Control Of Serum Phosphorus Levels Research Articles

Combined alkaline phosphatase and phosphorus levels as a predictor of mortality in maintenance hemodialysis patients.

Hyperphosphatemia-induced vascular calcification and higher alkaline phosphatase (ALP) levels-related high-turnover bone diseases are linked to mortality among patients with chronic kidney disease (CKD). Nonetheless, no large epidemiological study in patients with CKD has been conducted to investigate the interaction and joint effect of hyperphosphatemia and higher ALP levels on mortality.We analyzed 11,912 maintenance hemodialysis patients from January 2005 to December 2010. Unadjusted and adjusted hazard ratios (aHRs) of death were calculated for different categories of serum phosphorus and ALP using the Cox regression model. The modification effect between serum phosphorus and ALP on mortality was determined using an interaction product term.Both hypophosphatemia (<3.0 mg/dL) and hyperphosphatemia (>7.0 mg/dL) were associated with incremental risks of death (aHR: 1.25 [95% confidence intervals (CIs): 1.09–1.44], and 1.15 [95% CI: 1.01–1.31], respectively) compared to the lowest hazard ratio (HR) group (5 mg/dL ≤ phosphorus < 6 mg/dL). ALP levels were linearly associated with incremental risks for death (aHR: 1.58 [95% CI: 1.41–1.76] for the category of ALP > 150 U/L). In the stratified analysis, patients with combined higher ALP (>150 U/L) and hyperphosphatemia (>7.0 mg/dL) had the greatest mortality risk (aHR: 2.25 [95% CI: 1.69–2.98] compared to the lowest HR group (ALP ≤ 60 U/L and 4 mg/dL ≤ phosphorus < 5 mg/dL). Although the effect of hyperphosphatemia on mortality seemed stronger in higher ALP levels, the interaction was not statistically significant (P = 0.22).The association between serum phosphorus levels and mortality was not limited to higher ALP levels. Regardless of serum ALP levels, we may control serum phosphorus levels merely toward the normal range. While considering the joint effect of ALP and hyperphosphatemia on mortality, the optimal phosphorus range should be stricter.

Antibacterial Activity of Probiotic Bacteria Isolated From Broiler Feces and Commercial Strains

Background: The extensive use of antibiotics in animal farms to promote the growth rate and prevent the enteric pathogen has led to the development of antibiotic-resistant bacteria and drug residues in the birds body. In the recent years, probiotics have been constantly studied for their inhibitory effects on pathogenic bacteria. Objectives: The current study aimed to assess the effect of magnesium oxide on controlling serum phosphorus levels and evaluate its side effects. Materials and Methods: Antibacterial activity of local and commercial probiotic bacteria was investigated using colony overlay assay. Then antibacterial activity of local and commercial probiotics against each pathogen, Salmonella typhimurium, Escherichia coli and Staphylococcus aureus were compared. Results: Local strain of lactic acid bacteria had significantly higher antibacterial activity compared to those of the commercial probiotics. Local probiotics showed a significantly stronger activity against Staphylococcus aureus, Salmonella typhimurium and Escherichia coli compared to all commercial probiotics. Conclusions: Administration of mono strain of Lactobacillus salivarius ES1, or co-administration of ES1 and L. salivarius ES6, is not only more effective than commercial probiotics against Salmonella spp., Staphylococcus spp. and E.coli, but also, will have no negative effects on micro flora balance of local birds.

The Effect of Magnesium Oxide on Hyperphosphatemia in Female Hemodialysis Patients

Objectives: This study aims to assess the effect of magnesium oxide on controlling serum phosphorus levels and evaluate its side effects. Patients and Methods: We studied 39 hemodialysis patients with hyperphosphatemia. Patients were randomly divided into two groups, trial and control. The trial group received magnesium oxide. Its dose was titrated according to weekly magnesium levels that were checked for 4 weeks. Phosphorous was also checked weekly in both groups. Data were analyzed by SPSS 15 software. P-values less than 0.05 were considered significant. Results: A total of 27 males and 12 females with a mean age 54.01 ± 17.20 years were divided into the trial (21 patients) and control (18 patients) groups. Serum phosphorous levels did not significantly decrease (P = 0.994). However the mean phosphorous level in females showed significant correlation with time, as a significant quadratic trend throughout time was observed (P = 0.001). A significant ascending trend in mean magnesium levels was observed in the trial group compared to the control group at the end of the study (P < 0.001). Conclusions: Although magnesium oxide was well tolerated by the study patients and lacked serious complications, it could not decrease phosphorous levels. In order to better assess these results we recommend that larger, multicenter studies with longer follow up that uses other magnesium compounds be designed.

Timing of Return to Dialysis in Patients with Failing Kidney Transplants

In the last decade, the number of patients starting dialysis after a failed kidney transplant has increased substantially. These patients appear to be different from their transplant-naïve counterparts, and so may be the timing of dialysis therapy initiation. An increasing number of studies suggest that in transplant-naïve patients, later dialysis initiation is associated with better outcomes. Very few data are available on timing of dialysis reinitiation in failed transplant recipients, and they suggest that an earlier return to dialysis therapy tended to be associated with worse survival, especially among healthier and younger patients and women. Failed transplant patients may also have unique issues such as continuation of immunosuppression versus withdrawal or the need for remnant allograft nephrectomy with regard to dialysis reinitiation. These patients may have a different predialysis preparation work-up, worse blood pressure control, higher or lower serum phosphorus levels, lower serum bicarbonate concentration, and worse anemia management. The choice of dialysis modality may also represent an important question for these patients, even though there appears to be no difference in mortality between patients starting peritoneal versus hemodialysis. Finally, failed transplant patients returning to dialysis appear to have a higher mortality rate compared with transplant-naïve incident dialysis patients, especially in the first several months of dialysis therapy. In this review, we will summarize the available data related to the timing of dialysis initiation and outcomes in failed kidney transplant patients after returning to dialysis.

Beneficial effects of nocturnal hemodialysis in a hemodynamically unstable patient with AL‐amyloidosis

We present a patient with primary systemic AL-amyloidosis, who stabilized hemodynamically on nocturnal hemodialysis (NHD). The NHD allowed a significant reduction in ultrafiltration rates which likely underlies the procedural tolerability. It also provided an increase in urea clearance, better control of serum phosphorus levels without the use of any binders, and normalization of blood pressure despite the discontinuation of all antihypertensive agents. Given the autonomic derangements associated with AL-amyloidosis pathophysiology and the clinical benefits of NHD on hemodynamic stability, the use of intensive hemodialysis may be considered for the management of patients with unstable hemodynamic profiles.

Clinical use of non-calcium phosphate binder:an advance

Controlling serum phosphorus levels is critical in patients with renal failure. Currently phosphate-binding agents are widely used to reduce phosphate absorption in patients with endstage renal disease. If possible,serum phosphorus level should be reduced without disturbing calcium homeostasis or increasing accumulation of potentially toxic elements. Aluminum hydroxide and traditional calcium -based phosphate binders are commonly used to control serum phosphorus level. Aluminum hydroxide can effectively lower serum phosphorus level,but aluminum can accumulates in the body and results in toxic effect. Traditional calcium-based phosphate binders tend to promote hypercalcemia and calcium overloading,and accelerate cardiovascular calcification. Therefore aluminum -free and calcium-free phosphate-binding agents have become the focus of study; however,agents like sevelamer hydrochloride and lanthanum carbonate are not widely used due to high price,although they are effective in controlling serum phosphorus level. New generation of phosphate binders,such as colestilan,nicotinic acid and magnesium salt,are cheaper than their previous counterparts,but their long -term effect still needs to be observed. This article summarizes the progress of non-calcium phosphate binders in treatment of end-stage renal diseases,hoping to help clinical drug usage.

Sevelamer Carbonate

To review the pharmacology, pharmacokinetics, clinical efficacy, safety data, and place in therapy of sevelamer carbonate for the treatment of hyperphosphatemia in patients with chronic kidney disease (CKD). A literature search of MEDLINE and MEDLINE In-Process & Other Non-Indexed Citations Databases (1966-August 2009) was conducted using the key words chronic kidney disease, hyperphosphatemia, and sevelamer carbonate. All published articles regarding sevelamer carbonate were included. References of selected articles, data from multiple presentations, and abstract publications were reviewed. Available English-language data from reviews, abstracts, presentations, and clinical trials of sevelamer carbonate in humans were reviewed; relevant clinical data were selected and included. Sevelamer carbonate is approved to control serum phosphorus levels and treat hyperphosphatemia in patients with CKD who are on dialysis. In clinical trials, sevelamer carbonate has been shown to lower serum phosphorus levels and calcium-phosphorus product to a similar extent as sevelamer hydrochloride. Significantly fewer patients receiving treatment with sevelamer carbonate were likely to report any gastrointestinal adverse event compared with those on sevelamer hydrochloride treatment. Further, sevelamer carbonate is associated with significant effects on decreasing low-density lipoprotein cholesterol levels and may cause less metabolic acidosis than sevelamer hydrochloride. Additionally, sevelamer hydrochloride was removed from the market in October 2009; sevelamer carbonate is now the only available formulation. Sevelamer carbonate is a treatment option for hyperphosphatemia in patients with CKD who are on dialysis. Clinical data indicate that sevelamer carbonate effectively lowers serum phosphorus levels while having minimal effect on serum calcium or serum chloride levels. The role of sevelamer carbonate in the treatment of hyperphosphatemia relative to other phosphate-binding drugs, including calcium salts and lanthanum, has not yet been established.

Benefits and Harms of Phosphate Binders in CKD: A Systematic Review of Randomized Controlled Trials

Phosphate binders are widely used to control serum phosphorus levels in patients with chronic kidney disease (CKD). We analyzed the effects of phosphate binders on biochemical and patient-level end points in patients with CKD. Systematic review and meta-analysis by searching MEDLINE (1966 to April 2009), EMBASE (1980 to April 2009), and the Cochrane Renal Group Specialised Register and the Cochrane Central Register of Controlled Trials (CENTRAL). Patients with CKD. Randomized controlled trials. Phosphate binders. Serum phosphorus, calcium, and parathyroid hormone levels; incidence of hypercalcemia; all-cause mortality; adverse effects. 40 trials (6,406 patients) were included. There was no significant decrease in all-cause mortality (10 randomized controlled trials; 3,079 patients; relative risk [RR], 0.73; 95% confidence interval [CI], 0.46 to 1.16), hospitalization, or end-of-treatment serum calcium-phosphorus product levels with sevelamer compared with calcium-based agents. There was a significant decrease in end-of-treatment phosphorus and parathyroid hormone levels with calcium salts compared with sevelamer and a significant decrease in risk of hypercalcemia (RR, 0.47; 95% CI, 0.36 to 0.62) with sevelamer compared with calcium-based agents. There was a significant increase in risk of gastrointestinal adverse events with sevelamer in comparison to calcium salts (RR, 1.39; 95% CI, 1.04 to 1.87). Compared with calcium-based agents, lanthanum significantly decreased end-of-treatment serum calcium and calcium-phosphorus product levels, but with similar end-of-treatment phosphorus levels. Effects of calcium acetate on biochemical end points were similar to those of calcium carbonate. Existing data are insufficient to conclude for a differential impact of any phosphate binder on cardiovascular mortality or other patient-level outcome. Few long-term studies of the efficacy of phosphate binders on mortality and musculoskeletal morbidity, significant heterogeneity for many surrogate outcomes, and suboptimal reporting of study methods to determine trial quality. Currently, there are insufficient data to establish the comparative superiority of non-calcium-binding agents over calcium-containing phosphate binders for such important patient-level outcomes as all-cause mortality and cardiovascular end points. Additional trials are still required to examine the differential effects of phosphate-binding agents on these end points and the mineral homeostasis pathway.

Phosphorus Additives in Food and their Effect in Dialysis Patients

There is substantial epidemiologic evidence linking hyperphosphatemia and cardiovascular and all-cause mortality among dialysis patients (1,2). Therefore, control of hyperphosphatemia is a crucial element of the routine clinical care of dialysis patients. Theoretically, control of serum phosphorus levels can be achieved by the right combination of decreased dietary phosphorus intake, decreased GI phosphorus absorption by phosphate binders, and increased phosphorus elimination via dialysis. However, the clinical reality is that despite the widespread use of high-efficiency dialyzers, new phosphorus binders, and usual nutritional education, the average serum phosphorus in dialysis patients remains higher than the levels recommended by practice guidelines, except in patients on long nocturnal hemodialysis (3). The lack of attention by practicing nephrologists to dietary phosphorus restriction in general, and more specifically the lack of awareness regarding the increasing consumption of processed foods rich in phosphate additives, may significantly contribute to limit the efficacy of the current interventions (4). Estimation of the dietary intake of phosphorus should consider not only phosphorus contained in natural food, but also phosphorus added in processing food. In general, foods high in protein like meats, milk, eggs, and cereals are also naturally high in phosphorus and traditionally have represented the main source of dietary phosphorus (5). However, this is changing as phosphates are currently being added to a large and increasing number of processed foods, including meats, cheeses, dressings, beverages, and bakery products (6–8). As a result, and depending on the food choices, such additives may increase the phosphorus intake by as much as 1.0 g/d (7). Phosphorus in additives is more readily absorbed than that from foods naturally high in phosphorus; as a result, additives will have a greater effect on hyperphosphatemia than an equivalent amount of naturally …

Management of phosphate in chronic kidney disease--Phosphorus control by hemodialysis with long treatment time

Hyperphosphatemia is an almost universal finding in patients with end-stage renal disease and is associated with increased all-cause mortality, cardiovascular mortality, and vascular calcification. Although new phosphate binders lead to a easy control of serum phosphorus levels, treatment time of a dialysis session might be the most important factor for controlling hyperphosphatemia. Two alternatives to conventional thrice weekly dialysis (CHD) are nocturnal hemodialysis (NHD) and short daily hemodialysis (SDHD) . The total weekly phosphorus removal with NHD and SDHS is significantly greater than that removed by CHD and this is associated with a significantly lower average serum phosphorous.

Novel phosphate binders under development

Controlling serum phosphorus levels in patients with chronic kidney disease is crucial. Since hyperphosphatemia is an established risk factor for not only secondary hyperparathyroidism, but also cardiovascular mortality in these patients, the adequate control of serum phosphorus is necessary. The target levels of serum phosphorus, however, are not consistently being met. To achieve better control of serum phosphorus levels, some novel phosphate binders, which do not contain calcium or metal, have been developed. In this manuscript we discuss some novel phosphate binders, which are now in clinical trials.

Management of hyperphosphatemia ; phosphate-binder

Numerous experimental and clinical studies have recently addressed the underlying mechanisms in particular the marked increase in cardiovascular mortality in patients with CKD. Hyperphosphatemia is a major problem in these patients with advanced stage of CKD. Calcium carbonate became the most widely used phosphate binders ; however, increasing evidence now suggests that prolonged use of these agents increases the total body calcium load, induces adynamic bone, and potentially increases the risk of cardiovascular and soft tissue calcification. Sevelamer is the first phosphate-binding agent that is non-absorbed, calcium-free, and metal-free. To date, this agent has been shown to effectively control serum phosphorus levels in patients with CKD. It may also attenuate coronary and aortic calcification and has a number of other beneficial effects on lipid metabolism and inflammation among others.

Sevelamer carbonate in the management of hyperphosphatemia

Sevelamer carbonate appears to be a promising new agent in the control of serum phosphorus levels in subjects with chronic kidney disease. It contains the same active moiety as sevelamer hydrochloride, but has carbonate instead of chloride as the counterion. This substitution has resulted in a statistically significant improvement in serum bicarbonate levels in chronic kidney disease patients receiving chronic dialysis, and may support, in the future, the treatment of hyperphosphatemia in chronic kidney disease patients not yet on dialysis. It also offers the potential for improved gastrointestinal tolerability and the prospect of alternative formulations, such as a powder. However, most of the proposed benefits of sevelamer carbonate are extrapolated from the studies completed with sevelamer hydrochloride. Hence, the determination of an added benefit from sevelamer carbonate compared with sevelamer hydrochloride and other phosphorus binders will require direct comparison.

A new era in phosphate binder therapy: What are the options?

Dietary restriction of phosphorus and current dialysis prescription are unable to maintain phosphorus levels within the recommended range (2.7-5.5 mg/dl) in patients with advanced chronic kidney disease (CKD). Therefore, phosphate binders that limit the absorption of dietary phosphorus are commonly prescribed for this patient group. The first phosphate binders were introduced more than 30 years ago and included aluminum salts; however, although effective binders, the use of these agents was subsequently restricted because of concerns over aluminum accumulation in the central nervous system, bone, and hematopoietic cells. In subsequent years, calcium salts, namely calcium carbonate and calcium acetate, became the most widely used phosphate binders; however, increasing evidence now suggests that prolonged use of these agents increases the total body calcium load, induces adynamic bone, and potentially increases the risk of cardiovascular and soft tissue calcification. Sevelamer is the first phosphate-binding agent that is non-absorbed, calcium-free, and metal-free. To date, this agent has been shown to effectively control serum phosphorus levels in patients with CKD. It may also attenuate coronary and aortic calcification and has a number of other beneficial effects on lipid metabolism and inflammation among others. Lanthanum carbonate is another new agent that is reported to provide similar phosphate control to calcium-based phosphate binders but concerns that the long-term administration of such compound may lead to tissue accumulation may limit its use.

Effect of manipulating serum phosphorus with phosphate binder on circulating PTH and FGF23 in renal failure rats

Phosphorus directly controls parathyroid hormone (PTH) synthesis and secretion. Serum levels of the novel phosphate-regulating hormone, fibroblast growth factor 23 (FGF23), are positively correlated with hyperphosphatemia in patients with chronic renal insufficiency (CRI). We proposed that changes in serum PTH and FGF23 levels might be associated with changes in serum phosphorus levels caused by the phosphate binder sevelamer hydrochloride (sevelamer, i.e. crosslinked poly[allylamine hydrochloride]). Rats were fed a diet containing adenine for 4 weeks to establish CRI. Animals were then offered either a normal diet or a diet containing 1 or 3% sevelamer for 8 weeks continuously, or intermittently with sevelamer diet or a normal diet offered for alternating 2-week periods. Changes in the serum levels of phosphorus, calcium, PTH, FGF23, and 1alpha,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) were monitored over time. Adenine-treated rats developed severe CRI, with markedly elevated serum levels of phosphorus, PTH and FGF23, and reduced levels of serum 1,25(OH)(2)D(3). Continuous treatment with sevelamer suppressed these increases throughout the study period. Serum phosphorus, PTH, and FGF23 levels decreased rapidly when sevelamer treatments commenced and recovered rapidly once they were discontinued. However, the changes in serum FGF23 levels began after the onset of changes in serum phosphorus and PTH levels. In conclusion, circulating PTH, and FGF23 levels can be promptly manipulated through the control of serum phosphorus levels. Moreover, phosphate-binder treatment can effectively inhibit the elevation of serum FGF23 levels, as well as PTH levels, under conditions of CRI.

Lanthanum carbonate (Fosrenol®) efficacy and tolerability in the treatment of hyperphosphatemic patients with end-stage renal disease

High serum phosphorus levels are a common problem in patients receiving long-term dialysis treatment. Lanthanum carbonate (Fosrenol) is a new non-aluminum, non-calcium phosphate binder developed for the treatment of hyperphosphatemia in patients with end-stage renal disease (ESRD). We report data from a recent trial, which, for the first time, assessed the efficacy and tolerability of lanthanum carbonate treatment, compared with placebo, in Chinese patients with ESRD. Following a one- to three-week washout phase and a four-week, open-label lanthanum carbonate dose-titration phase, male and female hemodialysis patients were randomized (1:1) to receive either lanthanum carbonate or placebo for four weeks. The primary efficacy parameter of the study was the control of serum phosphorus levels (< or =1.8 mmol/l [< or = 5.6 mg/dl]). Secondary endpoints included the profile of serum phosphorus during titration and parathyroid hormone, calcium, and calcium x phosphorus (Ca x P) product levels. The safety and tolerability of lanthanum carbonate were assessed by monitoring adverse events throughout the study. Mean serum phosphorus level at the end of washout was 2.5 +/- 0.5 mmol/l (7.7 +/- 1.5 mg/dl; n=73), and there was no evidence of a difference in levels between the treatment groups pre-randomization. At the end of the study, lanthanum carbonate-treated patients had significantly lower phosphorus levels (1.6 +/- 0.5 mmol/l [5.1 +/- 1.5 mg/dl]; n=30) than those receiving placebo (2.3 +/- 0.4 mmol/l [7.2 +/- 1.3 mg/dl]; n=31; p < 0.001). In addition, a significantly higher proportion of patients receiving lanthanum carbonate had controlled serum phosphorus levels (60%) compared with the placebo group (10%; p < 0.001). Ca x P product levels were also significantly lower in the lanthanum carbonate group at the end of randomized treatment (p < 0.001). Lanthanum carbonate was well tolerated; only one serious adverse event was reported, which was unrelated to treatment. Lanthanum carbonate was shown to be an effective and well-tolerated phosphate binder for the treatment of hyperphosphatemia in Chinese patients with ESRD. This finding supports the results of previous US and European studies, which have also shown that lanthanum carbonate treatment effectively controls serum phosphorus levels.

The role of abnormal phosphorus metabolism in the progression of chronic kidney disease and metastatic calcification

The role of abnormal phosphorus metabolism in the progression of renal disease and metastatic calcification. Hyperphosphatemia is a common biochemical abnormality in advanced renal failure. The resulting increase serum calcium x phosphorus product results in the deposition of hydroxyapatite crystals. The crystalline properties of these deposits incite an inflammatory response manifested by encapsulated tumoral deposits around joints, acute inflammatory arthritis, and irritative conjunctivitis. These deposits occur in association with marked elevation of serum phosphorus levels, and are prevented and eradicated by normalizing serum phosphorus levels. The calcium-phosphate deposits which occur in heart and lungs are nonapatitic. These deposits were never clearly related to hyperphosphatemia. They are mainly of historic interest because currently they are rarely seen. Their eradication appears to be more of a result of improved dialytic techniques than correction of serum phosphorus levels. The presence, persistence, and progression of vascular calcification are more closely related to patient age and duration of dialysis than hyperphosphatemia. This suggests that these deposits are a result of dystrophic calcification occurring de novo in a diseased or damaged vessel wall. Phosphorous restriction has also been shown to be protective of renal functional deterioration in experimental renal disease. It is unclear whether the protective effect is mediated through phosphate restriction or phosphate depletion. In conclusion, control of serum phosphorus levels in dialyzed uremic patients has clearly decreased morbidity associated with periarticular, articular, and conjunctiva hydroxyapatite deposits. In contrast, phosphorous control has had little effect on the presence or severity of vascular calcification.

Improving phosphate-binder therapy as a way forward.

Aluminium- or calcium-based phosphate-binding agents traditionally have been used to treat hyperphosphataemia in patients with end-stage renal disease. Although these agents effectively lower serum phosphorus levels, they are associated with serious side effects. Aluminium-based agents are associated with bone toxicity, renal osteodystrophy and encephalopathy, and calcium-based agents increase the risk of hypercalcaemia and cardiovascular calcification. Consequently, there remains a need for new, safe and effective non-calcium-, non-aluminium-based alternative treatments. Fortunately, several new agents are now available or are in the late stages of development, including sevelamer hydrochloride and lanthanum carbonate. Although sevelamer hydrochloride represents a step forward in the management of hyperphosphataemia, it has several drawbacks and is far from being the ideal phosphate binder. Lanthanum carbonate is the most recent non-calcium, non-aluminium phosphate binder to be developed for the treatment of hyperphosphataemia. Animal studies have shown it to be as effective as aluminium, without the associated toxicity. In clinical studies, lanthanum carbonate significantly reduced serum phosphorus levels, compared with placebo. It shows a similar efficacy to calcium carbonate in controlling serum phosphorus levels, but requires lower doses. In addition, lanthanum carbonate is at least as well tolerated as calcium carbonate, but is not associated with hypercalcaemia. Importantly, it has a positive effect on bone histology, with no evolution towards low bone turnover. Lanthanum carbonate, therefore, moves closer to the ideal phosphate binder.

Importance of hyperphosphataemia in the cardio-renal axis.

Hyperphosphataemia occurs in nearly all patients with end-stage renal disease (ESRD). In the past, the need to manage hyperphosphataemia focused primarily on its role as a contributor to secondary hyperparathyroidism and renal osteodystrophy. There is now widespread recognition that disturbances in phosphorus metabolism and/or the therapeutic measures used to manage it are important risk factors for cardiovascular calcification. This serious complication of chronic kidney disease may contribute to the very high mortality rate from cardiovascular causes in patients undergoing long-term dialysis. New strategies for controlling serum phosphorus levels and for better management of mineral metabolism in general are required to address these issues in patients with ESRD.

Consequences of hyperphosphatemia and elevated levels of the calcium-phosphorus product in dialysis patients.

Control of serum phosphorus levels is a central goal in the management of patients with chronic renal failure. Inadequate control of serum phosphorus leads to elevated levels of the calcium-phosphorus product. This plays a pivotal role in vascular calcification, cardiovascular disease, calciphylaxis, and death. Elevated phosphorus and elevated levels of the calcium-phosphorus product are both significant predictors of cardiovascular mortality, at phosphorus and calcium-phosphorus product levels that were considered safe until recently. A lowering of levels such that phosphorus is maintained between 2.2 and 5.5 mg/dl, calcium-phosphorus product is below 55 mg(2)/dl(2), and serum calcium is at 9.2-9.6 mg/dl, respectively, might well be the goal of therapeutic management strategies.