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PubMed2005

Prospective randomized multicenter trial of sevelamer hydrochloride and calcium carbonate for the treatment of hyperphosphatemia in hemodialysis patients in Japan.

A prospective, randomized open-label trial of sevelamer hydrochloride with or without calcium carbonate (CC) involved 86 hemodialysis patients in Japan. The dosage of CC was fixed at 3.0 g/day for the 12-week study. After the first 4 weeks all subjects were changed from CC to sevelamer 3.0 g/day for another 4 weeks, then allocated randomly to three groups for the final 4 weeks: group A, sevelamer 6.0 g/day; group B, sevelamer 3.0 g/day and CC 3.0 g/day; group C, CC 3.0 g/day. The target serum phosphorous concentration (P)=5.5 mg/dL and the corrected calcium concentration (Ca) was 9.0-10.0 mg/dL. Of the 86 patients, 62 finished the study without a change of dosage and their data were analyzed (group A, N=16; group B, N=26; group C, N=20). At week 8 compared with week 4, the concentration of P increased from 5.7+/-1.4 to 6.4+/-1.7 mg/dL in group A, and decreased significantly in groups B and C, and in group B compared with groups A and C; groups A and C had similar concentrations at week 8. The Ca concentration decreased significantly from 9.7+/-1.0 to 9.1+/-0.7 mg/dL after the change to sevelamer. At week 8 Ca was not significantly changed in group A, whereas a significant increase occurred in groups B and C. Side-effects with sevelamer administration occurred in 34 of the 86 patients and 24 dropped out of the study, with a high frequency in group A (13/29; 44.8%). In conclusion, there was an additive effect of sevelamer for the treatment of hyperphosphatemia with CC. The combination therapy was better tolerated and showed higher patient compliance than CC or sevelamer monotherapy.

Analysis of Variance↗
PubMed1984

Tumoral calcinosis, diaphysitis, and hyperphosphatemia.

Three children with hyperphosphatemic tumoral calcinosis, including 2 siblings, presented with recurrent pain and swelling of the legs. Laboratory tests, radiographs, and biopsy showed reactive new bone formation of unknown etiology in the diaphyses. The authors hypothesize a relationship between tumoral calcinosis, hyperostosis, and hyperphosphatemia and consider possible mechanisms.

Adolescent↗
PubMed1992

Effects of hyperphosphatemia on diaphragmatic strength and endurance.

Effects of an infusion of Na2HPO4 on diaphragm strength, endurance, and magnitude of recovery were evaluated in in situ canine diaphragm strips. Results showed no effect on maximal isometric tetanic tension. Twitch tension and tension in the low- (10-Hz) frequency range were significantly increased (P less than 0.01). Time to fatigue (endurance) increased by 38 +/- 4.5% in the group that received phosphorus compared with its control and decreased by 18.5 +/- 2.5% in the group that received dextrose compared with its control (P less than 0.005). Recovery from fatigue was also significantly improved after the phosphorus infusion. Serum ATP and 2,3-diphosphoglycerate levels were unchanged throughout the experiment. The results of this study support the notion that hyperphosphatemia improves diaphragmatic endurance and recovery from fatigue. The mechanisms involved may in part be due to the phosphate-buffering effects, which limit the extent of the muscle intracellular acidosis produced with fatigue.

2,3-Diphosphoglycerate↗
PubMed2005

Efficacy, tolerability, and safety of lanthanum carbonate in hyperphosphatemia: a 6-month, randomized, comparative trial versus calcium carbonate.

BACKGROUND/AIMS: Hyperphosphatemia is an important clinical consequence of renal failure, and its multiple adverse systemic effects are associated with significantly increased risks of morbidity and mortality in dialysis patients. Existing oral phosphate binders have not permitted control of serum phosphate within currently accepted guidelines. This study compares lanthanum carbonate with calcium carbonate for control of serum phosphate in hemodialysis patients. METHODS: In this European multicentre study, 800 patients were randomised to receive either lanthanum or calcium carbonate and the dose titrated over 5 weeks to achieve control of serum phosphate. Serum levels of phosphate, calcium and parathryoid hormone were followed over the following 20 weeks. RESULTS: Around 65% of patients in each group achieved phosphate control, but in the calcium carbonate group this was at the expense of significant hypercalcemia (20.2% of patients vs. 0.4%). Consequently, calcium x phosphate product tended to be better controlled in the lanthanum group. CONCLUSION: This 6-month study demonstrates that serum phosphate control with lanthanum carbonate (750-3,000 mg/day) is similar to that seen with calcium carbonate (1,500-9,000 mg/day), but with a significantly reduced incidence of hypercalcemia. Lanthanum carbonate is well tolerated and may be more effective in reducing calcium x phosphate product than calcium carbonate.

Adult↗
PubMed2004

The role of sevelamer in achieving the kidney disease outcomes quality initiative (K/DOQI) guidelines for hyperphosphatemia.

BACKGROUND: End-stage renal disease (ESRD) is a chronic health care problem associated with multiple co-morbidities and escalating costs. Disregulation of mineral metabolism (principally hyperphosphatemia and hypercalcemia) contributes to substantial morbidity and mortality. Accordingly, new and more-aggressive Kidney Disease Outcomes Quality Initiative (K/DOQI) Guidelines from the National Kidney Foundation promote lower serum phosphorus (3.5-5.5 mg/dL), lower calcium (8.4-9.5 mg/dL), and lower calcium-phosphorus product (< 55 mg(2)/dL(2)) targets. REVIEW FINDINGS: Traditional calcium-based and metal-based phosphate binders are effective but are associated with side effects and toxicity that limit their use. Achieving rigorous K/DOQI goals demands higher therapeutic doses of phosphate binders and may require more-aggressive use of calcium-free and metal-free phosphate binders. Sevelamer hydrochloride is a calcium- and metal-free polymer that binds phosphate effectively without contributing to calcium load or metal accumulation. In the Treat-to-Goal trial, sevelamer-treated dialysis patients had less progression of coronary and aortic calcification than patients treated with calcium-based binders. This offers the potential promise of reducing cardiovascular morbidity and mortality. The 800-mg tablet (Renagel) increases the daily sevelamer dose while reducing the number of tablets required per meal. Nine of the 800-mg tablets per day (3 x 800-mg tablets tid with meals) of sevelamer monotherapy have been shown to achieve K/DOQI serum phosphorus and calcium-phosphorus product targets. CONCLUSION: In summary, this review of the current evidence-base concludes that the new, more-aggressive, K/DOQI goals limit the use of metal-based and calcium-based phosphate binders. Sevelamer offers the advantages of lowering serum phosphorus without the risks of calcium or metal accumulation - and offers the promise of slowing the progression of vascular calcification and potentially reducing the morbidity and mortality of hemodialysis patients.

Chronic Disease↗
PubMed1999

Hyperphosphatemia accelerates parathyroid cell proliferation and parathyroid hormone secretion in severe secondary parathyroid hyperplasia.

We studied the role of phosphorus retention in parathyroid cell proliferation and parathyroid hormone (PTH) oversecretion in severe secondary parathyroid hyperplasia. Mice transplanted with human parathyroid tissue from a patient who had undergone parathyroidectomy for severe secondary hyperparathyroidism were divided into four groups; each group was given a diet with a different phosphorus content (0.4, 0.7, 1.0, and 1.2%) to alter serum phosphorus concentrations. Histologic examinations of grafts by hematoxylin-eosin or by bromodeoxyuridine (BrdU) immunohistochemical staining were performed to assess parathyroid cell proliferation. Changes in serum phosphorus concentrations unidirectionally affected PTH secretion from the graft, because human PTH did not cross-react with mouse PTH. Serum phosphorus concentrations of 1.0P and 1.2P groups were significantly higher than those of 0.4P and 0.7P groups (p<0.05). Serum phosphorus concentrations were significantly correlated with the gradient of human PTH elevation with a coefficient of 0.48 and a p<0.05. Furthermore, serum phosphorus concentrations and the gradient of human PTH elevation were significantly higher in mice with BrdU-immunoreactive cells in the parathyroid graft than in mice without immunoreactive cells in the graft. These results indicate that uncontrolled hyperphosphatemia may accelerate the proliferation of parathyroid cells, exacerbating PTH oversecretion.

Animals↗
PubMed2006

Severe hyperphosphatemia and hypocalcemic tetany after oral laxative administration in a 3-month-old infant.

A 3-month-old infant presented to the pediatric emergency department with respiratory distress and tetany after ingestion of a phosphate-containing oral laxative. The initial phosphorus level was 38.3 mg/dL. With aggressive fluid resuscitation and intravenous calcium administration, the infant completely recovered. Although the risks of phosphate-containing enemas are well described, life-threatening hyperphosphatemia can also result from administration of phosphate-containing oral laxatives. Aggressive fluid hydration is the mainstay of treatment. Intravenous calcium administration may be necessary to avoid hemodynamic collapse despite the theoretical possibility of metastatic calcifications. Physicians should be alerted to the possibility of phosphate toxicity and hypocalcemic tetany in young children when treated with over-the-counter laxatives. Caregivers should be advised not to administer over-the-counter laxatives to infants without physician supervision.

Administration, Oral↗
PubMed2003

[Critical appraisal of sevelamer for the treatment of hyperphosphatemia in patients with chronic renal failure].

OBJECTIVE: To evaluate in patients with chronic renal failure (CRF) the effectiveness and the costs of sevelamer, a cationic polymer calcium- and aluminum-free, that is a new gastrointestinal phosphate binder. METHODS: Literature review and critical appraisal of six clinical trials about the effectiveness and two economic studies of sevelamer in CRF patients. RESULTS: Sevelamer is an effective phosphate binder (used in a mean daily dose of 3.5 g three times per day with meals) and with similar effect as that obtained with calcium salts, without the adverse manifestations of the latter (elevation of calcium x phosphorus product, hypercalcemia, vascular and cardiac calcifications, etc.). Moreover, sevelamer reduced serum LDL cholesterol in around 30%. Despite the greater direct costs of sevelamer compared with calcium salts, the total costs may be lower due to the reduction of costs with clinical complications and hospitalizations. CONCLUSIONS: Sevelamer has important therapeutic value in CRF patients with hyperphosphatemia. Economic analyses should be performed in our setting to define the cost-effectiveness relationship of sevelamer.

Calcium↗
PubMed1991

Bone mineral loss in patients on maintenance hemodialysis with hyperphosphatemia treated with 1 alpha-hydroxycholecalciferol and calcium carbonate.

We investigated the relationship between bone mineral density loss and mean serum phosphate level for one year in 58 men on maintenance hemodialysis who were treated with 1 alpha-hydroxycholecalciferol and calcium bicarbonate. Bone mineral density of the femur head and neck was measured twice, 8 months apart, by dual energy X-ray absorptiometry (Hologic QDR 1000). Patients were divided into two groups according to their mean serum phosphate level during the year of the study. Group A had almost normal serum phosphate levels (mean, less than 6.0 mg/dl) and group B had hyperphosphatemia (mean, greater than or equal to 6.0 mg/dl). In group A, the mean bone mineral density was 0.825 +/- 0.122 g/cm2 at the beginning of the study and 0.828 +/- 0.118 g/cm2 8 months later. In group B, these values were 0.787 +/- 0.167 g/cm2 at the beginning and 0.762 +/- 0.171 g/cm2 8 months later. Bone mineral density did not decrease in group A, but it decreased significantly in group B (p less than 0.01). For all patients, the percent increase in the bone mineral density was inversely correlated with the mean serum phosphate value for the year of the study (r = -0.274, p less than 0.05). These results indicate the importance of serum phosphate control in patients on maintenance hemodialysis, even when they are being treated with 1 alpha-hydroxycholecalciferol and calcium carbonate.

Adult↗
PubMedDate not supplied

Hypocalcemia and hyperphosphatemia due to primary hypoparathyroidism in a six-month-old kitten.

A six-month-old, intact female Himalayan kitten was presented to the University of Tennessee Veterinary Medical Teaching Hospital for evaluation of chronic lethargy, inappetance, muscle tremors, and seizures. Upon physical examination, the kitten was very small for her age. Bilateral, incipient-to-immature cataracts were seen on ophthalmic examination. Severe hypocalcemia and concurrent hyperphosphatemia were identified on initial diagnostic evaluation. A diagnosis of primary hypoparathyroidism was made by identifying reduced concentrations of parathyroid hormone (PTH). The kitten responded well to treatment with calcium, vitamin D, and aluminum hydroxide and is clinically normal 17 months after initiation of treatment.

Aluminum Hydroxide↗
PubMed1999

[Inhibition of gastric secretion by omeprazole and efficacy of calcium carbonate in the control of hyperphosphatemia in patients on maintenance hemodialysis].

UNLABELLED: Apparent contradictions exist in the literature regarding the effect of gastric secretion inhibition on phosphatemia. In healthy adults, omeprazole has been reported to prevent the increase of plasma phosphate or of phosphaturia observed after an acute phosphate load suggesting an inhibition of phosphate absorption. In patients on chronic hemodialysis their hyperphosphatemia is associated to gastric hypersecretion but the inhibition of this latter by ranitidine in patients taking CaCO3 has been reported to increase their plasma phosphate. Because of this contradiction, we have made an open cross-over study in 16 stable and compliant patients in chronic hemodialysis taking a mean daily dose of 9.4 +/- 4 g of CaCO3 and compared their predialysis plasma concentration of phosphate, calcium, protides, bicarbonates, intact PTH, urea and creatine for two successive periods of two months without or with 20 mg of omeprazole. Plasma phosphate did not increased significantly with omeprazole (from 1.80 +/- 0.38 to 1.89 +/- 0.42 mmol/l) whereas plasma corrected calcium significantly decreased from 2.41 +/- 0.18 to 2.36 +/- 0.16 mmol/l (p = 0.04) and plasma bicarbonate decreased significantly from 26.7 +/- 3.5 to 25.7 +/- 3.1 mmol/l (p < 0.05). No significant change was observed in plasma creatine and urea suggesting stability of dialysis efficiency and of protein and therefore phosphate intake. CONCLUSION: These data do not support that CaCO3 efficiency as phosphate binder is decreased with inhibition of the gastric secretion by omeprazole.

Adult↗
PubMed1999

Hemodiafiltration--a new treatment option for hyperphosphatemia in hemodialysis patients.

BACKGROUND: Hemodiafiltration is used to increase the convective transport and thereby the elimination of small and middle molecules, mainly beta2-microglobulin (beta2-M) across the dialysis membranes. There is little information concerning urea, creatinine, beta2-M and principally phosphate kinetics during hemodiafiltration in vivo. In this prospective study, we evaluated the transmembrane solute mass removal (TSR) and clearance (Kd) of urea, creatinine and phosphate as well as serum beta2-M reduction rate (beta2-MRR) and collected beta2-M in dialysate plus ultrafiltrate during high-flux hemodialysis (HD) and post-dilutional hemodiafiltration (HDF). PATIENTS AND METHODS: 16 patients were studied using a polysulfone capillary filter (1.6 m2 surface area, 40 microm fiber internal diameter and 200 microm, wall thickness) during 2 one-week periods: first week HD 1.6 m2 and second week HDF 1.6 m2. Treatment time was 4 hours, blood flow rate 300 ml/min with constant dialysate and ultrafiltration rates for HD and HDF periods. TSR, Kd, beta2-MRR and beta2-M collection were assessed during the mid-week treatment. In a second part of the study, we repeated the same protocol using a second high-flux polysulfone capillary filter (2.4 m2 surface area, 30 microm fiber diameter and 150 microm wall thickness). RESULTS: TSR and Kd of urea and creatinine were not improved by HDF, however, HDF increased TSR and Kd of phosphate. Phosphate clearance rose from 120 (HD 1.6 m2) to 159 (HDF 1.6 m2) (p < 0.005) and from 146 (HD 2.4 m2) to 206 (HDF 2.4 m2) (p < 0.005) ml/min. Beta2-MRR increased from 64.1 +/- 8.6 to 77.7 +/- 8.2% (p < 0.005) and from 75.0 +/- 5.1 to 82.9 +/- 8.5% (p < 0.005) during HDF 1.6 m2 and HDF 2.4 m2, respectively. Collected beta2-M remained unchanged. This discrepancy seems to be due to an enhanced beta2-M adsorption to the polysulfone membrane during HDF. CONCLUSION: Our results provide a strong evidence that HDF has no advantage over HD with respect to urea and creatinine removal in vivo. However, HDF did improve the elimination of phosphate and should be considered as an additional treatment option for hyperphosphatemia in dialysis patients. HDF improves significantly the elimination of beta2-M.

Biocompatible Materials↗
PubMed1999

Understanding and managing hyperphosphatemia in patients with chronic renal disease.

Controlling serum phosphorus levels continues to be a challenge in patients with chronic renal disease. Hyperphosphatemia is implicated in the development and worsening of secondary hyperparathyroidism and renal osteodystrophy (ROD) through its effects on serum calcium and calcitriol levels, parathyroid hormone (PTH) overproduction, and parathyroid cell hyperplasia. In the past serum phosphorus control with aluminum-containing phosphate binders was associated with insidious but serious development of aluminum toxicity. More recent approaches using non aluminum-containing calcium salts as phosphate binders are limited because of the excessive calcium load resulting from concomitant enhanced intestinal calcium absorption. Moreover serum phosphorus does not only result from dietary phosphate intake but also from enhanced bone breakdown due to secondary hyperparathyroidism. Strategies for managing ROD including early control of serum phosphorus and PTH, prevention of parathyroid hyperplasia; establishment of optimal PTH levels for bone health, and the availability of new therapeutic tools for controlling phosphorus may help prevent complications and improve patient outcomes.

Chronic Kidney Disease-Mineral and Bone Disorder↗
PubMed1992

Dose-dependent vitamin D3, 25-hydroxyvitamin D3 and 1,25-dihydroxyvitamin D3-induced hypercalcemia and hyperphosphatemia, and the correlative changes in the activity of ultimobranchial and parathyroid glands of the toad, Bufo andersoni Boulenger.

Vitamin D3, 25(OH) vitamin D3 and 1,25 (OH)2D3 were administered daily to unfed male Bufo andersoni for 15 days which resulted in a significant hypercalcemia and hyperphosphatemia in a dose-dependent fashion. 1,25(OH)2D3 is more potent than the other metabolites. The treatment activated ultimobranchial gland but induced degenerative changes in parathyroid of the toads.

Animals↗
PubMed2004

[Treatment of hyperphosphatemia with sevelamer in patients with chronic renal failure].

UNLABELLED: Sevelamer is a recent phosphate binder that is mineral-free, and represents a great advance in the treatment of hyperphosphatemia in patients with hypercalcemia and/or gastric intolerance to calcium-based phosphate binders. The communications about the experience with the use of sevelamer in patients non-yet in dialysis is scanty. The aim of our study is to investigate retrospectively the gastrointestinal tolerance of sevelamer, their efficacy as phosphate binder and other parameters in a group of 89 patients with chronic renal failure in predialysis. We have analysed the effects of sevelamer at baseline and after 1, 3 and 6 months on the following data and parameters: calcium, phosphate, intact PTH, venous bicarbonate, urea, creatinine, creatinine clearance, side-effects, number of patients that were discontinued, and co-treatment during the study period with phosphate-based binders, calcitriol, lipid-lowering drugs and sodium bicarbonate. RESULTS: 19 patients (21.3%) refused to continue with sevelamer at the first month (16 patients had digestive intolerance and 3 several symptoms). Serum phosphate fell at 3 months (5 +/- 0.8 mg/dl basal vs 4.8 +/- 0.7 mg/dl, p = 0.02) and 6 months (5 +/- 0.8 mg/dl basal vs 4.7 +/- 0.9 mg/dl, p = 0.07). Serum calcium fell at 6 months (9.8 +/- 0.7 mg/dl basal vs 9.4 +/- 0.6 mg/dl, p = 0.03). Venous bicarbonate and iPTH were unchanged, but the quantity of sodium bicarbonate administered increased significantly. Blood cholesterol fell at 1 months (193 +/- 49 mg/dl basal vs 173 +/- 52 mg/dl, p = 0.001) and 3 months (205 +/- 49 mg/dl basal vs 170 +/- 49 mg/dl, p = 0.004), in spite of a significant reduction of the dose of statins. CONCLUSIONS: Sevelamer is an effective phosphate binder in predialysis patients and also reduces significantly the serum cholesterol, improving the blood lipid profile. The levels of venous bicarbonate remained unchanged, at expenses of an increment in the dose of sodium bicarbonate supplementation.

Acid-Base Equilibrium↗
PubMed2004

[Hyperphosphatemia and cardiovascular risk in patients on dialysis].

Cardiovascular diseases are the leading causes of mortality among patients with end-stage renal disease (ESRD), with arterial disease and left ventricular hypertrophy being the two principal factors of the high mortality rate in this population. In addition to traditional risk factors (age, gender, diabetes, hypertension, lifestyle, hyperlipidemia, smoking, hyperhomocystinemia), inflammation, oxidative stress and disorders of mineral metabolism may contribute to cardiovascular risk in patients with uremic syndrome. High serum phosphate may influence vascular calcifications directly and indirectly, by worsening secondary hyperparathyroidism. Several treatment options are available for the treatment of hyperphosphatemia and secondary hyperparathyroidism in patients with ESRD. The treatment approach includes a diet low in phosphorus, with less than 1 g/kg/day of protein. Vitamin D supplementation is an important part of treatment. Phosphate binding agents are in most of the patients necessary in addition to diet. Aluminum hydroxide has been widely used for many years. It is very potent, but also very toxic, with severe encephalopathy as the most dangerous side effect. Calcium salts are less potent, and were considered safe for use in patients on dialysis. However, improvement in the understanding of vascular calcifications has demonstrated that calcium overload significantly contributes to widespread atherosclerosis in patients with ESRD. Sevelamer-hydrochloride is a novel non-aluminum, non-calcium containing phosphate binder, which is capable of reducing the levels of phosphorus as well as of low-density lipoprotein cholesterol, and increasing high-density lipoprotein cholesterol.

Blood Vessels↗
PubMed2004

[Front line of management of hyperphosphatemia in hemodialysis patients].

Management of hyperphosphatemia in hemodialysis patients is very important to prevent progress of renal hyperparathyroidism or ectopic calcification. Sevelamer hydrochloride is a Ca and Al free phosphate binder, and reduces serum phosphorus level, without any influence on serum Ca level, and Ca-P products. This compound is expected to reduce the incidence of arterial calcification, and improve the QOL (quality of life) of hemodialysis patients.

Calcinosis↗