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Results for “Hyperphosphatemia”

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At least 127 records · Page 7Linked to original sources

PubMed2005

Hyperphosphatemia in children receiving peritoneal dialysis--an educational program.

Hyperphosphatemia has been associated with the development of secondary hyperparathyroidism, renal osteodystrophy, cardiovascular calcification and increased risk of death. Using a one group, pretest-posttest study design, we sought to evaluate changes in serum phosphorus, calcium, parathyroid hormone and subject knowledge in response to a 3-month educational intervention. Mean serum phosphorus levels did not differ significantly between the three evaluation periods: pretreatment (5.69 mg/dl), treatment (5.84 mg/dl) and posttreatment (6.17 mg/dl). Mean serum calcium, calcium-phosphorus product and PTH values also did not differ significantly between the treatment periods. We observed no difference between the subject test scores between the two testing periods. Calcium-phosphorus product, serum phosphorus and PTH values on average, despite the education program, remained outside the K/DOQI target guidelines 44, 56 and 81% of the time, respectively. The results of this study suggest that an aggressive 3-month patient education program targeting dietary phosphorus knowledge, phosphate binder name and dosing, and knowledge of medical consequences associated with non-compliance had no effect on the serum phosphorus, calcium, PTH or phosphate binder need.

Adolescent↗

PubMed2005

Spurious hyperphosphatemia in a patient with alteplase-locked central venous catheter.

Alteplase has been shown to be effective in preventing central venous access clotting in patients on hemodialysis. Because of a high phosphorus content in its excipient, it can inadvertently contaminate blood samples, leading the physician in care of the patient to erroneously increase dialysis time or change diet in order to control the pseudo-hyperphosphatemia.

Catheterization, Central Venous↗

PubMed1985

Enema-induced hyperphosphatemia.

Severe hyperphosphatemia and hypocalcemia developed following the administration of a single hypertonic sodium phosphate enema in an adult with mild chronic renal insufficiency.

Aged↗

PubMedDate not supplied

Hyperphosphatemia: an objective marker for bulimia nervosa?

Phosphorus abnormalities among patients suffering from eating disorders, although cited, have received relatively little attention. Studies generally report decreased concentrations of phosphorus for both bulimia and anorexia nervosa. We have recently noted hyperphosphatemia in several consecutive hospitalized bulimic patients who appeared to have normal renal function and calcium levels. Case files of 30 inpatient and outpatient female bulimic patients and 30 sex- and age-matched physically healthy psychiatric inpatients and outpatients were reviewed. Phosphorus and electrolytes related to phosphorus metabolism were compared between the two groups. Twenty-four of 30 bulimic patients (80%) were found to have at least one elevated serum phosphorus concentration, whereas all but one of 30 age-matched controls had values within normal limits. Elevated phosphorus levels were generally in the mild to moderate range. No correlation was found between phosphorus levels and any of the other electrolytes examined in both patients and controls. No correlation was found between phosphorus levels and the reported frequency of bingeing and vomiting or the number of laxatives ingested. Since bulimic patients are generally of normal weight and tend to deny their disturbed eating habits, diagnosis is often delayed. However, bulimia may be suspected from biochemical abnormalities such as hypokalemia, hypochloremia, elevated amylase, and acid-base disturbances. This preliminary study indicates that elevated serum phosphorus levels may serve as an additional objective marker for the presence of bulimia nervosa.

Adult↗

PubMed1989

Colonic intussusception secondary to a calcium phosphate bezoar in a child receiving calcium carbonate for hyperphosphatemia.

We report a case of a calcium phosphate bezoar resulting in colonic intussusception in a boy with chronic renal failure who received calcium carbonate to control hyperphosphatemia. Because of concerns about aluminum-related disease in patients receiving aluminum hydroxide phosphate binders, calcium carbonate is being used more frequently to manage phosphate retention in renal failure. The development of bezoars may complicate this new form of therapy.

Bezoars↗

PubMed1977

Hypocalcemia, hyperphosphatemia, and dehydration following a single hypertonic phosphate enema.

Previous reports of hypocalcemia and hyperphosphatemia following use of phosphate enemas have either been in patients with renal disease or followed prolonged abuse of these products. The two patients described here had marked elevation of serum phosphate and concomitant lowering of serum calcium secondary to absorption of phosphate from a single administered enema. Associated moderate dehydration resulted in poor renal excretion of the absorbed phosphate and prolongation of hypocalcemia. Hydration was effective in permitting clearance of phosphate and restoration of normocalcemia.

Child, Preschool↗

PubMed1989

Severe hyperphosphatemia, hypocalcemia, acidosis, and shock in a 5-month-old child following the administration of an adult Fleet enema.

We report the case of a 5-month-old girl who was given an adult Fleet enema by her mother because of her concern that the baby was constipated. Within minutes the child became extremely ill. She developed shock, hyperphosphatemia, hypocalcemia, and acidosis. This case is presented to demonstrate that life-threatening events may result after the injudicious use of enemas in children.

Acidosis↗

PubMed2000

Re-evaluation of risks associated with hyperphosphatemia and hyperparathyroidism in dialysis patients: recommendations for a change in management.

Hyperphosphatemia is a predictable consequence of chronic renal failure and is present in most patients on dialysis. Traditionally, the risk associated with elevated serum phosphorus has focused on its impact on renal osteodystrophy. A growing body of evidence, however, suggests that abnormalities in serum phosphorus, calcium-phosphorus product (CaxP), and parathyroid hormone (PTH) levels are resulting in vascular and visceral calcification, thereby contributing to the substantially increased risk of cardiovascular death in this population. In this analysis, we review in detail the literature that describes these associations. We show that the current treatment paradigm for serum phosphorus and secondary hyperparathyroidism is ineffective for a large segment of dialysis patients. Currently, 60% of hemodialysis patients have phosphorus greater than 5.5 mg/dL, and 40% have CaxP greater than 60 mg(2)/dL(2). It is our belief that prevention of uremic calcification, cardiac death, and vascular disease should assume primary importance when evaluating the risks associated with elevated levels of phosphorus, CaxP, and PTH. We recommend that target levels should become 9.2 to 9.6 mg/dL for calcium, 2.5 to 5.5 mg/dL for phosphorus, less than 55 mg(2)/dL(2) for CaxP product, and 100 to 200 pg/mL for intact PTH.

Calcinosis↗

PubMed1997

Severe hyperphosphatemia following phosphate administration for bowel preparation in patients with renal failure: two cases and a review of the literature.

Two cases of severe hyperphosphatemia following phosphate bowel preparation are described and a review of the literature is presented. Impairment of renal function appears to be a risk factor in those patients without primary bowel pathology. One of our patients died, and the mortality rate combining our cases with all other reported cases is 33%. Repeated doses of phosphate bowel preparations/purgatives can be dangerous in patients with renal impairment.

Acute Disease↗

PubMed2003

Hyperphosphatemia in dialysis patients: is there a role for focused counseling?

BACKGROUND: Elevated serum phosphorus (P) and calcium-P product (CaXP) are associated with cardiac mortality in dialysis patients. A CaXP <55 is considered acceptable by most authorities. Because nutrition practices can modulate CaXP, we designed a survey to study the impact of the patients' levels of education and disease awareness on their CaXP. METHODS: A survey questionnaire with 5 didactic questions pertaining to hyperphosphatemia and P-binders and 5 questions related to patient attitudes and beliefs was administered to all patients in a hemodialysis unit. The association of CaXP >55 with the patients' level of education, their score on the survey (didactic part, score 0 to 5), parathyroid hormone (PTH) levels, hyperkalemia, hypertension, and vascular disease were studied. RESULTS: Of the 117 patients (61 men, age 56.5 +/- 18 years) who participated in the survey, 49 (42%) had CaXP >55 and 100 (85%) were on P binders. Thirty-seven (31.6%) had at least some college education. Eighty-seven patients (74%) failed to identify foods rich in P; 61% were unaware of complications related to high CaXP. Patients with CaXP >55 were less likely to have college education (20% versus 39%, P =.04), and had lower survey scores (2.4 +/- 1.3 versus 2.6 +/- 1.4, P = NS). Patients with college education scored higher (2.9 +/- 1.1 versus 2.3 +/- 1.4, P =.014). Furthermore, CaXP >55 was significantly associated with hyperkalemia (P =.02), high PTH levels (P <.001), and hypertension (P =.02), but not with >Kt/V, URR, type of hemodialysis access, or vascular diseases. CONCLUSION: The majority of patients in the survey were ignorant of basic facts pertaining to high P and CaXP. The association of CaXP >55 with hyperkalemia, and not with Kt/V, suggests dietary noncompliance rather than inadequate dialysis. Patients with less education were more likely to have CaXP >55. Because this related mostly to misperception of simple facts that affect dietary habits, there is need for focused counseling of these patients at a level appropriate for their literacy skills.

Calcium Phosphates↗

PubMed1992

Chronic respiratory alkalosis induces renal PTH-resistance, hyperphosphatemia and hypocalcemia in humans.

The effects of chronic respiratory alkalosis on divalent ion homeostasis have not been reported in any species. We studied four normal male subjects during a four-day control period (residence at 500 m), during six days of chronic respiratory alkalosis induced by hypobaric hypoxia (residence at 3450 m), followed by a six-day eucapnic recovery period (500 m) under metabolic balance conditions. Chronic respiratory alkalosis (delta PaCO2, -8.4 mm Hg, delta[H+] -3.2 nmol/liter) resulted in a sustained decrement in plasma ionized calcium concentration (delta[IoCa++]p, -0.10 mmol/liter, P less than 0.05) and a sustained increment in plasma phosphate concentration (delta[PO4]p, +0.14 mmol/liter, P less than 0.005) associated with increased fractional excretion of Ca++ (+0.5%, P less than 0.005), decreased phosphate clearance (-6.1 ml/min, P less than 0.025) and decreased excretion of nephrogenous cAMP (-1.5 nmol/100 ml GFR, P less than 0.0025). Urinary phosphate excretion decreased by 15.4 mmol/24 hr on day 1 of chronic respiratory alkalosis (P less than 0.0025), but returned to control values by day 6 despite hyperphosphatemia. Serum intact [PTH] did not change. Sustained hypomagnesuria (-0.8 mmol/24 hr, P less than 0.05) occurred during chronic respiratory alkalosis and was accounted for, at least in part, by decreased fractional excretion of Mg++ (-0.7%, P less than 0.05) in the absence of change in plasma magnesium concentration. Serum 1,25(OH)2D levels were unchanged by chronic respiratory alkalosis. In conclusion, the decrease in nephrogenous cAMP generation despite unchanged serum intact PTH concentration suggests that chronic respiratory alkalosis results in impaired renal responsiveness to PTH as manifested by alterations in PTH-dependent renal calcium and phosphate transport.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2003

Treatment of hyperphosphatemia with sevelamer hydrochloride in hemodialysis patients: a comparison with calcium acetate.

BACKGROUND: Sevelamer hydrochloride is a recently approved calcium- and aluminium-free phosphate binder. A randomized study comparing sevelamer and calcium acetate was performed to assess the control of hyperphosphatemia in hemodialysis patients. METHODS: Administration of phosphate binders was discontinued during a two-week washout period. The patients were then randomized to receive sevelamer or calcium acetate. The laboratory tests were performed monthly for 34 weeks. RESULTS: There was a statistically significant decrease of serum phosphorus in both sevelamer and calcium acetate treatments. In addition, sevelamer improved the lipid profile. CONCLUSION: This study confirms that sevelamer is effective at lowering serum phosphorus in hemodialysis patients and that it has several striking properties that could be beneficial in atherosclerosis in dialysis patients.

Acetates↗

PubMed2001

Calciphylaxis is associated with hyperphosphatemia and increased osteopontin expression by vascular smooth muscle cells.

Calciphylaxis or calcific uremic arteriolopathy (CUA) is a fatal disease in dialysis patients due to calcification of cutaneous blood vessels. The pathogenesis has been attributed to elevated parathyroid hormone (PTH). However, recent studies evaluating vascular calcification in nondialysis patients have found that the smooth muscle cells play an active role, including production of the bone matrix protein osteopontin. To examine the involvement of various clinical parameters and smooth muscle cells of CUA, we performed a case-control analysis comparing 10 CUA patients with our current dialysis patients. Available histologic sections were immunostained for osteopontin, markers of smooth muscle cells, endothelial cells, and macrophages. Compared with our current dialysis population, patients with CUA were more likely to be obese, white, and female (P < 0.02). Comparison of laboratory values found CUA patients with lower serum albumin, greater serum phosphorus, and greater calcium X phosphorus product (P < 0.01). In contrast, there was no difference in the concentration of PTH or calcium between the 2 groups. Immunostaining of calcified blood vessels showed that all calcified vessels stained positive for osteopontin, whereas all the noncalcifed vessels showed no osteopontin localization. Staining for smooth muscle alpha-actin decreased in the medial layer with calcification, with cells appearing to be sloughed off, leading to near occlusion of the vessel lumen. Our case-control study demonstrates that hyperphosphatemia and an elevated calcium X phosphorus product is associated with CUA. Histologic examination suggests that the calcification is associated with increased expression of osteopontin by smooth muscle cells.

Adult↗

PubMed2005

Hyperphosphatemia and vascular calcification in end-stage renal disease.

Vascular calcification is a common finding in atherosclerosis and a serious problem in uremic patients. Because of the correlation of hyperphosphatemia and vascular calcification, the ability of extracellular inorganic phosphate levels to regulate human aortic smooth muscle cell (HSMC) culture mineralization in vitro was examined. HSMC cultured in media containing normal physiologic levels of inorganic phosphate (1.4 mM) did not mineralize. In contrast, HSMC cultured in media containing phosphate levels comparable with those seen in hyperphosphatemic individuals (>1.4 mM) showed dose-dependent increases in mineral deposition. Mechanistic studies showed that elevated phosphate treatment of HSMC also enhanced the expression of the osteoblastic differentiation markers osteocalcin and osf2/Cbfa-1. The effects of elevated phosphate on HSMC were mediated by a sodium-dependent phosphate cotransporter (NPC) as indicated by the ability of the specific NPC inhibitor phosphonoformic acid to dose-dependently inhibit phosphate-induced calcium deposition as well as osteocalcin and Cbfa-1 gene expression. The NPC in HSMC was identified as Pit-1, a member of the novel type III NPCs. These data suggest that elevated phosphate may directly stimulate HSMC to undergo phenotypic changes that predispose to calcification and offers a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions. Furthermore, we examined the factors affecting peripheral vascular calcification in 332 nondiabetic hemodialysis patients. There were 45 nondiabetic patients with vascular calcification. In multivariate logistic regression, the significant factors affecting vascular calcification were advanced age, longer duration of hemodialysis, increased phosphate concentrations, male gender, and lower predialysis diastolic pressure. Our findings suggest that an elevated phosphate level may directly stimulate HSMC to undergo phenotypic changes that predispose to calcification and offer a novel explanation of the phenomenon of vascular calcification under hyperphosphatemic conditions.

Aorta↗

PubMed1989

Extensive extraosseous localization of bone imaging agent in a patient with renal failure and rhabdomyolysis accompanied by combined hypercalcemia and hyperphosphatemia.

Four sequential Tc-99m pyrophosphate (PYP) imaging studies were performed in a 28-year-old man with high fever and exudate pharyngitis associated with renal failure. Radiotracer localization in the left ventricle (LV), lungs, kidneys, and skeletal muscles were seen in two, initial imaging studies. In the second and third imaging studies, area of increase in activity was seen in the left-sided bowel. In studies done two months later (in the third study), the radioactivity in the skeletal muscles was no longer seen. Studies obtained nine months (in the fourth study) after the first imaging showed less radiotracer localization in the LV, lungs, and kidneys as compared to that seen in the initial study. Myocardial necrosis and microcalcification were proved by LV biopsy. The exact mechanism of extraosseous bone-imaging agent localization is unknown. However, this phenomenon may be related to renal failure, rhabdomyolysis, hypercalcemia, hyperphosphatemia, or elevated parathyroid hormone. The Tc-99m PYP imaging study is useful and sensitive in the detection of extraosseous tissue calcification and monitoring of the disease process.

Acute Kidney Injury↗

PubMed1997

Hyperphosphatemia associated with phosphorus-containing laxatives in a patient with chronic renal insufficiency.

A patient with chronic renal insufficiency had hyperphosphatemia, hypocalcemia, hypomagnesemia, hypokalemia, metabolic acidosis, and QT prolongation on electrocardiogram after taking prescribed laxatives containing phosphorus. Clinical findings included tetany in the form of Chvostek's and Trousseau's signs. Symptoms resolved after careful rehydration and electrolyte replacement. The interactions between these electrolytes are described. Patients with moderate to severe renal dysfunction should avoid use of laxatives containing phosphorus. If these laxatives are used in patients with mild renal dysfunction, careful monitoring is indicated.

Adult↗

PubMed2003

Severe hyperphosphatemia resulting from high-dose liposomal amphotericin in a child with leukemia.

Children with acute lymphoblastic leukemia (ALL) are at risk for serious electrolyte abnormalities. The authors report their experience in managing a child with ALL who developed severe hyperphosphatemia as a consequence of a large exogenous load of phosphorus from high-dose liposomal amphotericin B. Health care providers need to recognize this potentially life-threatening complication of liposomal amphotericin B, since early detection and intervention can prevent significant morbidity.

Amphotericin B↗

PubMed2004

Age as a predictor of hyperphosphatemia after oral phosphosoda administration for colon preparation.

BACKGROUND AND AIM: It has been reported that oral phosphosoda (OPS), commonly used in bowel cleansing, may cause complications such as hyperphosphatemia and hypocalcemia. This has been observed in patients with normal kidney function and in those with renal insufficiency. Few controlled studies have been performed with respect to age on healthy subjects after OPS administration. METHODS: Seventy patients (38 men and 32 women; mean age 47 +/- 12 years, range 25-80 years) were enrolled in the present study. Half of the 90 mL total volume of OPS was ingested 18 h before colonoscopy, and the other half 6 h before the procedure. Creatinine clearance rate (CCR) and serum levels of sodium, potassium, calcium and phosphate were measured before and after OPS administration. RESULTS: After OPS administration, serum calcium and potassium were significantly lower (P < 0.05), and serum phosphate and sodium were significantly higher than pretreatment levels (P < or = 0.01). The statistically significant changes in serum sodium, potassium and calcium were within normal laboratory ranges. The mean change in serum phosphate was positively correlated with age (Pearson's r = 0.705; p < 0.001). CONCLUSION: Administration of OPS causes a significant rise in serum phosphate, even in patients with normal CCR. The elevation is significantly greater in elderly patients. Administration of OPS can be considered safe for young and middle-aged patients with normal renal function; however, it should be used with caution in elderly patients, even in those with normal CCR and serum creatinine values.

Administration, Oral↗