Spurious Hyperphosphatemia in a Patient with Chronic Kidney Disease - a Rare Case of Alteplase Contamination.

Spurious hyperphosphatemia, a rare occurrence, typically arises from substances in a patient's blood interfering with the colorimetric method for serum phosphate measurement. We present a case of factitious hyperphosphatemia caused by alteplase-contaminated blood samples in an 88-year-old CKD patient on hemodialysis, leading to misleadingly high phosphorus levels. Thorough investigations ruled out other etiologies, highlighting the necessity of stringent adherence to blood collection protocols to prevent sample contamination and avert erroneous laboratory results. This unique cause of hyperphosphatemia should be considered in the differential diagnosis when encountering unexplained elevations in phosphorus levels, particularly in the context of normal blood calcium levels.

A 47-Year-Old Man with Hyperphosphatemia Due to Chronic Renal Failure Treated with Lanthanum Carbonate Tablets Presenting Acutely with Partial Large Bowel Obstruction.

BACKGROUND Hyperphosphatemia is a complication of chronic renal failure (CRF) due to reduction in the glomerular filtration rate. Lanthanum carbonate is a commonly used phosphate binder for patients with CRF and hyperphosphatemia, but has adverse effects if patients are not monitored. This report is of a 47-year-old man with hyperphosphatemia due to CRF treated with lanthanum carbonate tablets who presented acutely with partial large bowel obstruction. The incidence of lanthanum carbonate causing intestinal obstruction is rare, and few cases in the literature have described the course of the disease in detail. CASE REPORT A 47-year-old man diagnosed with diabetic nephropathy underwent hemodialysis treatment and was prescribed 0.5 g/day of chewable lanthanum carbonate tablets. After taking lanthanum carbonate for 5 months, the patient experienced symptoms of decreased bowel movements and exhaustion, which progressively worsened. Abdominal computed tomography (CT) revealed multiple hyperdensities in the large bowel, indicating the presence of lanthanum deposition. Lanthanum carbonate was promptly discontinued. After undergoing enema and catharsis treatment, the large bowel obstruction was relieved, and the hyperdensities in the abdominal CT disappeared. The colonoscopy and histologic examination revealed ulcerations and inflammatory changes in the large bowel mucosa. CONCLUSIONS This report highlights the rare association between the use of lanthanum carbonate tablets and intestinal obstruction. Healthcare providers should enhance their vigilance regarding lanthanum carbonate-induced serious gastrointestinal adverse reactions and actively seek to detect lanthanum deposition by abdominal CT or radiography (X-ray). After the occurrence of lanthanum deposition, drug withdrawal and promotion of defecation are primary treatment methods.

Hypervitaminosis D has no positive effects on goat tuberculosis and may cause chronic renal lesions.

BACKGROUND: There is evidence for a link between vitamin D deficiency and active tuberculosis (TB). In human beings, several trials have evaluated the role of vitamin D supplementation in TB treatment with conflicting results. However, the role of vitamin D supplementation in animal TB control has received less attention. The authors evaluated the benefit of vitamin D supplementation for preventing mycobacterial infection or reducing TB lesions (TBL) in a controlled trial with goats naturally exposed to Mycobacterium caprae. METHODS: Two groups of goats, a vitamin D-supplemented group and a non-supplemented control group, were housed for 10 months in direct contact with M caprae-infected adult goats. Upon contact with the infected adult goats, all animals were TB-tested every two months. RESULTS: No experimental evidence of a protective effect of vitamin D supplementation based on M caprae culture prevalence, TBL prevalence, median TBL score or the proportion of single versus multiple organs presenting TBL was observed. CONCLUSION: The results indicate that, in the conditions used in this study, vitamin D supplementation in goats does not reduce TB infection risk nor the diffusion and severity of TBL. In addition, vitamin D-supplemented goats presented hyperphosphataemia and renal injury with calcifications suggestive of vitamin D intoxication.

Phosphate supplementation for hypophosphatemia during continuous renal replacement therapy in adults.

BACKGROUND: Hypophosphatemia is common during continuous renal replacement therapy (CRRT) in critically ill patients and can cause generalized muscle weakness, prolonged respiratory failure, and myocardial dysfunction. This study aimed to investigate the efficacy and safety of adding phosphate to the dialysate and replacement solutions to treat hypophosphatemia occurring in intensive CRRT in critically ill patients. METHODS: We retrospectively analyzed 73 patients treated with intensive CRRT (effluent flow ≥35 ml/kg/hr) in the intensive care unit. The control group (group 1, n = 22) received no phosphate supplementation. The treatment groups received dialysate and replacement solution phosphate supplementation at 2.0 mmol/L (group 2, n = 26) or 3.0 mmol/L (group 3, n = 25). RESULTS: The CRRT-induced hypophosphatemia incidence was 59.0%. Correction of hypophosphatemia with phosphate supplementation changed the mean serum phosphorus levels to 1.24 ± 0.37 and 1.44 ± 0.31 mmol/L in groups 2 and 3, respectively (p = .02). The time required for correction was 1.65 ± 0.80 and 1.39 ± 1.43 days for groups 2 and 3, respectively and was significantly longer in group 2 (p = .02). After supplementation, hypophosphatemia, and hyperphosphatemia both occurred in 7% of group 2. Group 3 developed no hypophosphatemia, but 20% developed hyperphosphatemia. The serum phosphate levels in hyperphosphatemia cases returned to normal within 2.0 days (group 2) and 1.0 day (group 3) after stopping phosphate supplementation. CONCLUSION: Phosphate supplementation effectively corrected CRRT-induced hypophosphatemia in critically ill patients with an acute kidney injury. The use of 2 mmol/L phosphate is appropriate in patients with CRRT-induced hypophosphatemia, but a different concentration could be required to prevent hypophosphatemia at the start of CRRT.

Nutritional status and survival of maintenance hemodialysis patients receiving lanthanum carbonate.

Background: Hyperphosphatemia and poor nutritional status are associated with increased mortality. Lanthanum carbonate is an effective, calcium-free phosphate binder, but little is known about the long-term impact on mineral metabolism, nutritional status and survival. Methods: We extended the follow-up period of a historical cohort of 2292 maintenance hemodialysis patients that was formed in late 2008. We examined 7-year all-cause mortality according to the serum phosphate levels and nutritional indicators in the entire cohort and then compared the mortality rate of the 562 patients who initiated lanthanum with that of the 562 propensity score-matched patients who were not treated with lanthanum. Results: During a mean ± SD follow-up of 4.9 ± 2.3 years, 679 patients died in the entire cohort. Higher serum phosphorus levels and lower nutritional indicators (body mass index, albumin and creatinine) were each independently associated with an increased risk of death. In the propensity score-matched analysis, patients who initiated lanthanum had a 23% lower risk for mortality compared with the matched controls. During the follow-up period, the serum phosphorus levels tended to decrease comparably in both groups, but the lanthanum group maintained a better nutritional status than the control group. The survival benefit associated with lanthanum was unchanged after adjustment for time-varying phosphorus or other mineral metabolism parameters, but was attenuated by adjustments for time-varying indicators of nutritional status. Conclusions: Treatment with lanthanum is associated with improved survival in hemodialysis patients. This effect may be partially mediated by relaxation of dietary phosphate restriction and improved nutritional status.

[Tetany secondary to phosphate enema toxicity, case report]. / Tetania severa por uso de enemas fosfatados, reporte de caso.

Phosphate enemas are frequently used in the treatment of constipation. Errors in dosage and administration can lead to severe complications. OBJECTIVE: To report a case of severe toxicity of phosphate enemas in a child with no risk factors. CASE: 2 years old female, with functional constipation, was brought to emergency department because abdominal pain. She was diagnosed with fecal impaction and received half a bottle of Fleet Adult® (Laboratorio Synthon, Chile) two times, with no clinical resolution, deciding to start proctoclisis in pediatric ward. Soon after admission, she presented painful tetany, but alert and oriented. Patient was transferred to PICU where severe hyperphosphatemia and secondary hypocalcemia were confirmed. Her treatment included electrolyte correction; removal of residual phosphate enema and hyperhydration. Tetany resolved over 2 hours after admission and no other complications. Proctoclisis was performed and patient was discharged three days after admission with pharmacological management of constipation. CONCLUSION: Phosphate enemas may cause serious complications in children with no risk factors. Errors in dosage, administration and removal of the enema are causes of toxicity in this group. Pediatricians and health personnel must be aware of risks and signs of toxicity of phosphate enema.

Tetania severa por uso de enemas fosfatados, reporte de caso / Tetany secondary to phosphate enema toxicity, case report

Los enemas fosfatados son utilizados frecuentemente en el tratamiento de la constipación. Errores en la posología pueden producir complicaciones graves. Objetivo: Reportar un caso de toxicidad grave por enema fosfatado en un pre escolar sin factores de riesgo. Caso clínico: Paciente de 2 años con constipación funcional, evaluada en servicio de urgencia por dolor abdominal a quién se le diagnosticó un fecaloma impactado. Recibió 2 dosis de enema de fosfato, “medio frasco” de Fleet® adulto (Synthon, Chile) por vez, sin resolución de su fecaloma, decidiéndose hospitalización para proctoclisis. Posterior al ingreso presentó un cuadro clínico de tetania. Ingresó a la Unidad de Paciente Crítico donde se confirmó una hiperfosfemia e hipocalcemia secundaria. Se realizó corrección electrolítica progresiva, retiro de enema fosfatado residual del recto e hiperhidratación forzando diuresis. La tetania cedió 2 horas después del ingreso sin otras complicaciones. Se realizó proctoclisis y fue dada de alta a los 3 días. Conclusión: Los enemas fosfatados pueden presentar complicaciones graves en niños sin factores de riesgo. Errores en la posología son la causa más frecuente de toxicidad en este grupo, pero esta puede estar favorecida también por una administración y eliminación inadecuadas. Pediatras y personal de salud que atiende a niños deben conocer factores de riesgo, signos y síntomas de intoxicación por enemas fosfatados.

Phosphate enemas are frequently used in the treatment of constipation. Errors in dosage and administration can lead to severe complications. Objective: To report a case of severe toxicity of phosphate enemas in a child with no risk factors. Case: 2 years old female, with functional constipation, was brought to emergency department because abdominal pain. She was diagnosed with fecal impaction and received half a bottle of Fleet Adult® (Laboratorio Synthon, Chile) two times, with no clinical resolution, deciding to start proctoclisis in pediatric ward. Soon after admission, she presented painful tetany, but alert and oriented. Patient was transferred to PICU where severe hyperphosphatemia and secondary hypocalcemia were confirmed. Her treatment included electrolyte correction; removal of residual phosphate enema and hyperhydration. Tetany resolved over 2 hours after admission and no other complications. Proctoclisis was performed and patient was discharged three days after admission with pharmacological management of constipation. Conclusion: Phosphate enemas may cause serious complications in children with no risk factors. Errors in dosage, administration and removal of the enema are causes of toxicity in this group. Pediatricians and health personnel must be aware of risks and signs of toxicity of phosphate enema.

Efficacy and safety of paricalcitol in children with stages 3 to 5 chronic kidney disease.

BACKGROUND: Elevated intact parathyroid hormone (iPTH) levels can contribute to morbidity and mortality in children with chronic kidney disease (CKD). We evaluated the pharmacokinetics, efficacy, and safety of oral paricalcitol in reducing iPTH levels in children with stages 3-5 CKD. METHODS: Children aged 10-16 years with stages 3-5 CKD were enrolled in two phase 3 studies. The stage 3/4 CKD study characterized paricalcitol pharmacokinetics and compared the efficacy and safety of paricalcitol with placebo followed by an open-label period. The stage 5 CKD study evaluated the efficacy and safety of paricalcitol (no comparator) in children with stage 5 CKD undergoing dialysis. RESULTS: In the stage 3/4 CKD study, mean peak plasma concentration and area under the time curve from zero to infinity were 0.13 ng/mL and 2.87 ng•h/((or ng×h/))mL, respectively, for 12 children who received 3 µg paricalcitol. Thirty-six children were randomized to paricalcitol or placebo; 27.8% of the paricalcitol group achieved two consecutive iPTH reductions of ≥30% from baseline versus none of the placebo group (P = 0.045). Adverse events were higher in children who received placebo than in those administered paricalcitol during the double-blind treatment (88.9 vs. 38.9%; P = 0.005). In the stage 5 CKD study, eight children (61.5%) had two consecutive iPTH reductions of ≥30% from baseline, and five (38.5%) had two consecutive iPTH values of between 150 and 300 pg/mL. Clinically meaningful hypercalcemia occurred in 21% of children. CONCLUSIONS: Oral paricalcitol in children aged 10-16 years with stages 3-5 CKD reduced iPTH levels and the treatment was well tolerated. Results support an initiating dose of 1 µg paricalcitol 3 times weekly in children aged 10-16 years.

Severe hyperphosphatemia after oral laxative administration in a 7-year-old patient.

Sodium phosphate based laxatives are commonly used for constipation and pre-procedural bowel cleansing. Phosphate intoxication related with these preparations is well recognized. Herein, we present a case of severe hyperphosphatemia and seizure in a 7-year-old male patient after administration of an oral sodium phosphate based laxative. At the time of admission, serum phosphorus level was 25.6 mg/dl. Aggressive fluid therapy was started. Although serum phosphorus level decreased to 20.9 mg/dl eight hours after admission, hemodialysis was performed because of the preexisting renal disease and declined glomerular filtration rate. Serum phosphorus level and blood gas analysis returned to normal after hemodialysis and the patient was discharged on hospital day two. In conclusion, sodium phosphate based laxatives should be used carefully in patients with preexisting renal diseases. Intravenous hydration and correction of hypocalcemia are important components of treatment. Hemodialysis is indicated in patients with renal failure.

Prevalence of Phosphorus-Based Additives in the Australian Food Supply: A Challenge for Dietary Education?

OBJECTIVE: Phosphorus-based food additives may pose a significant risk in chronic kidney disease given the link between hyperphosphatemia and cardiovascular disease. The objective of the study was to determine the prevalence of phosphorus-based food additives in best-selling processed grocery products and to establish how they were reported on food labels. DESIGN: A data set of 3000 best-selling grocery items in Australia across 15 food and beverage categories was obtained for the 12 months ending December 2013 produced by the Nielsen Company's Homescan database. The nutrition labels of the products were reviewed in store for phosphorus additives. The type of additive, total number of additives, and method of reporting (written out in words or as an E number) were recorded. MAIN OUTCOME MEASURES: Presence of phosphorus-based food additives, number of phosphorus-based food additives per product, and the reporting method of additives on product ingredient lists. RESULTS: Phosphorus-based additives were identified in 44% of food and beverages reviewed. Additives were particularly common in the categories of small goods (96%), bakery goods (93%), frozen meals (75%), prepared foods (70%), and biscuits (65%). A total of 19 different phosphorus additives were identified across the reviewed products. From the items containing phosphorus additives, there was a median (minimum-maximum) of 2 (1-7) additives per product. Additives by E number (81%) was the most common method of reporting. CONCLUSION: Phosphorus-based food additives are common in the Australian food supply. This suggests that prioritizing phosphorus additive education may be an important strategy in the dietary management of hyperphosphatemia. Further research to establish a database of food items containing phosphorus-based additives is warranted.

[Phosphate Intoxication after Application of Enema--a Life-threatening Iatrogenic Complication]. / Phosphatintoxikation nach Klysmagabe--eine lebensgefährliche iatrogene Komplikation.

INTRODUCTION: Enemas are used in pediatric patients with constipation. Retention of phosphate containing enemas with prolonged resorption or reduced renal elimination of phosphate can result in life-threatening hyperphosphatemia with subsequent lethal hypocalcemia and acidosis. CASE PRESENTATION: We report the case of a 6-month-old child who received phosphate-containing enema to treat acute aggravation of constipation. The used enema here was not licensed for this age group. Phosphate intoxication resulted (phosphate 19.87 mmol/l) and presented like a sepsis. Hyperphosphatemia was treated by hemodialysis. A non-diagnosed Hirschsprung disease had led to prolonged resorption of phosphate containing enema and to an ileus and toxic megacolon that had to be operated. CONCLUSION: Insufficient elimination of phosphate containing enema can result in lethal or life threatening hyperphosphatemia, hypocalcemia and metabolic acidosis. These can be treated efficaciously by hemodialysis. Because of the high risk of intoxication in using enemas containing phosphate in infants or in patients with gastrointestinal or renal comorbidities, physicians treating constipation should choose enemas without phosphate but with ingredients with lower risk like glycerol or sorbitol in this age group.

Hemodialysis for near-fatal sodium phosphate toxicity in a child receiving sodium phosphate enemas.

OBJECTIVE: This study aimed to demonstrate the importance of considering hemodialysis as a treatment option in the management of sodium phosphate toxicity. METHODS: This is a case report of a 4-year-old who presented to the emergency department with shock, decreased mental status, seizures, and tetany due to sodium phosphate toxicity from sodium phosphate enemas. RESULTS: Traditional management of hyperphosphatemia with aggressive hydration and diuretics was insufficient to reverse the hemodynamic and neurological abnormalities in this child. This is the first report of the use of hemodialysis in a child without preexisting renal failure for the successful management of near-fatal sodium phosphate toxicity. CONCLUSIONS: Hemodialysis can safely be used as an adjunctive therapy in sodium phosphate toxicity to rapidly reduce serum phosphate levels and increase serum calcium levels in children not responding to conventional management.

Pseudohyperphosphatemia in children treated with liposomal amphotericin B.

PURPOSE: The results of a study to determine the frequency of pseudohyperphosphatemia in a sample of pediatric patients treated with i.v. liposomal amphotericin B are reported. METHODS: A single-site retrospective study was conducted to identify evidence of pseudohyperphosphatemia in the medical records of patients 18 years of age or younger who received at least five doses of amphotericin B liposome; the maximum dose was calculated for each regimen and categorized as either ≤5 or >5 mg/kg/day. The primary objective was to ascertain the rate of pseudohyperphosphatemia (i.e., abnormally high serum phosphate without elevated serum calcium). The secondary objective was to compare rates of pseudohyperphosphatemia at the higher and lower amphotericin B dosage levels. A multivariate generalized estimating equation (GEE) regression model was used to identify potential predictors of pseudohyperphosphatemia. RESULTS: Data were collected on 72 courses of amphotericin B liposome administered during a 13-month period to 47 patients; based on a review of chart notations and clinical data, it was determined that 36 regimens (50%) involved pseudohyperphosphatemia. The GEE model revealed no significant association between pseudohyperphosphatemia and any evaluated variable, including age, weight, duration of therapy, and concurrent use of medications known to alter serum phosphorus. CONCLUSION: In children receiving amphotericin B liposome, half of the regimens were associated with pseudohyperphosphatemia. Although no factors were found to predict pseudohyperphosphatemia, on average, patients who developed the abnormality were significantly older and heavier and received a significantly higher absolute initial dosage of amphotericin B liposome than those who did not develop the condition.

[Metabolic encephalopathy secondary to vitamin D intoxication]. / Encefalopatía metabólica secundaria a intoxicación por vitamina D.

The association between vitamin D deficiency and increased risk of, among others, cardiovascular and autoimmune diseases has lead in the last years to an enhanced interest in the usage of supplements to achieve the normalization of plasmatic values at 25(OH) D. Apparently this search for normalization is resulting in an higher incidence on vitamin D intoxication. We present the case of an 81 years old woman with metabolic encephalopathy and renal failure secondary to iatrogenic vitamin D intoxication. Calcium and vitamin D oral supplements were prescribed after an osteoporotic vertebral fracture. The patient improved clinically as well as analytically after receiving treatment with diuretics and hydration. We emphasize the importance of discarding hypercalcemia as a cause of metabolic encephalopathy; moreover we highly recommend keeping vitamin D intoxication in mind as an uncommon although always possible etiology of reversible hypercalcemia and renal failure.

La asociación entre la deficiencia de vitamina D y un mayor riesgo de diversas enfermedades, entre ellas cardiovasculares y autoinmunes, ha aumentado en los últimos años el uso de suplementos para la normalización de los valores plasmáticos de esta vitamina. Desde entonces se ha descrito un mayor número de casos de intoxicación iatrogénica por vitamina D. Presentamos una enferma de 81 años con encefalopatía metabólica e insuficiencia renal secundarias a una intoxicación por vitamina D. Los suplementos orales con calcio y vitamina D se le prescribieron después de sufrir una fractura vertebral osteoporótica. La enferma mejoró clínica y analíticamente tras hidratación y diuréticos. Es importante destacar la hipercalcemia como causa de encefalopatía metabólica y considerar la intoxicación por vitamina D como etiología poco frecuente pero posible de hipercalcemia e insuficiencia renal reversibles.

Is parenteral phosphate replacement in the intensive care unit safe?

Hypophosphatemia is well recognized in the intensive care setting, associated with refeeding and continuous forms of renal replacement therapy (CCRT). However, it is unclear as to when and how to administer intravenous phosphate supplementation in the general intensive care setting. There have been recent concerns regarding phosphate administration and development of acute kidney injury. We therefore audited our practice of parenteral phosphate administration. We prospectively audited parenteral phosphate administration (20 mmol) in 58 adult patients in a general intensive care unit in a University tertiary referral center. Fifty-eight patients were audited; mean age 57.2 ± 2.0 years, 70.7% male. The median duration of the infusion was 310 min (228-417), and 50% of the patients were on CRRT. 63.8% of patients were hypophosphatemic (<0.87 mmol/L) prior to the phosphate infusion, and serum phosphate increased from 0.79 ± 0.02 to 1.07 ± 0.03 mmol/L, P < 0.001. Two patients became hyperphosphatemic (>1.45 mmol/L). There was no correlation between the change in serum phosphate and the pre-infusion phosphate. Although there were no significant changes in serum urea, creatinine or other electrolytes, arterial ionized calcium fell from 1.15 ± 0.01 to 1.13 ± 0.01 mmol/L, P < 0.01. Although infusion of 20 mmol phosphate did not appear to adversely affect renal function and corrected hypophosphatemia in 67.7% of cases, we found that around 33% of patients who were given parenteral phosphate were not hypophosphatemic, and that the fall in ionized calcium raises the possibility of the formation of calcium-phosphate complexes and potential for soft tissue calcium deposition.

Massive hyperphosphatemia in a patient with neuronal intestinal dysplasia after bowel preparation with oral sodium phosphate.

Oral sodium phosphate-based laxatives are frequently used for bowel preparation or relief of constipation in some countries. However, these agents are not without risk. Small and clinical insignificant increments on serum phosphorus levels are observed in almost all individuals after use of oral sodium phosphate. Some patients are prone to severe hyperphosphatemia such as elders, those with chronic or acute renal disease and those with poor bowel motility. Severe hyperphosphatemia accompanied with hypocalcemia may be life-threatening in these patients. We present an 18-year-old woman with neuronal intestinal dysplasia who developed symptomatic and severe hyperphosphatemia after bowel preparation with oral sodium phosphate enema. Urgent hemodialysis was performed two times for severe hyperphosphatemia.

Phosphate additives in food--a health risk.

BACKGROUND: Hyperphosphatemia has been identified in the past decade as a strong predictor of mortality in advanced chronic kidney disease (CKD). For example, a study of patients in stage CKD 5 (with an annual mortality of about 20%) revealed that 12% of all deaths in this group were attributable to an elevated serum phosphate concentration. Recently, a high-normal serum phosphate concentration has also been found to be an independent predictor of cardiovascular events and mortality in the general population. Therefore, phosphate additives in food are a matter of concern, and their potential impact on health may well have been underappreciated. METHODS: We reviewed pertinent literature retrieved by a selective search of the PubMed and EU databases (www.zusatzstoffe-online.de, www.codexalimentarius.de), with the search terms "phosphate additives" and "hyperphosphatemia." RESULTS: There is no need to lower the content of natural phosphate, i.e. organic esters, in food, because this type of phosphate is incompletely absorbed; restricting its intake might even lead to protein malnutrition. On the other hand, inorganic phosphate in food additives is effectively absorbed and can measurably elevate the serum phosphate concentration in patients with advanced CKD. Foods with added phosphate tend to be eaten by persons at the lower end of the socioeconomic scale, who consume more processed and "fast" food. The main pathophysiological effect of phosphate is vascular damage, e.g. endothelial dysfunction and vascular calcification. Aside from the quality of phosphate in the diet (which also requires attention), the quantity of phosphate consumed by patients with advanced renal failure should not exceed 1000 mg per day, according to the guidelines. CONCLUSION: Prospective controlled trials are currently unavailable. In view of the high prevalence of CKD and the potential harm caused by phosphate additives to food, the public should be informed that added phosphate is damaging to health. Furthermore, calls for labeling the content of added phosphate in food are appropriate.

Lanthanum carbonate reduces urine phosphorus excretion: evidence of high-capacity phosphate binding.

The effectiveness of phosphate binders can be assessed by evaluating urinary phosphorus excretion in healthy volunteers, which indicates the ability of the phosphate binder to reduce gastrointestinal phosphate absorption. Healthy volunteers were enrolled into one of five separate randomized trials; four were open label and one double blind. Following a screening period of ≤28 days, participants received differing tablets containing lanthanum carbonate [LC, 3000 mg/day of elemental lanthanum (in one study other doses were also used)]. Participants received a standardized phosphate diet and remained in the relevant study center throughout the duration of each treatment period. The end point in all studies was the reduction in urinary phosphorus excretion. Reductions in mean 24-h urinary phosphorus excretion in volunteers receiving a lanthanum dose of 3000 mg/day were between 236 and 468 mg/day over the five separate studies. These data in healthy volunteers can be used to estimate the amount of reduction of dietary phosphate absorption by LC. The reduction in 24-h urinary phosphorus excretion per tablet was compared with published data on other phosphate binders. Although there are limitations, evidence suggests that LC is a very effective phosphate binder in terms of binding per tablet.