PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Hyperphosphatemia”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed2002

[Complete control of hyperphosphatemia with daily nocturnal hemodialysis].

Because the removal of phosphate by the conventional hemodialysis (HD) is absolutely insufficient, phosphate-binding agents has been indispensable. Although, renewed daily HD regiments have taken the strong interest in the issues of dialysis adequacy, quality of life, and clinical outcomes. Short-time daily HD, or nocturnal daily HD showed the desirable control of hyperphosphatemia. Especially, nocturnal daily HD revealed the complete results of serum phosphate control without any phosphate-binders.

English Abstract↗
PubMed2002

[Hyperphosphatemia and diet therapy].

Hyperphosphatemia cause not only renal bone disease but also poor prognosis in hemodialysis patients. We should control serum phosphate levels within near normal range. Although many patients are prescribed phosphate binder, they should restrict oral phosphate intake. There are poor prognosis in malnutrition patients, they should take sufficient protein. Contents of phosphate in foods increase proportionaly with protein contents. It is important that they should take foods with low phosphate contents and low phosphate/protein ratio. They should restrict preserved food, confectionary, seasoning which contain phosphate compounds as food additive. It is useful to take special low phosphate food.

English Abstract↗
PubMed2002

[Therapeutic agents for hyperphosphatemia].

Hyperphosphatemia is one of the major causes of secondary hyperparathyroidism (II degrees HPT) in dialysis patients. Aluminum (Al) hydroxide was commonly used as a phosphate binder in Japan until the beginning of the 1990's, when it was replaced by calcium(Ca) compounds to eliminate undesirable side effects. Although Ca compounds are effective phosphate binders, the concomitant use of vitamin D derivatives can often result in hypercalcemia. For the reason, physicians today have been requesting phosphate binders that contain neither Al nor Ca. In this paper, we introduce several such phosphate binders. Sevelamer hydrocholoride (SH) is a new phosphate binder that contains neither Al nor Ca, and is not absorbed from the gastrointestinal tract. Several short-term clinical studies have established that SH is as efficient as calcium carbonate at lowering serum phosphorus (P) levels, with significant improvement in the Ca x P product and lipids metabolism. Furthermore, a long-term (52 weeks) study revealed that SH attenuated the progression of coronary and aortic calcification in hemodialysis (HD) patients. SH is considered a highly effective phosphate binder in protecting against the progression of II degrees HPT and cardiovascular death in HD patients.

English Abstract↗
PubMed2001

[Hyperphosphatemia and parathyroid hyperplasia].

A hypophosphatemic patient with adult onset osteomalacia was treated with oral phosphate agents for more than 10 years, when tertiary hyperparathyroidism developed. Gene analysis of the enlarged four parathyroid glands revealed MEM1 gene abnormalities in the two glands and microsatellite instability in the one gland, suggesting that hyperphosphatemia per se was involved in the development of nodular hyperplasia or adenoma in this patient, irrespective of renal function.

English Abstract↗
PubMed1990

Calcium ketovaline as new therapy for uremic hyperphosphatemia.

Since treatment of uremic hyperphosphatemia still represents a major problem and phosphate-binding agents carry the well-known risk of aluminum intoxication, we carried out a study to determine whether calcium ketovaline, a keto acid containing calcium, would show phosphate-binding effects comparable to those obtained with a mixture of amino acids and calcium salts of ketoanalogues tested previously. In vitro as well as in vivo studies show convincingly that calcium ketovaline is a valuable intestinal phosphate binder. Dialysis patients treated for 6 weeks showed a significant (p less than 0.05) decrease in serum phosphate from 2.36 +/- 0.19 to 1.81 +/- 0.16 mmol/l.

Hemiterpenes↗
PubMed1990

Hyperphosphatemia in infantile hypophosphatasia: implications for carrier diagnosis and screening.

Twenty obligate carriers of infantile hypophosphatasia (HOPS), a severe autosomal recessive metabolic bone disorder, were studied and compared with 36 controls. Decreased serum alkaline phosphatase activity and increased urinary phosphoethanolamine excretion were confirmed in the HOPS carriers. Relative hyperphosphatemia was documented for the first time in the carriers. Logistic regression analysis was used to develop models for the diagnosis of and screening for HOPS carriers in the high-risk population of Manitoba Mennonites. Models based on serum alkaline phosphatase activity and on serum phosphate levels with or without urinary phosphoethanolamine excretion were used for diagnostic purposes. A model based on serum alkaline phosphatase activity and on the serum phosphate level was the most suitable for screening.

Adult↗
PubMed1990

[Calcium carbonate for the treatment of hyperphosphatemia in chronic hemodialysis patients].

Hyperphosphatemia in chronic hemodialysis patients is usually treated with aluminium containing phosphate binders. In recent years there has been increasing evidence of serious complications due to aluminium accumulation. We have investigated a new calcium carbonate preparation with an HCl-resistant capsule designed to prevent gastrointestinal side effects. Its phosphate binding capacity in comparison to aluminium chloride hydroxide was investigated in 17 chronic hemodialysis patients. The dose of the phosphate binder was adjusted regularly so that the serum phosphorus levels were below 1.8 mmol/l. The mean dose of aluminium chloride hydroxide was 3.36 g/day and of calcium carbonate 4.96 g/day. The mean (+/- SD) serum calcium level was 2.58 +/- 0.11 mmol/l under aluminium chloride hydroxide and 2.50 +/- 0.25 mmol/l under calcium carbonate. The mean phosphorus level was 1.69 +/- 0.31 mmol/l under aluminium chloride hydroxide and 1.71 +/- 0.33 under calcium carbonate. Serum aluminium fell from 64.5 +/- 14.4 micrograms/l to 28.5 +/- 17.5 micrograms/l after 3 months.

Adult↗
PubMed1989

[Hypercalcemia and hyperphosphatemia in thyrotoxoicosis and the therapeutic effect of propranolol].

Measured levels of serum calcium, phosphate, alkaline phosphatase, and urinary hydroxyproline were measured and calcium-phosphate product was calculated in 20 hyperthyroid patients and 20 normal controls. Eleven of the patients took propranolol 160 mg per day for 28 days. We found that the serum level of calcium was higher than that of normal controls. The incidence of hypercalcaemia in hyperthyroid patients was 10%. The serum level of phosphate and the calcium-phosphate product increased (P less than 0.01). Elevation of alkaline phosphatase and bone alkaline phosphatase were also observed (P less than 0.01). The urinary hydroxyproline was also elevated (P less than 0.01). After treatment with propranolol serum calcium and triiodothyronine decreased (P less than 0.05). It is suggested that the major mechanism of hypercalcaemia and hyperphosphatemia in hyperthyroidism was increase of bone absorption stimulated by triiodothyronine. Propranolol decreased the serum level of calcium through decreasing triiodothyronine level and through beta-receptor blocking effect as well as its direct effect on bone.

Adolescent↗
PubMed1989

Calcium salts of ketoacids as a new treatment strategy for uremic hyperphosphatemia.

Hyperphosphatemia and secondary hyperparathyroidism are regular complications in patients suffering from end-stage renal failure. Aluminum-containing drugs are widely used to control serum phosphate, but this therapy carries the well-known risk of aluminum toxicity. Previously we demonstrated that a mixture of ketoacids is very effective in lowering increased serum phosphate and serum PTH levels. Recent studies to clarify the underlying mechanisms whereby these compounds lower serum phosphate revealed that ketoacids act as intestinal phosphate binders. In balance studies we demonstrated that intestinal phosphorus uptake decreased in normal subjects (decrease of absorption during ingestion: 0.7-3.14 mmol/day). Additional in vitro studies not only confirmed the in vivo results but also showed that ketoacids are as efficient as calcium carbonate although they provide less calcium. It is of further interest that ketoacids reached their greatest binding efficiency when the pH is 7.0, whereas calcium carbonate binds phosphate predominantly when the pH is 2.0 or 5.0. Ketoacids represent a further therapy to lower serum phosphate in uremia. As they provide less calcium than calcium carbonate, they could be considered as an advantageous, less dangerous alternative.

Absorption↗
PubMed1989

The causes and value of hyperphosphatemia in experimental strangulation obstruction.

In model experiments with mongrel dogs, intestinal strangulation obstruction was induced by occluding the superior mesenteric veins, and a rise in the inorganic phosphate value of the blood was observed. The high inorganic phosphate values of the fluid exuding from the strangulated bowel suggest that intestinal factors associated with the strangulated bowel may be partly responsible for this elevated phosphatemia. However, hyperphosphatemia was also found in a model experiment in which the route through which the fluid was absorbed into the blood from the peritoneal cavity was interrupted by keeping the strangulated bowel in an intestinal bag. After this, in the model experiments in which a systemic blood pressure depression curve with a percentage reduction similar to that of the decreasing arterial blood pressure resulting from strangulation was produced (by exsanguination, and even by exsanguination with adequate perfusion of the gut), plasma inorganic phosphate values also increased. Therefore it is undeniable that systemic factors other than the above-mentioned local factors are related to the rise in plasma inorganic phosphate values in experimental strangulation obstruction. Because it is not possible to assert that phosphatemia is specific to intestinal strangulation, the importance of a rise in inorganic phosphate values in the early diagnosis of intestinal strangulation cannot be considered very great.

Animals↗
PubMed1986

The role of metabolic acidosis in causing uremic hyperphosphatemia.

Metabolic acidosis was corrected within 1 h in 7 chronic anuric uremic patients on maintenance hemodialysis and, in the course of a week, in 11 other patients on conservative therapy. These patients were on a diet supplying constant amounts of phosphate throughout the duration of the study. In the former group the intravenous infusion of sodium bicarbonate was used, and, in the latter, the oral administration of sodium citrate. In both groups serum phosphate was found to decrease significantly. In the patients on conservative therapy, phosphaturia also had significantly decreased while no changes occurred in their daily fecal loss of phosphate that was measured in 3 patients. These findings indicate that metabolic acidosis is one of the causes of hyperphosphatemia in chronic uremic patients.

Acidosis↗
PubMedDate not supplied

Hyperostosis with hyperphosphatemia: a case report and review of the literature.

This is a report of a 6-year-old girl with the rare syndrome of hyperostosis with hyperphosphatemia. Only eight cases have been previously reported. The main features of this syndrome are repeated attacks of bone pain and swelling, the radiologic finding of periosteal reaction with cortical hyperostosis, and the laboratory finding of increased serum phosphorus level with normal serum calcium and parathyroid hormone levels. The purpose of this article is to review the clinical picture, laboratory and radiological findings, and the differential diagnosis.

Biopsy↗
PubMed1988

Cardiac arrest after acute hyperphosphatemia.

Symptoms of hyperphosphatemia usually relate to the associated hypocalcemia. In a 33-year-old patient accidental infusion of a bolus of potassium phosphate (5 ml intravenously) was immediately followed by cardiac arrest. During CPR, clinically important hypocalcemia or hyperkalemia was not detected, but serum phosphorus was significantly increased. Because acute phosphate load can precipitate life-threatening cardiac arrhythmias, familiarity with doses and rate of infusion of phosphate is extremely important.

Acute Disease↗
PubMed1983

[Hyperphosphatemia and tetany following phosphate enema].

Two patients with renal failure presented postoperatively with marked hyperphosphatemia and symptomatic hypocalcemia. This phosphate intoxication was due to a commonly used phosphate-containing enema. An increase in phosphatemia was also seen in two other patients prospectively followed after receiving the same product. The phosphate increase depends upon the retention duration of the enema. The use of phosphate-containing enemas in patients with renal failure is not entirely risk-free.

Enema↗
PubMed1995

[Enema-induced hyperphosphatemia in ileus of the small and large intestine].

We report a case of severe hyperphosphatemia following repeated use of phosphate-containing enemas in a patient with small and large bowel ileus, who died from acute renal and cardiovascular failure. Refractory hypocalcemia presumably resulted from precipitation of calcium-phosphate. Hypocalcemia may induce alterations which seriously compromise the clinical course.

Aged↗