positive vasculitis diagnosed with cardiac calcifications while receiving maintenance dialysis. Hyperphosphatemia and an elevated CaxP product were seen in both patients and probably contributed to the development of extraskeletal calcifications. In addition, both patients had an underlying systemic inflammatory disease and significant weight loss/malnutrition that may have contributed to the early and rapid onset of cardiac calcifications.

Adolescent↗

PubMed1985

Dynamic changes in serum phosphorus levels in diabetic ketoacidosis.

The dynamic changes in serum phosphorus levels in 69 episodes of ketoacidosis in 48 diabetic patients were retrospectively evaluated. The mean age was 41 +/- 2 years (mean +/- SEM), and the duration of diabetes mellitus was 7 +/- 1 years. The serum phosphorus levels determined within the first six hours of admission were analyzed. Before initiation of therapy, the incidence of hyperphosphatemia was 94.7 percent. At the end of 12 hours, the mean serum phosphorus level fell from 9.2 +/- 0.6 to 2.8 +/- 0.3 mg/dl. Before therapy, the serum phosphorus level correlated positively with the serum glucose level, the effective plasma osmolality, and anion gaps, and correlated negatively with the serum chloride level. It is concluded that hyperphosphatemia is common in diabetic ketoacidosis before therapy. The increase in serum phosphorus is likely to be due to a transcellular shift. Potential factors responsible for the shift are serum glucose, through its osmotic effect, and the organic anions.

Adult↗

PubMed1994

The role of vitamin D in chorioallantoic membrane calcium transport.

1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) is essential for the transport of eggshell calcium to the embryo across the chorioallantoic membrane (CAM). CAM contains the vitamin D receptor that increases following 1,25-(OH)2D3 injection into embryos at day 10 of incubation. Further, a single injection of 100 ng of 1,25-(OH)2D3 into vitamin D-deficient quail eggs at day 10 of incubation resulted in a significant increase in both body and yolk calcium. This is accompanied by an increase in carbonic anhydrase from low levels in deficiency to normal levels. Acetazolamide (AZ), a specific carbonic anhydrase inhibitor injected into the quail embryos, caused hypocalcemia and hyperphosphatemia. This is similar to the hypocalcemia and hyperphosphatemia found in vitamin D-deficient embryos. These results suggest that one mechanism of action of vitamin D in the mobilization of eggshell calcium is the activation of carbonic anhydrase that acidifies the calcium carbonate shell.

Acetazolamide↗

PubMed1995

Limitations of pulse oral calcitriol therapy in continuous ambulatory peritoneal dialysis patients.

Calcitriol is increasingly used for therapy of secondary hyperparathyroidism in patients with end-stage renal disease. Its therapeutic efficacy, however, often has been limited by the associated increase in intestinal calcium and phosphorus absorption. Previous studies reported that these side effects could be avoided by intermittent administration of calcitriol in high doses, subsequently referred to as pulse therapy. The present study was designed to investigate pulse oral calcitriol therapy in a patient subgroup especially susceptible to the development of hypercalcemia and hyperphosphatemia under standard continuous calcitriol treatment. We examined 15 peritoneal dialysis patients with moderate degrees of hyperparathyroidism (intact parathyroid hormone [iPTH] levels, 150 to 903 pg/mL) ingesting between 1.5 and 6 g of calcium salts as the sole phosphate binders. Treatment consisted of 0.5 microgram calcitriol twice weekly. Eight of these patients had been previously converted to low calcium dialysate to tolerate the necessary doses of phosphate-binding calcium salts. During the study period, comprising 8 pretreatment weeks and 8 weeks of therapy, dialysates and doses of calcium salts were not changed, so that only calcitriol influenced the determined parameters. As expected, iPTH levels decreased rapidly in all patients (P < 0.0001). However, within 4 weeks of treatment a marked increase in calcium phosphorus products was observed (P < 0.0001). Overt hypercalcemia developed in five patients. We concluded that pulse oral calcitriol has to be carefully monitored in peritoneal dialysis patients receiving high doses of calcium salts because of the increased risk for hypercalcemia and hyperphosphatemia.

Administration, Oral↗

PubMed1995

The importance of dosing intravenous calcitriol in dialysis patients with severe hyperparathyroidism.

The current study evaluates the use of intravenous (IV) calcitriol in 10 patients with severe hyperparathyroidism (HPTH). Patients with parathyroid hormone (PTH) > 1,200 pg/m and serum P < 6.5 mg/dL were studied. Ten patients with a mean PTH of 1,826 +/- 146 pg/mL were treated for a mean of 48 weeks with a dose of IV calcitriol commensurate to the level of PTH. The initial calcitriol dose had to be increased in seven patients. The mean maximum dose of calcitriol was 3.8 micrograms thrice weekly. There was a dramatic decrease in PTH levels, and by the end of the study it was 211 +/- 48 pg/mL. Alkaline phosphatase decreased from 582 +/- 3 to 120 +/- 12 IU/L. Serum Ca and P remained unchanged in most patients. There were three episodes of hyperphosphatemia in one patient, and another had a hypercalcemic episode. In conclusion, patients with severe HPTH respond very well to IV calcitriol, provided that dosing of calcitriol is commensurate to PTH levels, and hyperphosphatemia is kept under control.

Adult↗

PubMed1995

Successful treatment of hyperphosphatemic tumoral calcinosis with long-term acetazolamide.

We describe a patient with tumoral calcinosis, in which acetazolamide (ACZ) was, for the first time, tested for its therapeutic efficacy. The 19-year-old Japanese man had been suffering from multiple recurrent calcific masses with tenderness around the finger, knee, and toe joints since 10 months of age. Radiographs revealed several calcific subcutaneous masses around the finger joints, and calcific myelitis around the right knee joint and in the calvarium. The patient had hyperphosphatemia with elevated maximal threshold of renal phosphate excretion in the presence of normal kidney function and normocalcemia, suggesting a reduced ability to excrete phosphorus in the urine. A delay of disappearance of orally administered phosphate from the blood stream was found. A serum parathyroid hormone (PTH) level was normal, and responses to PTH and ACZ were also normal regarding the induction of phosphaturia. Since the masses tended to recur easily despite repeated surgical resections, we started medical treatment with phosphorus deprivation by oral aluminum hydroxide. However, the drug alone had no effect on hyperphosphatemia or calcific lesions, and ACZ was added in expectation of making the patient's phosphorus balance negative by its phosphaturic effect. Fourteen years of administration of the two drugs apparently improved the patient's symptoms, the biochemical findings, and the calcific lesions on radiographs. Thus, ACZ appeared to be useful for tumoral calcinosis resistant to phosphorus deprivation by aluminum hydroxide alone.

Acetazolamide↗

PubMed2003

Regulation of stanniocalcin 1 and 2 expression in the kidney by klotho gene.

The klotho gene product and stanniocalcin (STC) 1 and 2 are recently identified molecules implicated in calcium and phosphorus homeostasis. In the present study, we investigated the regulation of STC1 and STC2 gene expression in the kidney by klotho gene expression. Mice deficient in klotho expression (klotho mice) have hypercalcemia and hyperphosphatemia, and increased renal gene expression of STC1 and STC2 compared with wild-type mice. Administration of vitamin D or CaCl(2) to wild-type mice causes upregulation of STC1 but STC2 gene expression is not altered significantly. On the other hand, treatment of klotho mice with low phosphorus diet results in partial decrease in STC2 gene expression with normalization of hyperphosphatemia. These findings indicate that klotho gene expression plays a crucial role in the regulation of renal stanniocalcin gene expression in vivo, at least partly, through the control of circulating calcium and phosphate concentrations.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed2004

Arterial calcification in chronic kidney disease.

Hyperphosphatemia is associated with soft-tissue calcification and bone disease. Nephrologists prescribe phosphate binders to decrease dietary phosphate absorption, reduce serum phosphorus concentrations, and minimize the risk for soft-tissue calcification and bone disease. Recent data suggest that the dose of calcium used as a phosphate binder may contribute to the risk for cardiovascular calcification. Chronic positive calcium balance from diet, dialysis, and calcium-based phosphate binders or intermittent hypercalcemia may favor precipitation of calcium and phosphate into tissues. Calcium suppresses parathyroid hormone (PTH) secretion and bone turnover, limiting the ability of bone to incorporate calcium and phosphorus. Sevelamer, a non-absorbed polymer, allows physicians to bind dietary phosphate and decrease serum phosphorus without unwanted absorption of metals or calcium or over-suppression of PTH. In a comparative trial, calcium-based phosphate binders were associated with progressive coronary artery and aortic calcification that was attenuated by sevelamer. The optimal phosphate binder is one that controls hyperphosphatemia prevents soft-tissue calcification and preserves bone health.

Arteries↗

PubMed2004

Management of calcium and bone abnormalities in hemodialysis patients.

In chronic renal failure, hyperphosphatemia, hypocalcemia, hyperparathyroidism, reduced activation of vitamin D, decreased level of calcium-sensing receptor, osteitis fibrosa, and osteomalacia are features related to calcium abnormalities. Hyperparathyroidism is a risk factor for survival of hemodialysis patients as well as hypoparathyroidism, which is another feature in hemodialysis patients. Treatment of these abnormalities includes control of parathyroid hormone (PTH) secretion, counteracting hyperphosphatemia, correction of hypocalcemia, and others. Various kinds of vitamin D analogs have been introduced recently in addition to calcitriol and alfacalcidol, which have a rather long history (eg, maxacalcitol and falecalcitriol). Sevelamer is a newly developed phosphate binder to treat soft-tissue calcification.

Bone Diseases↗

PubMed1999

Paricalcitol, a new agent for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis.

Patients with end-stage renal disease commonly develop secondary hyperparathyroidism. Calcitriol may be administered to such patients to decrease the synthesis and secretion of parathyroid hormone (PTH) and to help maintain calcium and phosphorus homeostasis. However, the doses of calcitriol required to suppress serum PTH concentrations can lead to hypercalcemia or hyperphosphatemia in many patients undergoing hemodialysis. Paricalcitol is a new vitamin D analogue that is safe and effective in suppressing elevated concentrations of PTH in patients with established hyperparathyroidism who are maintained on chronic hemodialysis. As with vitamin D, the biologic action of paricalcitol is mediated through activation of the vitamin D receptor (VDR). The VDR functions as a ligand-induced transcription factor regulating the rate of expression of genes that are involved in controlling not only calcium homeostasis and bone remodeling but also hormone secretion, inhibition of cell growth, and induction of cell differentiation. In vitro studies have shown that paricalcitol inhibits PTH secretion from bovine parathyroid cells in a dose-dependent manner. Studies in renally insufficient rats demonstrated that paricalcitol caused approximately 10 times less elevation of serum calcium concentrations than calcitriol. In clinical studies, paricalcitol effectively decreased PTH by about 60% over a 12-week period. Mean serum concentrations of calcium were significantly increased but remained within the normal range. There were occasional (5/414 determinations) transient elevations in serum calcium above the upper limit of normal in some (5/401) patients. Serum phosphorus values did not change significantly compared with baseline, although they tended to be slightly higher in the paricalcitol-treated group than in the group receiving placebo. Elevations of the calcium-times-phosphorus product were relatively few but occurred more often in the paricalcitol than in the placebo group. The terminal half-life of paricalcitol was 5 to 7 hours in healthy subjects; in patients undergoing hemodialysis, it was 14 hours. Adverse events associated with paricalcitol use included, among others, chills, feeling unwell, fever, sepsis, palpitations, dry mouth, gastrointestinal bleeding, nausea, vomiting, edema, light-headedness, and pneumonia. Paricalcitol should be considered as an alternative to calcitriol in the treatment of patients who are undergoing maintenance hemodialysis for end-stage renal disease, as it has a decreased potential to induce hypercalcemia and hyperphosphatemia. Additional studies are required to determine the long-term effects of therapy.

Animals↗

PubMed1991

Uremic tumoral calcinosis: preliminary observations suggesting an association with aberrant vitamin D homeostasis.

Periarticular tumoral calcification is a unique form of soft tissue calcification that occurs infrequently in patients with end-stage renal disease. The mechanism underlying such massive periarticular calcifications is unknown. The radiographic similarity between uremic tumoral calcifications and those found in hereditary tumoral calcinosis, a disorder of calcitriol and phosphorus homeostasis, caused us to examine whether abnormalities in vitamin D metabolism were associated with uremic calcinosis as well. We examined two uremic subjects with massive periarticular tumoral calcifications and found that they had inappropriately high serum calcitriol levels for the degree of renal function, hyperparathyroidism, and hyperphosphatemia. The source of calcitriol could not be identified in one subject, but likely was derived from granulomatous tissue in the other. In the subject with marrow granulomas, we found that calcitonin administration further stimulated calcitriol production. Although epidemiological studies are needed to confirm this preliminary association between calcitriol and uremic tumoral calcinosis, our observations suggest that normal serum calcitriol levels in association with hyperphosphatemia may be a contributing factor in the development of this rare disorder.

Adult↗

PubMed1988

Efficacy and safety of long-term treatment with calcium carbonate as a phosphate binder.

The efficacy and safety of calcium carbonate as a phosphate binder was evaluated in 20 patients on chronic hemodialysis who had previously received aluminum hydroxide. During the control period the patients were on aluminum hydroxide and calcitriol therapy and had plasma phosphorus levels less than 6 mg/dL (4.95 +/- 0.8 mg/dL). Aluminum hydroxide was then discontinued and no phosphate binder was prescribed for 1 month. Every patient developed hyperphosphatemia so that calcium carbonate treatment was begun and calcitriol dose was adjusted in relation to plasma calcium changes. After 24 months of calcium carbonate therapy, plasma phosphorus was 4.85 +/- 0.7 mg/dL, using a daily dose of calcium carbonate of 2.57 +/- 1.3 g (range, 1 to 6 g). The daily dose per patient of calcitriol was not different from that prescribed during the control period, but in five patients calcitriol was permanently withdrawn for hypercalcemia. At the end of the study plasma calcium, magnesium, bicarbonate, alkaline phosphatase, and parathyroid hormone values were unchanged in comparison with the control period, whereas a significant reduction in plasma aluminum and plasma aluminum increase induced by deferoxamine infusion was observed. The frequency of hypercalcemic and hyperphosphatemic episodes during the last 12 months of calcium carbonate therapy (6.2% and 16.6%, respectively) was not different from that observed during the 12 months on aluminum hydroxide therapy preceding the control period (4.5% and 14.7%, respectively). It was concluded that calcium carbonate is effective in the control of hyperphosphatemia and secondary hyperparathyroidism in patients on chronic hemodialysis and that the incidence of hypercalcemia is low when the daily dosage is less than 6 g.

Adult↗