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PubMed1997

Hypocalcemia and hyperphosphatemia after phosphate enema use in a child.

The authors present a 3-year-old girl in whom severe hyperphosphatemia and hypocalcemia developed after the administration of three adult-sized hypertonic phosphate enemas. The commonly held notion that these enemas are not absorbed and therefore are systemically inactive is incorrect. With early intervention and treatment, the child survived without sequelae despite a serum phosphate level (74.7 mg/dL) that is greater than those previously reported. The treatment of hyperphosphatemia is reviewed as well as underlying pathology such as altered gastrointestinal motility and renal insufficiency, which may predispose the patient to this problem. Physicians should be aware of the possible adverse effects that can be caused by hypertonic phosphate enemas.

Calcium Gluconate↗
PubMed1981

The syndrome of hyperostosis and hyperphosphatemia.

Six children, five girls and one boy, presented with recurrent episodes of swelling, pain, and tenderness of the long bones. On roentgenographic examination all had cortical hyperostosis of the affected areas. Serum phosphate concentration was persistently elevated, and calcium values were normal. Bone biopsy and histologic examination in three patients revealed periosteal new bone formation. The Ellsworth-Howard test was performed on three patients; all had a normal phosphaturic response and an increase in urinary c'AMP to exogenous PTH. The EDTA test, performed on one patient, demonstrated significant phosphaturic response, but a minimal drop in serum phosphate concentration. These findings suggest that the association of cortical hyperostosis and hyperphosphatemia is a distinct clinical entity, and that hyperphosphatemia results from decreased renal excretion of phosphate.

Adolescent↗
PubMed2003

Unexplained transient hyperphosphatemia is more common in acute psychiatric disorders than in acute medical-surgical conditions.

Increased serum inorganic phosphorus associated with elevated serum calcium has been demonstrated to coincide with the onset of agitation and mania in periodic psychoses and bipolar disorders. We tested the hypothesis that unexplained transient hyperphosphatemia (UTHP) is more common in patients with psychiatric disorders than in controls with medical or surgical conditions. We studied 100 patients admitted to a psychiatric ward and 100 controls admitted to a medical-surgical ward. All subjects (patients and controls) underwent acute admission to the same general hospital. The serum phosphorus was measured upon admission and, if elevated, followed during the hospital course. Twenty patients (20%) with psychiatric disorders had unexplained hyperphosphatemia compared with four medical-surgical controls (4%). UTHP occurred in six patients with psychiatric disorders and no controls. Hypophosphatemia did not occur in subjects with psychiatric disorders. This study shows an increased incidence of UTHP in acutely ill, hospitalized patients with psychiatric disorders relative to acutely ill, hospitalized controls with medical-surgical conditions. These data extend previous findings by linking UTHP to acute psychiatric disturbances across varied psychiatric diagnoses independent of hypercalcemia. Potential explanations include trazodone administration and transient hypocalcemia.

Acute Disease↗
PubMed2003

Randomized, double-blind, placebo-controlled, dose-titration, phase III study assessing the efficacy and tolerability of lanthanum carbonate: a new phosphate binder for the treatment of hyperphosphatemia.

BACKGROUND: Lanthanum carbonate is a novel, non-calcium, non-aluminum phosphate binder under evaluation for the treatment of hyperphosphatemia in end-stage renal disease (ESRD) patients receiving either hemodialysis or continuous ambulatory peritoneal dialysis. METHODS: This 16-week study assessed the control of serum phosphorus with lanthanum carbonate, and its effects on serum calcium, calcium x phosphorus product, and parathyroid hormone (PTH). Hemodialysis patients > or =18 years old entered into a 1- to 3-week washout period during which serum phosphorus levels rose to >5.9 mg/dL (1.90 mmol/L). In total, 126 patients were titrated with lanthanum carbonate at doses containing 375, 750, 1,500, 2,250, or 3,000 mg/d elemental lanthanum, given in divided doses with meals over a 6-week period, to achieve serum levels < or =5.9 mg/dL. By the end of dose titration, 11/126 (9%) patients received < or =750 mg/d of lanthanum, 25 (20%) received 1,500 mg/d, 37 (29%) received 2,250 mg/d, and 53 (42%) received 3,000 mg/d. Following titration, patients were randomized to receive either lanthanum carbonate or placebo during a 4-week, double-blind maintenance phase. RESULTS: At the study endpoint, the mean difference in serum phosphorus between the lanthanum carbonate and placebo treatment arms was 1.91 mg/dL (0.62 mmol/L) (P < 0.0001). Calcium x phosphorus product (P < 0.0001) and serum PTH levels (P < 0.01) were also significantly lower with lanthanum carbonate versus placebo. The incidence of drug-related adverse events was similar between placebo- and lanthanum carbonate-treated patients. CONCLUSION: Lanthanum carbonate is an effective and well-tolerated agent for the treatment of hyperphosphatemia in patients with ESRD.

Aged↗
PubMed1992

Hyperphosphatemia: its consequences and treatment in patients with chronic renal disease.

Control of phosphorus accumulation in chronic renal insufficiency is crucial to the prevention of secondary hyperparathyroidism and metastatic calcification. In early renal failure, calcitriol levels are normal and parathyroid hormone levels are elevated. The phosphorus levels are maintained in the normal range by the phosphaturia induced by hyperparathyroidism. In this situation, dietary phosphorus restriction increases calcitriol levels and suppresses parathyroid hormone secretion. As renal failure progresses into late stages, hyperphosphatemia is evident along with low levels of calcitriol and worsening hyperparathyroidism. Phosphorus restriction will not affect calcitriol concentrations, yet parathyroid levels may decline. During long-term dialysis, urinary excretion of phosphorus is usually minimal. Therefore, phosphorus balance is determined primarily by the net amount absorbed by the bowel and the quantity removed during dialytic therapy. Given an adequate diet, no form of conventional dialysis is able to fully compensate for the gastrointestinal absorption of phosphorus. Hence, compounds that bind phosphorus in the bowel are often necessary. With the realization that the use of phosphorus binders containing aluminum leads to aluminum accumulation and its sequelae: osteomalacia, dementia, myopathy, and anemia, other phosphorus binders have been evaluated. Calcium carbonate has been investigated the most thoroughly and is in wide use. It is inexpensive and contains a high percent of elemental calcium. However, it is only modestly potent in the binding of phosphorus, and large doses are often necessary to attain satisfactory control of phosphorus. This may lead to hypercalcemia. One approach to this problem is to decrease the concentration of calcium in the dialysate. Alternatively, a more effective phosphorus binder may be used. Calcium acetate has been shown in acute studies to have twice the binding capacity of phosphorus per calcium absorbed than calcium carbonate. Whether use of this compound decreases the incidence of hypercalcemia is unproven. Calcium citrate increases the gastrointestinal absorption of aluminum and offers no advantage over calcium carbonate. Other compounds, such as calcium ketoacids and calcium alginate, have not been extensively studied and are not generally available. The use of phosphorus binders containing magnesium in conjunction with a dialysate low in magnesium may be efficacious. Large doses of magnesium will cause diarrhea and thus limit its use as a single agent. Reasons for failure to control hyperphosphatemia include poor compliance, improper prescription of binders, poor dissolution rates seen with some generic brands of calcium carbonate, and the presence of severe hyperparathyroidism. Optimal control of serum phosphorus in dialysis patients should always be viewed in the context of adequate nutrition and protein intake.

Aluminum↗
PubMed1997

Poly[allylamine hydrochloride] (RenaGel): a noncalcemic phosphate binder for the treatment of hyperphosphatemia in chronic renal failure.

Dietary phosphate restriction and the oral administration of calcium and aluminum salts have been the principal means of controlling hyperphosphatemia in individuals with end-stage renal disease over the past decade. Although relatively well-tolerated, a large fraction of patients treated with calcium develop hypercalcemia, particularly when administered concurrently with calcitriol, despite a lowering of the dialysate calcium concentration. We evaluated the efficacy of cross-linked poly[allylamine hydrochloride] (RenaGel; Geltex Pharmaceuticals, Waltham, MA), a nonabsorbable calcium- and aluminum-free phosphate binder, in a randomized, placebo-controlled, double-blind trial of 36 maintenance hemodialysis patients followed over an 8-week period. RenaGel was found to be as effective as calcium carbonate or acetate as a phosphate binder. The reduction in serum phosphorus was significantly greater after 2 weeks of treatment with RenaGel (6.6 +/- 2.1 mg/dL to 5.4 +/- 1.5 mg/dL) compared with placebo (7.0 +/- 2.1 mg/dL to 7.2 +/- 2.4 mg/dL; P = 0.037). There was no significant change in serum calcium concentration in either treatment group. The total serum cholesterol and low-density lipoprotein cholesterol fraction were significantly reduced in RenaGel-treated patients compared with placebo-treated patients (P = 0.013 and P = 0.003, respectively) without a concomitant reduction in high-density lipoprotein cholesterol (P = 0.93). There was no difference among recipients of RenaGel and placebo in terms of adverse events. RenaGel is a safe and effective alternative to oral calcium for the management of hyperphosphatemia in end-stage renal disease.

Adult↗
PubMed1999

Hyperphosphatemia in end-stage renal disease patients: pathophysiological consequences.

A study of 6407 end-stage renal disease (ESRD) patients has shown that hyperphosphatemia is increasingly important as a risk for mortality. Half of the patients showed serum phosphorus levels of over 6.0 mg/dl; at the same time, an elevated calcium x phosphorus product indicated increased risk of mortality. These observations lead to questions regarding the mechanisms at work in both the observed phenomena and the way in which they affect mortality. To answer these questions, an understanding of the pathophysiological consequences of hyperphosphatemia is necessary.

Animals↗
PubMed2004

The effect of diet education on the laboratory values and knowledge of hemodialysis patients with hyperphosphatemia.

OBJECTIVE: The purpose of this study was to evaluate the effectiveness of 20 to 30 minutes per month of additional diet education on monthly laboratory values (phosphorus, calcium, parathyroid hormone, and calcium/phosphorus product) and knowledge of dietary phosphorus management in hemodialysis patients with hyperphosphatemia. DESIGN: A quasi-experimental design. SETTING: Three outpatient dialysis centers owned by the same corporation in 1 southern state. PATIENTS: Based on a 3-month average serum phosphorus >6.0 mg/dL, 70 patients were selected for participation; 63 dialysis patients completed the study, 32 in the experimental group and 31 in the control group. INTERVENTION: All patients completed a before-and-after knowledge test and had monthly blood samples drawn. Each month, the same registered dietitian provided the routine laboratory results review with control group. The experimental group received the routine laboratory review plus 20 to 30 minutes of additional diet education specifically targeting phosphorus. Main outcome measures Before-and-after knowledge test results and baseline and final serum calcium, phosphorus, parathyroid hormone, and calcium/phosphorus product levels. RESULTS: At baseline, there were no significant differences in any of the laboratory values, but the knowledge level of the experimental group was greater (P <.05) After 6 months, gains in knowledge were significantly higher in the intervention group, and the serum phosphorus and calcium/phosphorus product levels were significantly lower (P <.01) than in the control group. CONCLUSION: Based on this research, those patients who received extra education monthly showed positive changes, which may be beneficial in reducing hyperphosphatemia.

Adult↗
PubMed1986

The acidosis of cholera. Contributions of hyperproteinemia, lactic acidemia, and hyperphosphatemia to an increased serum anion gap.

To study the metabolic acidosis that occurs during the diarrhea of cholera, we examined the serum anion gap in 21 patients with hypovolemic shock due to Vibrio cholerae infection. Measurements of serum electrolytes, as well as divalent cations and the anionic contributions of serum proteins, lactate, phosphate, and serum creatinine, were made at the time of admission, after rehydration, and during convalescence. At the time of admission, the mean serum concentration of sodium was 134.8 mmol (meq) per liter, that of chloride was 103.2 mmol per liter, and that of bicarbonate was 11.4 mmol per liter; the mean anion gap was 20.2 mmol per liter. The mean serum creatinine concentration was 2.48 mg per deciliter. The low serum bicarbonate level and the high serum anion gap were corrected by rehydration. The increased serum anion gap was caused by hyperproteinemia, lactic acidemia, and hyperphosphatemia, with anionic contributions to the rise in anion gap estimated as protein, 5.5 meq per liter; lactate, 2.5 meq per liter; and phosphate, 2.5 meq per liter. The hyperproteinemia was attributed to dehydration, the lactic acidemia to shock, and the hyperphosphatemia to acidosis and transient renal failure. The mean concentrations of serum calcium and magnesium were slightly elevated but did not affect the increased anion gap. These results indicate that severe cholera causes acidosis with relatively little change in serum chloride but an increased serum anion gap. The acidosis is more profound than would be expected on the basis of stool losses of bicarbonate, because of superimposed lactic acidemia and renal failure.

Acid-Base Equilibrium↗
PubMedDate not supplied

Hyperphosphatemia in a burn patient.

Hypophosphatemia has been observed in severely burned patients and has been associated with increased mortality. Hyperphosphatemia has rarely been described in this population. We present a burn patient with hyperphosphatemia, hypercalciuria, and suppressed parathyroid hormone level 5 months after the initial burn. The patient's presentation is most consistent with the effect of immobilization on bone and calcium metabolism.

Adult↗
PubMed1986

Lactic acidosis associated with cirrhosis, hepatoma, hemoperitoneum, and hyperphosphatemia.

A patient with cirrhosis developed hemoperitoneum, lactic acidosis, and hyperphosphatemia in the absence of shock. At post-mortem examination occult multicentric hepatocellular carcinoma eroding the liver capsule was present. The case emphasizes the central role of the liver in lactic acidosis, indicates that hemoperitoneum may precipitate this complication, and documents the association of lactic acidosis and hyperphosphatemia.

Acidosis↗
PubMed2002

Fatal hyperphosphatemia from a phosphosoda bowel preparation.

Oral phosphosoda is increasingly being used as a bowel preparation for colonoscopy, as it requires that a much smaller volume be ingested and is equally effective and less costly than polyethylene glycol-based electrolyte solutions. Oral phosphosoda has a good safety record, but complications of its use may occur. We describe a patient who died as a result of severe hyperphosphatemia after an oral phosphosoda bowel preparation. A 55-year-old man was admitted with rectal bleeding, abdominal pain, and vomiting. He had a history of diabetes, hypertension, and end-stage renal disease and had successful renal transplant 3 years prior. His initial serum creatinine, calcium, phosphate, and electrolyte levels were normal. He vomited after polyethylene glycol-based electrolyte solution, and an alternate bowel preparation with oral phosphosoda was recommended. He received 90 mL of oral phosphosoda as a single dose. Six hours later, he had cardiorespiratory arrest and was found to have hyperphosphatemia (serum phosphate, 17.8 mg/dL), a high anion gap acidosis, hypoxia, and oliguric renal failure. Resuscitation was unsuccessful. Autopsy showed ischemic colitis. We conclude that bowel preparation with phosphosoda may be associated with severe complications and should be avoided if there is any suggestion of impaired renal function or poor gut motility.

Administration, Oral↗
PubMed2003

Calcium salts in the treatment of hyperphosphatemia in hemodialysis patients.

PURPOSE OF REVIEW: Hyperphosphatemia in patients with end-stage renal disease leads to secondary hyperparathyroidism and renal osteodystrophy, and is independently associated with mortality risk. How hyperphosphatemia increases mortality risk is unknown but it may promote cardiovascular calcification. It is recommended that dialysis patients be treated to maintain normal serum phosphorus. Although calcium-based phosphate binders are cost-effective, their long-term safety has been questioned because of their postulated role in progression of cardiovascular calcification. In this regard, sevelamer hydrochloride has been recommended as an alternative phosphate binder. In this review, we will examine these issues and provide rational guidelines for the use of calcium-based phosphate binders. RECENT FINDINGS: Results from the calcium acetate Renagel evaluation study indicate that calcium acetate is more effective than sevelamer in controlling serum phosphorus and calcium x phosphorus product in hemodialysis patients. However, in the Treat-to-Goal study dialysis patients treated with sevelamer had less progression of coronary and aortic calcification than patients treated with calcium-containing binders. The mechanism underlying the slower rate of progression of cardiovascular calcification in sevelamer-treated patients remains uncertain but may relate to decreased calcium loading or to dramatic reductions in LDL cholesterol. SUMMARY: At present, evidence incriminating calcium-containing phosphate binders in the progression of cardiovascular calcification in end-stage renal disease remains largely circumstantial. As calcium acetate is more efficacious and cost-effective than sevelamer, it remains an accepted first-line drug. Treatment with sevelamer hydrochloride should be considered for patients with persistent hypercalcemia during calcium-based binder therapy despite appropriate adjustment of vitamin D therapy.

Acetates↗
PubMed2004

Nicotinamide suppresses hyperphosphatemia in hemodialysis patients.

BACKGROUND: The use of calcium- or aluminum-based phosphate binders against hyperphosphatemia is limited by the adverse effects of hypercalcemia or aluminum toxicity in long-term hemodialysis. Because nicotinamide is an inhibitor of sodium-dependent phosphate cotransport in rat renal tubule and small intestine, we examined whether nicotinamide reduces serum levels of phosphorus and intact parathyroid hormone (iPTH) in patients undergoing hemodialysis. METHODS: Sixty-five hemodialysis patients with a serum phosphorus level of more than 6.0 mg/dL after a 2-week washout of calcium carbonate were enrolled in this study. Nicotinamide was administered for 12 weeks. The starting dose was 500 mg/day, and the dose was increased by 250 mg/day every 2 weeks until serum phosphorus levels were well controlled at less than 6.0 mg/dL. A 2-week posttreatment washout period followed the cessation of nicotinamide. Blood samples were collected every week for measurement of serum calcium, phosphorus, lipids, iPTH, and blood nicotinamide adenine dinucleotide (NAD). RESULTS: The mean dose of nicotinamide was 1080 mg/day. The mean blood NAD concentration increased from 9.3 +/- 1.9 nmol/105 erythrocytes before treatment to 13.2 +/- 5.3 nmol/105 erythrocytes after treatment (P < 0.01). The serum phosphorus concentration increased from 5.4 +/- 1.5 mg/dL to 6.9 +/- 1.5 mg/dL with the pretreatment washout, then decreased to 5.4 +/- 1.3 mg/dL after the 12-week nicotinamide treatment (P < 0.0001), and rose again to 6.7 +/- 1.6 mg/dL after the posttreatment washout. Serum calcium levels decreased during the pretreatment washout from 9.1 +/- 0.8 mg/dL to 8.7 +/- 0.7 mg/dL with the cessation of calcium carbonate. No significant changes in serum calcium levels were observed during nicotinamide treatment. Median serum iPTH levels increased with pretreatment washout from 130.0 (32.8 to 394.0) pg/mL to 200.0 (92.5 to 535.0) pg/mL and then decreased from the maximum 230.0 (90.8 to 582.0) pg/mL to 150.0 (57.6 to 518.0) pg/mL after the 12-week nicotinamide treatment (P < 0.05). With nicotinamide, serum high-density lipoprotein (HDL) cholesterol concentrations increased from 47.4 +/- 14.9 mg/dL to 67.2 +/- 22.3 mg/dL (P < 0.0001) and serum low-density lipoprotein (LDL) cholesterol concentrations decreased from 78.9 +/- 18.8 mg/dL to 70.1 +/- 25.3 mg/dL (P < 0.01); serum triglyceride levels did not change significantly. CONCLUSION: Nicotinamide may provide an alternative for controlling hyperphosphatemia and hyperparathyroidism without inducing hypercalcemia in hemodialysis patients.

Aged↗
PubMed2004

Treatment of hyperphosphatemia in hemodialysis patients: The Calcium Acetate Renagel Evaluation (CARE Study).

BACKGROUND: Hyperphosphatemia underlies development of hyperparathyroidism, osteodystrophy, extraosseous calcification, and is associated with increased mortality in hemodialysis patients. METHODS: To determine whether calcium acetate or sevelamer hydrochloride best achieves recently recommended treatment goals of phosphorus </=5.5 mg/dL and Ca x P product </=55 mg(2)/dL(2), we conducted an 8-week randomized, double-blind study in 100 hemodialysis patients. RESULTS: Comparisons of time-averaged concentrations (weeks 1 to 8) demonstrated that calcium acetate recipients had lower serum phosphorus (1.08 mg/dL difference, P= 0.0006), higher serum calcium (0.63 mg/dL difference, P < 0.0001), and lower Ca x P (6.1 mg(2)/dL(2) difference, P= 0.022) than sevelamer recipients. At each week, calcium acetate recipients were 20% to 24% more likely to attain goal phosphorus [odds ratio (OR) 2.37, 95% CI 1.28-4.37, P= 0.0058], and 15% to 20% more likely to attain goal Ca x P (OR 2.16, 95% CI 1.20-3.86, P= 0.0097). Transient hypercalcemia occurred in 8 of 48 (16.7%) calcium acetate recipients, all of whom received concomitant intravenous vitamin D. By regression analysis hypercalcemia was more likely with calcium acetate (OR 6.1, 95% CI 2.8-13.3, P < 0.0001). Week 8 intact PTH levels were not significantly different. Serum bicarbonate levels were significantly lower with sevelamer hydrochloride treatment (P < 0.0001). CONCLUSION: Calcium acetate controls serum phosphorus and calcium-phosphate product more effectively than sevelamer hydrochloride. Cost-benefit analysis indicates that in the absence of hypercalcemia, calcium acetate should remain the treatment of choice for hyperphosphatemia in hemodialysis patients.

Acetates↗
PubMed2004

Treatment of hyperphosphatemia in patients with chronic kidney disease on maintenance hemodialysis: results of the CARE study.

Most patients with end-stage renal disease develop hyperphosphatemia because their dietary intake exceeds phosphorus elimination by intermittent thrice-weekly dialysis. Inadequately treated hyperphosphatemia plays a central role in the pathogenesis of secondary hyperparathyroidism and extraosseous calcification. Moreover, in the last 15 years, this biochemical abnormality has become increasingly important following the publication of two epidemiologic studies that demonstrated an association between elevated serum phosphorus and increased mortality risk in patients with end-stage renal disease. As a result, the National Kidney Foundation Kidney Disease Outcome and Quality Initiative (K/DOQI) Bone Metabolism and Chronic Kidney Disease Guidelines recommend that serum phosphorus levels be maintained between 3.5 and 5.5 mg/dL. Unfortunately, cross-sectional studies have shown a mean serum phosphorus of 6.2 mg/dL in the maintenance hemodialysis population in the United States. An alarming 60% of patients have serum phosphorus in excess of the 5.5 mg/dL level recommended by K/DOQI guidelines. In order to achieve this new target for serum phosphorus, the most efficacious and cost-effective phosphate binders currently available should be utilized. In this review, we discuss the results of the Calcium Acetate Renagel Evaluation (CARE study), which clearly demonstrated the superiority of calcium acetate over sevelamer hydrochloride for controlling serum phosphorus and calcium-phosphate product to the levels recommended by the K/DOQI guidelines.

Acetates↗
PubMed2005

An introduction to phosphate binders for the treatment of hyperphosphatemia in patients with chronic kidney disease.

Chronic kidney disease has the potential to induce sequelae that can have severe and mortal outcomes. In particular, impaired glomerular filtration can cause a hyperphosphatemic state, which, if left unchecked, can lead to secondary hyperparathyroidism, vascular calcification, and renal osteodystrophy. Therapeutic management of hyperphosphatemia must maintain both phosphorus and calcium serum concentrations within the recommended guidelines. The balance of both minerals is regulated by parathyroid hormone; thus, an imbalance of one affects the other. In end-stage renal disease, patients often present with hypocalcemic levels due to the kidneys' inability to generate active vitamin D to promote calcium absorption in the intestine. Absorption of calcium can be increased by the administration of active vitamin D analogues. Minimizing phosphorus intake through a strict dietary regimen, combined with the use of phosphate binders to absorb excess ingested phosphate, can help to maintain serum phosphate levels near the recommended concentration of 5.5 mg/dL. Phosphate-binding compounds have evolved from the original aluminum-based binders pioneered in the 1970s to calcium-based binders such as calcium acetate, and more recently, to the following additions to the nephrologist's armamentarium: sevelamer--a polyhydrochloride polymer, and lanthanum carbonate. One of the top 2 common clinical treatments for hyperphosphatemia, calcium acetate, has an established history of efficacy since the 1980s, and has been shown to be cost effective and well tolerated, as well.

Chronic Disease↗