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PubMed2005

Consequences and management of hyperphosphatemia in patients with renal insufficiency.

Consequences and management of hyperphosphatemia in patients with renal insufficiency. Progressive renal insufficiency leads to hyperphosphatemia, hypocalcemia, and secondary hyperparathyroidism. Bone demineralization in secondary hyperparathyroidism may induce fractures, while joint and subcutaneous precipitations of calcium pyrophosphate limit mobility, and may cause crippling. Strategies to preempt bone and joint destruction in chronic kidney disease and end-stage renal disease have focused on limiting dietary phosphorus, intra-gut binding of ingested phosphorous, enhancing calcium absorption, and limiting parathyroid hormone secretion. Deciding which regimen is most effective to meet these treatment objectives challenges nephrologists; they often uncover conflicting evidence about which abnormal metabolite should be the prime treatment objective. Especially vexing is the question of whether hypercalcemia is a cardiotoxic consequence of calcium-based phosphate binders.

Acetates↗

PubMed2006

Management of hyperphosphatemia.

Hyperphosphatemia is a well recognized risk factor for cardiovascular mortality in dialysis patients. Despite advanced technology and regular and efficient dialysis treatment the prevalence of hyperphosphatemia is still high. The goal of normalization of serum phosphorus (iP) levels can only be reached by optimization of dialysis prescription in combination with individualized dietary and medical strategies. Due to the unique characteristics of intradialytic iP kinetics, dialysis treatment time and frequency are the most effective factors governing intradialytic iP removal. Although the combination of diffusive and convective removal by hemodiafiltration allows a further increase in iP mass removal, a neutral phosphorus balance without dietary restrictions and the use of phosphate binders has only be achieved by daily nocturnal hemodialysis. Strict dietary phosphate restriction bears the risk of inadequate protein intake and the development of protein/calorie malnutrition. Although phosphate binders (PB) can effectively lower serum iP levels into the normal range, this is rarely achieved in clinical practice probably due to inadequate relation of PB dose to dietary phosphorus intake. Developing methods to enable patients to self-adjust phosphate binder dose to individual meal phosphate content, similar to adjusting insulin dose to carbohydrate intake, may lead to further improvements in phosphate management.

Blood Flow Velocity↗

PubMed1985

Pathogenesis of hyperphosphatemia in lactic acidosis: disparate effects of racemic (DL-) and levo (L-) lactic acid on plasma phosphorus concentration.

The mechanism(s) for the hyperphosphatemia associated with lactic acidosis is unknown. Experimental lactate-induced hyperphosphatemia appears to require acidemia because we have shown that prevention of acidemia with NaHCO3 obviates increases in plasma phosphorus concentration ([P]). Since the rate of lactate metabolism (by utilizing NAD or other mechanisms) might modulate transcellular movement of phosphorus, we assessed the plasma [P] response to 3-h infusions of DL-lactic acid versus L-lactic acid. The dog metabolizes primarily the L-moiety of DL-lactic acid (thereby consuming H+), so more L-lactic acid is needed to produce the degree of acidemia attained with DL-lactic acid. Group 1 (n = 6) mongrel dogs received 12 mequiv./kg DL-lactic acid; group 2 (n = 6) 12 mequiv./kg L-lactic acid, and group 3 (n = 7) 16-19 mequiv./kg L-lactic acid. Prior to acid loading, the plasma [P] and acid-base status of the three groups were similar. After 3 h, blood pH and [HCO3] and change from base line in plasma [P], in both milligrams per decilitre and percent, were as follows: group 1: 7.05 +/- 0.02, 9 +/- 2 mM, 1.9 +/- 0.4 mg/dL, 38 +/- 10%; group 2: 7.28 +/- 0.02, 18 +/- 1, 0.9 +/- 0.3, 17 +/- 6; group 3: 7.06 +/- 0.04, 12 +/- 1, 1.1 +/- 0.3, 26 +/- 10, respectively. Thus, there was a tendency for both infusion rates of L-lactic acid to increase [P] less than DL-lactic acid, suggesting the importance of other factors in addition to pH.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed2006

Correlation between hyperphosphatemia and type II Na-Pi cotransporter activity in klotho mice.

Recent studies have demonstrated that klotho protein plays a role in calcium/phosphate homeostasis. The goal of the present study was to investigate the regulation of Na-P(i) cotransporters in klotho mutant (kl/kl) mice. The kl/kl mice displayed hyperphosphatemia, high plasma 1,25(OH)(2)D(3) levels, increased activity of the renal and intestinal sodium-dependent P(i) cotransporters, and increased levels of the type IIa, type IIb, and type IIc transporter proteins compared with wild-type mice. Interestingly, transcript levels of the type IIa/type IIc transporter mRNA abundance, but not transcripts levels of type IIb transporter mRNA, were markedly decreased in kl/kl mice compared with wild-type mice. Furthermore, plasma fibroblast growth factor 23 (FGF23) levels were 150-fold higher in kl/kl mice than in wild-type mice. Feeding of a low-P(i) diet induced the expression of klotho protein and decreased plasma FGF23 levels in kl/kl mice, whereas colchicine treatment experiments revealed evidence of abnormal membrane trafficking of the type IIa transporter in kl/kl mice. Finally, feeding of a low-P(i) diet resulted in increased type IIa Na-P(i) cotransporter protein in the apical membrane in the wild-type mice, but not in kl/kl mice. These results indicate that hyperphosphatemia in klotho mice is due to dysregulation of expression and trafficking of the renal type IIa/IIc transporters rather than to intestinal P(i) uptake.

Animals↗

PubMed2006

Practical approaches to management of hyperphosphatemia: can we improve the current situation?

Despite advanced technology and regular and efficient dialysis treatment, the prevalence of hyperphosphatemia still is unacceptably high. Nevertheless, a neutral phosphorus balance level can generally be achieved by optimization of dialysis prescription in combination with individualized dietary and medical strategies. Besides increasing the fraction of inorganic phosphate (iP) removed by convection through the application of hemodiafiltration, extension of daily or weekly treatment time is the most promising way to neutralize phosphorus balance. Dietary phosphate restriction, the second corner stone of phosphate management, bears the risk of development of protein malnutrition. Phosphate binders (PBs) effectively reduce intestinal iP absorption, but are mostly dosed inadequately in relation to meal phosphorus content. Phosphate management may be substantially improved by enabling patients to self-adjust the PB dose to individual meal phosphate content, similar to self-adjusting insulin dose to carbohydrate intake by diabetics. A recently developed Phosphate Education Program (PEP) provides simple training tools to instruct patients to eye-estimate meal phosphorus content based on newly defined phosphorus units instead of milligrams. PEP is the first approach applying the concept of patient empowerment in the management of hyperphosphatemia in dialysis patients.

Hemodiafiltration↗

PubMed1988

Treatment of uremic hyperphosphatemia--is there still a need for aluminum salts?

Aluminum-containing phosphate binders have been widely employed in the past in the management of uremic hyperphosphatemia. However, an increasing number of reports on aluminum toxicity has stimulated efforts to replace this therapy by safer methods. The aim of the present review is to critically evaluate other treatment strategies. It appears that aluminum-containing phosphate binders should no longer be considered the treatment of choice for controlling uremic hyperphosphatemia. Calcium carbonate, calcium citrate, magnesium carbonate and a mixture of ketoanalogues and amino acids present important therapeutical alternatives which could replace aluminum-containing phosphate binders in the majority of patients. However, it is mandatory, as these therapies also carry some risks, that side effects are detected early.

Alum Compounds↗

PubMed1996

High frequency of marked hyperphosphatemia during intravenous calcitriol therapy in hemodialysis patients with refractory hyperparathyroidism.

Efficacy and safety of intermittent intravenous calcitriol therapy were studied in 8 chronic hemodialysis patients with marked hyperparathyroidism refractory to oral therapy with calcium salts and daily vitamin D. They were followed for 20 weeks (32 weeks for 2 patients). At the start of the study, serum calcium was < 2.65 mmol/l and phosphate levels were controlled with calcium-based binders only. The phosphate content of the prescribed diet (< 1 g/day) remained unchanged during the study, and a low-calcium dialysate was used (1.38 mmol/l). The initial postdialysis calcitriol dose was 1 microgram and was increased to 2 micrograms in 6 patients. Intravenous calcitriol effectively improved hyperparathyroidism in 7 patients, with a significant decrease of the intact parathyroid hormone level from 650 +/- 433 to 195 +/- 208 pg/ml (p < 0.05). Hypercalcemia > 2.7 mmol/l occurring in 3 patients was observed in only 11% of the weekly laboratory controls and always resolved rapidly. In contrast, hyperphosphatemia > or = 2.0 mmol/l was observed in 7 patients and in 40% of the weekly laboratory controls. In 15% of the cases the phosphate values even exceeded 2.4 mmol/l. The phosphate binder therapy had to be intensified accordingly, not only by increasing the dose of calcium-based binders, but also by introducing aluminum salts in 6 patients. In summary, our data show that intravenously administered calcitriol is effective in the treatment of severe hyperparathyroidism in most hemodialysis patients resistant to oral therapy. However, its usefulness seems to be limited by frequency and severity of hyperphosphatemia, frequently necessitating additional prescription of aluminum-based binders. These undesirable secondary events may thus limit the long-term utility of intravenously administered calcitriol.

Administration, Oral↗

PubMed1989

[Extreme hyperphosphatemia with hypocalcemia within the scope of cell lysis syndrome in a child with T-ALL].

In a 10 3/4-year-old girl suffering from a T-ALL with an extremely high leukocyte blood cell count (400,000/microliters) we observed a tumor-lysis syndrome with hyperphosphatemia and hypocalcemia accompanied by clinical signs of tetany. The therapeutic application of calcium gluconate resulted in vascular calcification by exceeding by far the calcium-phosphate solubility product. The fast lysis of T-lymphoblasts with their high phosphate concentration is etiologically involved in the hyperphosphatemia. Our patient died of multiorganic failure. Regular monitoring of phosphate in urine might be helpful in instituting early therapeutic procedures.

Antineoplastic Combined Chemotherapy Protocols↗

PubMed2005

Effectiveness of aluminum hydroxide timing administration in relation to meals in controlling hyperphosphatemia in dialysis patients.

Phosphate binder compounds contribute to the control of hyperphosphatemia in hemodialysis (HD) patients. However, the most effective schedule of administration of phosphate binders in relation to meals is not well documented. We examined the effectiveness of aluminum hydroxide intake as the sole phosphate binder in relation to meals. Eighty-five patients on regular HD (45 male, 40 female), age 21-72 years, with a duration of 6-216 months HD participated in the study. In all patients, phosphate binders were discontinued for a one month period. Thereafter, and according to the protocol, all patients were advised to take aluminum hydroxide [Al(OH)3 ] 30 min before, during and 30 min after meals for 3 periods of one month each, in a random order. One month washout period preceded the periods of Al(OH)3 ingestion. When Al(OH)3 was administered 30 min prior to the meals, serum phosphate decreased by 7.0% (0.59 mg/dL), while when administrated with or 30 min after meals, it decreased statistically significantly by 28.5% (2.08 mg/dL), and 16% (1.29 mg/dL) respectively. Our results suggest that the efficacy of Al(OH)3 to bind phosphate salts and thus to prevent the hyperphosphatemia in HD patients is higher when this drug is taken with meals.

Adult↗

PubMed1996

Severe hyperphosphatemia induced by a phosphate-containing oral laxative.

OBJECTIVE: To describe a case of severe hyperphosphatemia following unintentional overdosage with an oral phosphate laxative, and raise attention to the risk of using such medications in the elderly. CASE SUMMARY: An 84-year-old white woman was admitted with confusion 8 hours after inadvertently ingesting 12 fluid ounces of Fleet Phospho-Soda (instead of the prescribed 1 1/2 fluid ounces) prior to a colonoscopy. Her serum phosphate and ionized calcium concentrations were 10.3 mmol/L and 0.56 mmol/L, respectively. She was treated conservatively with oral phosphate binders and made an uneventful recovery. DISCUSSION: Several previous reports have described hyperphosphatemia in association with phosphate laxatives, especially in patients with renal or colonic disease. Our case again presents two important issues in the use of phosphate laxatives by the elderly: (1) the frequently overlooked underlying renal insufficiency in which, despite "normal" serum creatinine values, renal phosphate handling may be impaired; and (2) the potential for drug misuse and poor compliance in the elderly. CONCLUSIONS: Caution should be taken with the use of phosphate laxatives in the elderly in the face of potentially serious metabolic abnormalities that may be generated.

Aged↗

PubMed2004

FGF-23 is elevated by chronic hyperphosphatemia.

The Identification and characterization of FGF-23 has provided an opportunity to gain new insight into phosphorus metabolism. Circulating FGF-23 promotes renal excretion of phosphorus, and FGF-23 is measurable in the serum of normal subjects. Serum levels of FGF-23 are elevated in patients with renal phosphate wasting disorders such as tumor induced osteomalacia, X-linked hypophosphatemia and fibrous dysplasia. However, the factors that alter its serum concentration are not known. The study of serum FGF-23 is confounded by the fact that high serum calcium, PTH, and any other putative phosphotonins, have similar effects on serum and urine phosphorus. To circumvent the confounding effect of serum PTH and calcium, we studied serum FGF-23 and phosphate levels in patients with chronic hypoparathyroidism and hyperphosphatemia. Serum was collected in the morning after an overnight fast from three groups: 1) 9 patients with chronic hypoparathyroidism on stable treatment with calcium and calcitriol, 2) 9 patients with primary hyperparathyroidism, and 3) 77 normal controls. Patients with hypoparathyroidism had predictably higher levels of serum phosphorus than patients with hyperparathyroidism or normal controls (5.6 +/- 1.1, 3.1 +/- 0.6, and 3.1 +/- 0.5 mg/dL, mean +/- 1 SD, respectively (p < 0.01 for hypoparathyroid vs. either group)). They also had higher levels of FGF-23 (150 +/- 120 vs. 70 +/- 60, or 55 +/- 20 RIU/ml, respectively (p < 0.05 vs. either group)). In conclusion, serum FGF-23 levels are elevated in patients with hyperphosphatemia and chronic hypoparathyroidism, suggesting a feedback system in which serum FGF-23 responds to serum phosphorus and regulates it. However, in the setting of chronic hypoparathyroidism, the degree of elevation of FGF-23 is insufficient to normalize serum phosphorus.

Adult↗

PubMed2003

[Pharmacological and clinical trial data on a novel phosphate-binding polymer (sevelamer hydrochloride), a medicine for hyperphosphatemia in hemodialysis patients].

Hyperphosphatemia is one of the major complications of hemodialysis patients and plays a key role in the pathogenesis of cardiovascular calcification and secondary hyperparathyroidism. Dietary phosphate restriction and removal of phosphate by dialysis are insufficient to control hyperphosphatemia. Therefore, almost all patients undergoing hemodialysis should take oral phosphate binders. Sevelamer hydrochloride (sevelamer) is a novel phosphate-binding polymer that contains neither aluminum nor calcium, and it is not absorbed from the gastrointestinal tract. In rat models with progressive chronic renal insufficiency, in addition to lowering effects on serum levels of phosphorus, calcium x phosphorus product, and parathyroid hormone, dietary treatment of sevelamer can prevent parathyroid hyperplasia, vascular calcification, high turnover bone lesion, and renal functional deterioration. In clinical studies with hemodialysis patients, sevelamer lowers serum phosphorus and calcium x phosphorus product without any incidence of hypercalcemia. Switching calcium-containing phosphate binders to sevelamer can decrease the percentage of hypoparathyroidism and hyperparathyroidism by negative calcium balance and increased dosage of vitamin D, respectively. Sevelamer also decreases serum low-density lipoprotein cholesterol levels by its bile acid-binding capacity. A long-term clinical study has demonstrated that the progression of coronary and aortic calcification in hemodialysis patients is attenuated by sevelamer. Thus, sevelamer offers the promise of impacting cardiac calcification and thereby reducing morbidity and mortality of hemodialysis patients.

Animals↗

PubMed2005

Control of hyperphosphatemia among patients with ESRD.

Derangements of mineral metabolism occur during the early stages of chronic kidney disease (CKD). Hyperphosphatemia develops in the majority of patients with ESRD and has long been associated with progression of secondary hyperparathyroidism and renal osteodystrophy. More recent observational data have associated hyperphosphatemia with increased cardiovascular mortality among dialysis patients. Adequate control of serum phosphorus remains a cornerstone in the clinical management of patients with CKD not only to attenuate the progression of secondary hyperparathyroidism but also possibly to reduce the risk for vascular calcification and cardiovascular mortality. These measures include dietary phosphorus restriction, dialysis, and oral phosphate binders. Dietary restriction is limited in advanced stages of CKD. Phosphate binders are necessary to limit dietary absorption of phosphorus. Aluminum hydroxide is an efficient binder; however, its use has been nearly eliminated because of concerns of toxicity. Calcium salts are inexpensive and have been used effectively worldwide as an alternative to aluminum. Concerns of calcium overload have led to the investigation of alternatives. Currently, only two Food and Drug Administration-approved noncalcium, nonaluminum binders are available. Sevelamer hydrochloride is an exchange resin and was not as effective as calcium acetate in meeting new guideline recommendations in one double-blind clinical trial. Lanthanum carbonate is a rare earth element and has been studied less extensively. Concerns of long-term administration and toxicity exist. Furthermore, these agents are significantly more expensive than calcium salts, which may contribute to patient noncompliance.

Humans↗

PubMed1992

Treatment of uraemic hyperphosphatemia with calcium acetate: a safe alternative to calcium carbonate.

Clinical usefulness of calcium acetate (CAA) as phosphorus binder was assessed in 19 stable hemodialysis patients with persistent hyperphosphatemia. All were dialysed thrice weekly with a constant dialytic schedule and a dialysate calcium of 3.5 mEq/l. One month prior the study beginning all patients stopped assumption of Ca and vitamin D supplements. In the first period of the study CAA (mean daily doses 2.2 g) was administered for one month followed by 15 days of withdrawal. The mean serum phosphorus decreased from 7.6 +/- 1.4 to 5.8 +/- 0.8 mg% (p < 0.005). After 15 days of withdrawal mean serum phosphorus reached the pretreatment value. Then the patients entered a long term study with personalized doses of CAA (between 1 and 4 g/day) and administration in 8 of them of alpha-calcidol. After a mean follow-up period of 5.4 +/- 1.5 months serum phosphorus was reduced from 7.5 +/- 1.1 to 5.6 +/- 1.1 mg% (p < 0.0005) while calcemia increased from 9.0 +/- 0.7 to 9.6 +/- 0.6 mg% (p < 0.005). Only one patient developed mild hypercalcemia. We concluded that CAA is a safe alternative to calcium carbonate for the control of hyperphosphatemia of uraemic patients for the most efficient phosphorus binding and the lesser absorption of calcium.

Acetates↗

PubMed2006

Lanthanum carbonate versus standard therapy for the treatment of hyperphosphatemia: safety and efficacy in chronic maintenance hemodialysis patients.

AIMS: No conventional phosphate binder is entirely satisfactory for the treatment of hyperphosphatemia in patients with end-stage renal disease (ESRD). Consequently, there is a need for new agents. One such agent is lanthanum carbonate (La). This large-scale study compares the safety of La with standard therapy (any approved phosphate binder) in patients who were treated for up to 2 years. Efficacy, having previously been demonstrated, was a secondary endpoint. MATERIALS AND METHODS: After washout, patients were randomized to receive La (n=682) or their pre-study phosphate binder (n=677). Over a 6-week period, La was titrated to a maximum daily dose of 3000 mg elemental lanthanum (serum phosphorus target levels for titration were < or = 5.9 mg/dl (1.90 mmol/l)). Safety assessments included adverse events (AEs), full laboratory parameters and blood profiles. Efficacy assessments included serum phosphorus, calcium, calcium x phosphorus product and parathyroid hormone (PTH) levels. RESULTS: Average treatment exposure was greater in the standard therapy group (501.4 days) than in the La group (370.3 days) because standard therapy patients who switched or combined treatments were allowed to continue in the study. The most common AEs were gastrointestinal. The incidences of AEs in the La and treatment exposure-corrected standard therapy groups were nausea, 37 versus 29%; vomiting, 27 versus 22% and diarrhea (24% in each group). Hypercalcemia that was reported as an AE (La versus treatment exposure-corrected standard therapy) occurred in 4.3% and 8.4% of patients, respectively. There was no indication of liver toxicity, suppression of erythropoiesis or changes in the mini-mental state examination. Over 2 years, phosphorus control was similar in both groups; in the La group, however, serum calcium was lower and serum PTH levels were maintained in the range recommended by the National Kidney Foundation Kidney Disease Outcomes Quality Initiative (K/DOQI). CONCLUSIONS: The 2-year tolerability and efficacy of La are similar to those seen with standard therapy, although lower serum calcium levels and improved PTH levels were observed in the La group. These results support La as a viable new option for the management of hyperphosphatemia in ESRD.

Female↗

PubMed1999

[Role of the time of administration of calcium carbonate (before or during mealtime) in the control of hyperphosphatemia in patients on maintenance hemodialysis].

UNLABELLED: A study has claimed that at equal elemental calcium dose, CaCO3 was not less but equally efficient in controlling predialysis hyperphosphatemia as calcium acetate provided both calcium salts were given five minutes before the meals instead of during the meals because the higher acidity of a fasting gastric juice would allow a better dissociation of CaCO3. To examine the point that CaCO3 is more efficient if it is taken five minutes before compared to during the meal, we performed a two month randomised cross-over trial in twelve reliable and stable patients maintained on chronic hemodialysis while their treatment and diet remained constant. Comparison of the plasma concentrations measured during the two modes of administration showed no significant difference in creatinine, urea, bicarbonate, intact-PTH. Mean (+/- SD) plasma PO4 was significantly higher (1.93 +/- 0.50 versus 1.72 +/- 0.40 mmol/l; p = 0.02) whereas corrected plasma Ca was significantly lower (2.30 +/- 0.15 versus 2.38 +/- 0.17 mmol/l; p = 0.01) when CaCO3 was given before the meals than during the meals. CONCLUSIONS: a) administration of CaCO3 before the meal decreases its efficiency in controlling hyperphosphatemia since plasma PO4 was actually slightly higher with this timing of administration; b) administration of CaCO3 before the meal is associated with significantly lower plasma corrected calcium suggesting a smaller absorption of calcium which may be an advantage but only in hypercalcemic patients; c) there is no reason other than the prevention of its hypercalcemic effect to recommend the administration of CaCO3 just before the meals than during the meals.

Aged↗

PubMed2004

[Acute hyperphosphatemia secondary to phosphate administration for bowel preparation].

We report a 75-years-old woman, stable on a three-weekly hemodialysis program over a period of 3 years, who develop acute hyperphosphatemia secondary to phosphate administration for bowel preparation. The quick clinical diagnosis and the treatment with intensive hemodialysis resulted in a correction of hyperphosphatemia, hypocalcemia, acidemia and other electrolyte abnormalities. The phosphate cathartics are contraindicated in patients with severe renal insufficient or in dialysis program. Our case shows the severe side effects secondary to injudicious use of sodium phosphate cathartics.

Acute Disease↗

PubMed2001

[The role of hyperphosphatemia in the pathogenesis of secondary hyperparathyroidism].

Renal phosphate handling plays key role in phosphate metabolism. Kidney dysfunction induced hyperphosphatemia. The phosphatemia with renal insufficiency, especially uremia, indirectly progresses into secondary hyperparathyroidism via suppression of vitamin D/Ca system. This indirect effect on parathyroid is called "Trade-off theory". Recently, the direct effect of hyperphosphatemia on parathyroid has been reported independent of vitamin D/Ca system in renal failure. The control of serum phosphate is certainly important by restriction of phosphate intake in renal failure patients.

English Abstract↗