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PubMed2001

[Renal dysfunction and hyperphosphatemia--role of hyperphosphatemia on vascular calcification].

Coronary-artery calcification was present in 14 of 16 hemodialysis patients who were 20 to 30 years old by electron-beam computed tomography. Bone matrix protein, such as osteopontin produced by infiltrating macrophages into the atherosclerotic arterial lesions, is thought to be associated with vascular calcification. Therefore, it is required to recognize the interaction between abnormal bone metabolism and vascular calcification. Control of serum phosphorus levels is likely to be most important for the prevention and treatment of vascular calcification in patients with end-stage renal diseases.

English Abstract↗

PubMed2005

Hyperphosphatemia among end-stage renal disease patients in developing countries: a forgotten issue?

The prevalence of hyperphosphatemia and increased calcium-phosphorus product has never been evaluated in a large multicenter study in a developing country. Our aim is to study the prevalence of hyperphosphatemia in 38 HD centers in Egypt (as an example of a developing country) and to correlate it with different co-morbid conditions and the patient's demographic data. This is a cross-sectional study conducted on 1005 chronic kidney disease stage 5 patients (CKD-stage 5) on HD for a period of more than 1 year in 38 dialysis centers in Egypt. All patients were receiving calcium-based salts as a phosphate binder. Hyperphosphatemia and increased calcium-phosphorus product were evaluated and correlated with different parameters including age, sex, knowledge by diet parameters, HD session duration, the frequency of HD per week, the type of dialysis membrane, the surface area of the dialyzer, dialyzer phosphorus clearance (phosphorus KoA), and the type of dialysate. Other co-morbid medical conditions and evidence of IHD were also investigated. Hyperphosphatemia was present in 69.1% of cases and a high calcium-phosphorus product was present in 30.2%. A higher calcium-phosphorus product was found among males. 83.2% of those with a poor knowledge by diet parameters had hyperphosphatemia compared with 67.6% in patients with a satisfactory knowledge by diet parameters. 72.3% of patients using a membrane with low-to-medium clearance had hyperphosphatemia, compared with 67.2% using a membrane with a high clearance. Seventy-two percent of patients with IHD were hyperphosphatemic compared with 67.6% of the non-ischemic patients. Hyperphosphatemia is a major problem in dialysis patients in developing countries, reflecting differences from developed countries regarding dietary habits, ethnic factors, dialysis quality, types of dialysis membranes, as well as economic factors hampering the use of the more expensive phosphate binders. Extended dialysis hours may be a good alternative solution in developing countries.

Developing Countries↗

PubMed2005

Mild hyperphosphatemia and mortality in hemodialysis patients.

BACKGROUND: Severe hyperphosphatemia (serum phosphate level > 6.5 mg/dL [>2.10 mmol/L]) has been associated directly with increased overall and cardiovascular mortality in hemodialysis (HD) patients. Currently, clinical guidelines recommend maintaining phosphate levels within normal range (3.0 to 5.0 mg/dL [0.97 to 1.61 mmol/L]). However, mild hyperphosphatemia (phosphate, 5.01 to 6.5 mg/dL [1.62 to 2.10 mmol/L]) is still to be addressed as an independent mortality risk factor in HD patients. METHODS: The association between serum phosphate level and survival in maintenance HD patients was explored prospectively in 385 incident patients from 1990 to 2001. Cox regression was performed using phosphate level as: (1) a continuous variable; (2) stratified as low phosphate level (<3 mg/dL [<0.97 mmol/L]), normal phosphate level (3.0 to 5.0 mg/dL [0.97 to 1.61 mmol/L]), mild hyperphosphatemia (phosphate, 5.01 to 6.5 mg/dL [1.62 to 2.10 mmol/L]), or severe hyperphosphatemia (phosphate > 6.5 mg/dL [>2.10 mmol/L]); and (3) phosphate level greater or less than 5.0 mg/dL (> or <1.61 mmol/L). RESULTS: As a continuous variable, relative risk (RR) for mortality for serum phosphate level was 1.26 (confidence interval [CI], 1.09 to 1.47) after adjusting for age, sex, diabetes, Kt/V, albumin level, hemoglobin level, serum calcium level, normalized protein catabolic rate, and parathyroid hormone level. Compared with a normal phosphate level, mild hyperphosphatemia showed an adjusted mortality RR of 1.94 (CI, 1.17 to 3.19), and severe hyperphosphatemia, an RR of 2.02 (CI, 1.10 to 3.73). Patients with a phosphate level cutoff value greater than 5.0 mg/dL (>1.61 mmol/L) showed a 2-fold increase in adjusted RR for mortality compared with those with a phosphate level of 5.0 mg/dL or less (< or =1.61 mmol/L; RR, 2.11; CI, 1.44 to 3.08). CONCLUSION: A serum phosphate level greater than 5.0 mg/dL (>1.61 mmol/L) is independently associated with an increased risk for death in HD patients.

Aged↗

PubMed2002

Hyperphosphatemia modestly retards parathyroid hormone suppression during calcitriol-induced hypercalcemia in normal and azotemic rats.

BACKGROUND/AIMS: In in vitro studies, a high phosphate concentration has been shown to directly stimulate parathyroid hormone (PTH) secretion in a normal calcium concentration and to reduce PTH suppression in a high calcium concentration. In hemodialysis patients during dialysis-induced hypercalcemia, the effect of hyperphosphatemia on PTH secretion was less than in vitro studies. Our goal was to determine whether hyperphosphatemia retards PTH suppression during calcitriol-induced hypercalcemia in azotemic rats with hyperparathyroidism. METHODS: Rats underwent a two-stage 5/6 nephrectomy or sham operations. After surgery, rats received a high phosphate diet (P 1.2%, Ca 0.6%) for 4 weeks to induce hyperparathyroidism and then were placed on a normal diet (P 0.6%, Ca 0.6%) for two additional weeks to normalize serum calcium values in azotemic rats. At week 7, rats were divided into five groups and before sacrifice received at 24-hour intervals, three doses of calcitriol (CTR) or its vehicle. The five groups and dietary phosphate content were: group 1--normal renal function (NRF) + 0.6% P + vehicle; group 2--NRF + 0.6% P + CTR; group 3--renal failure (RF) + 0.6% P + vehicle; group 4--RF + 1.2% P + CTR; and group 5--RF + 0.6% P + CTR. RESULTS: In the two CTR-treated groups with marked hypercalcemia (groups 2 and 5), 15.52 +/- 0.26 and 15.12 +/- 0.13 mg/dl, respectively, stepwise regression showed that hyperphosphatemia retarded PTH suppression. When the two azotemic groups treated with CTR (groups 4 and 5) were combined to expand the range of serum calcium values, stepwise regression showed that hypercalcemia suppressed and hyperphosphatemia modestly retarded PTH suppression. Similarly, in groups 4 and 5 combined, correlations were present between PTH and both serum calcium (r = -0.70, p < 0.001) and serum phosphate (r = 0.64, p = 0.001). CONCLUSIONS: Hypercalcemia and high doses of calcitriol markedly reduced PTH secretion in azotemic rats despite severe hyperphosphatemia. Even though hyperphosphatemia did retard PTH suppression during hypercalcemia, its effect was small.

Animals↗

PubMed2007

Hyperostosis-hyperphosphatemia syndrome: a congenital disorder of O-glycosylation associated with augmented processing of fibroblast growth factor 23.

UNLABELLED: Two hyperphosphatemic patients with mutations in GALNT3 showed low intact FGF23 levels with marked increase of processed C-terminal fragments. FGF23 protein has three O-linked glycans and FGF23 with incomplete glycosylation is susceptible to processing. Silencing GALNT3 resulted in enhanced processing of FGF23. Decreased function of FGF23 by enhanced processing is the cause of hyperphosphatemia in patients with GALNT3 mutation. INTRODUCTION: Hyperostosis-hyperphosphatemia syndrome (HHS) is an autosomal recessive entity manifesting as severe hyperphosphatemia associated with episodic bone pain and radiological findings of cortical hyperostosis and periosteal reaction. Persistent hyperphosphatemia is not counterbalanced by PTH or 1,25-dihydroxyvitamin D, posing a mirror image of hypophosphatemic states attributed to increased fibroblast growth factor (FGF)23 activity. MATERIALS AND METHODS: We describe two children with HHS who were found to be homozygous for a mutation in GALNT3 encoding a peptide involved in mucin-type O-glycosylation (ppGaNTase-T3). FGF23 levels were evaluated by two ELISAs and Western blotting. FGF23 protein was analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry. Effect of silencing GALNT3 was evaluated using siRNA in cells transfected with expression vector for FGF23. RESULTS: Both patients had low levels of the full-length FGF23 with markedly augmented amounts of the inactive fragments. Biologically active FGF23 has three O-linked glycans. FGF23 with only one or two O-linked glycans is processed into inactive fragments. Decreasing the expression of the GALNT3 gene by RNA interference resulted in enhanced processing of FGF23. CONCLUSIONS: The primary defect in HHS is impairment of glycosylation of FGF23 resulting from mutations in GALNT3 and leading to augmented processing of FGF23. These changes in FGF23 abolish its phosphaturic effect and lead to severe persistent hyperphosphatemia. This study provides the pathogenetic mechanism of the first mucin-type O-glycosylation defect identified.

Amino Acid Sequence↗

PubMed2006

Hyperphosphatemia is prevalent among children with nephrotic syndrome and normal renal function.

The aim of the study was to analyze systematically our observation that children with severe nephrotic syndrome (NS) have hyperphosphatemia despite normal kidney function. Forty-seven children with NS and normal glomerular filtration rate (GFR) were studied [26 with steroid-sensitive nephrotic syndrome (SSNS) and 21 with persistent NS]. The plasma phosphate level was expressed as the number of standard deviations (SDs) from the mean levels in age- and gender-matched controls. In SSNS plasma phosphate concentration was elevated (+3.7+/-2.0 SDs) during relapse and normalized (-0.7+/-1.7 SDs) in remission. In persistent NS the phosphate level was +4.0+/-2.1 SDs. Patients with marked hyperphosphatemia (>4 SDs) were younger (p<0.001), had lower plasma albumin (p<0.001), and had higher urinary protein levels (p<0.05). Hyperphosphatemia did not correlate with GFR, plasma calcium, or urinary sodium levels. Children with persistent NS had decreased serum 25(OH)D(3) and insulin-like growth factor 1 (IGF-1) concentrations. Hyperphosphatemia is prevalent among children with persistent nephrotic syndrome and normal renal function, correlates with its severity, and may result from increased urinary IGF-1 wasting.

Adolescent↗

PubMed1995

Review of the literature: severe hyperphosphatemia.

A patient with a markedly elevated serum phosphorus level (23.9 mg/dL) is described, followed by a brief review of severe hyperphosphatemia. Elevated serum phosphorus levels may be artifactual or true. True hyperphosphatemia is usefully subdivided according to (a) whether phosphorus is added to the extracellular fluid from a variety of exogenous or endogenous sources, or (b) whether the urinary excretion of phosphorus is reduced from either decreased glomerular filtration or increased tubular reabsorption. Severe hyperphosphatemia, defined herein as levels of 14 mg/dL or higher, is almost invariably multifactorial--usually resulting from addition of phosphorus to the extracellular fluid together with decreased phosphorus excretion. The hyperphosphatemia of the patient described herein appeared to result from a combination of dietary phosphorus supplementation, acute renal failure, acute pancreatitis, and ischemic bowel disease, complicated by lactic acidosis.

Acid-Base Equilibrium↗

PubMed2004

Consequences of hyperphosphatemia in patients with end-stage renal disease (ESRD).

Hyperphosphatemia is invariably present among patients with end-stage renal disease (ESRD) and is becoming an increasingly important clinical entity. Despite concerted efforts by patients, dietitians, and nephrologists to control serum phosphorus, a recent study by Block et al found that more than 60% of patients on hemodialysis in the United States have serum phosphorus levels above the recommended goal of 5.5 mg/dL. Historically, nephrologists have been concerned about the central role of elevated serum phosphorus in the pathogenesis of secondary hyperparathyroidism and extraosseous calcification. However, the consequences of untreated hyperphosphatemia have assumed more importance in the last few years, largely due to recent clinical studies that revealed a more sinister role of elevated serum phosphorus in increasing the mortality risk among patients with ESRD. Hemodialysis patients with serum phosphorus greater than 6.5 mg/dL were reported to have a 27% higher mortality risk than patients with serum phosphorus between 2.4 and 6.5 mg/dL. The pathophysiologic mechanisms by which persistent hyperphosphatemia enhances the mortality risk in dialysis patients are not yet completely understood. However, given that inadequate control of serum phosphorus contributes to elevated calcium-phosphorus product (Ca x P), untreated hyperphosphatemia may play a key role in cardiovascular calcification. In response to these findings, the National Kidney Foundation Kidney Disease Outcome Quality Initiative (K/DOQI) Clinical Practice Guidelines for Bone Metabolism and Disease in Chronic Kidney Disease have recently recommended more stringent levels for controlling serum phosphorus and Ca x P product in order to improve patients' quality of life and longevity.

Calcinosis↗

PubMed2004

Adverse effects of hyperphosphatemia on myocardial hypertrophy, renal function, and bone in rats with renal failure.

BACKGROUND: Hyperphosphatemia and disturbances in calcium or parathyroid hormone (PTH) metabolism contribute to the high incidence of cardiovascular disease and renal osteodystrophy in chronic renal failure (CRF). We evaluated the effect of hyperphosphatemia on the cardiovascular system, on renal function, and on bone in experimental uremia. METHODS: Wistar rats were submitted to parathyroidectomy (PTx) and 5/6 nephrectomy (Nx) with minipump implantation, delivering 1-34 rat PTH (physiologic rate), or were sham-operated and received vehicle. Only phosphorus content (low-phosphorus (LP) 0.2%; high-phosphorus (HP) 1.2%) differentiated diets. We divided the groups as follows: PTx +Nx +LP; sham + LP; PTx + Nx + HP; and sham + HP. Tail-cuff pressure and weight were measured weekly. After 2 months, biochemical, arterial, and myocardial histology and bone histomorphometry were analyzed. RESULTS: Heart weight normalized to body weight (heart weight/100 g body weight) was higher in PTx + Nx + HP rats (PTx + Nx + HP = 0.36 +/- 0.01 vs. sham + HP = 0.29 +/- 0.01, PTx + Nx + LP = 0.32 +/- 0.01, sham + LP = 0.28 +/- 0.01) (P < 0.05). Serum creatinine levels were higher in PTx + Nx + HP rats than in PTx + Nx + LP rats (1.09 +/- 0.13 vs. 0.59 +/- 0.03 mg/dL) (P < 0.05). Levels of PTH did not differ significantly between the groups. Myocardial and arterial histology detected no vascular calcification or fibrosis. Bone histomorphometry revealed an association, unrelated to uremia, between HP diets and decreased trabecular connectivity. CONCLUSION: Myocardial hypertrophy, impaired renal function, and adverse effects on bone remodeling were associated with hyperphosphatemia and were not corrected by PTH replacement. Although no vascular calcification was observed in this model, we cannot rule out an adverse effect of hyperphosphatemia on the vascular bed. Our finding underscores the importance of phosphorus control in reducing morbidity and mortality in CRF patients.

Animals↗

PubMed2007

Phosphate salivary secretion in hemodialysis patients: implications for the treatment of hyperphosphatemia.

BACKGROUND/AIMS: Hyperphosphatemia is recognized as contributing to the increased risk of cardiac death in end-stage renal disease (ESRD) and hemodialysis (HD) patients. Currently available pharmacologic treatment for hyperphosphatemia is based on phosphate binders but, despite treatment, only half of the patients fall within the range for serum phosphorus of the K/DOQI guidelines. Therefore, there is a need to identify other therapeutic approaches in order to reduce serum phosphate. Salivary fluid contains phosphate which, if related to the daily salivary secretion (1,000-1,880 ml), may raise interest in order to identify further additive approaches to phosphorus removal in uremic patients, while data about salivary phosphate secretion in ESRD patients are controversial. METHODS: This study evaluates salivary phosphate secretion in 68 HD patients compared with 30 healthy subjects. Saxon's test confirmed normal salivary function in patients and controls. Salivary calcium and serum phosphate, calcium and PTH were also measured. RESULTS: HD patients had significantly higher salivary phosphorus levels compared with healthy controls: 30.35 (26.5-34.6) vs. 12.1 (10.58-14.73) mg/dl (p < 0.0001), and this significantly correlated (p < 0.0001) with serum phosphorus. Multiple regression analysis confirmed serum phosphorus as the only predictor (p < 0.0001) of salivary phosphorus. CONCLUSIONS: Given the functional secretive similarity between salivary glands and the kidneys, this increased salivary phosphate secretion might be interpreted as being compensatory in the presence of renal failure. Absorption of the increased salivary phosphate secretion, however, may worsen hyperphosphatemia; therefore, the binding of salivary phosphate might be considered as a further therapeutic approach to hyperphosphatemia in ESRD.

Female↗

PubMed2005

Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease.

Hyperphosphatemia, calcitriol deficiency, and secondary hyperparathyroidism (SHPT) are common complications of chronic kidney disease (CKD). Fibroblast growth factor-23 (FGF-23) is a novel phosphaturic hormone that also inhibits renal 1alpha-hydroxylase activity and thus may be involved in the pathogenesis of SHPT. Several hypotheses were tested: that FGF-23 increases as renal function declines; is linearly associated with serum phosphate levels; is associated with increased phosphaturia independent of parathyroid hormone (PTH); and is associated with decreased calcitriol levels independent of renal function, hyperphosphatemia, and vitamin D stores. FGF-23, PTH, 25(OH)D3, calcitriol, calcium, phosphate, and urinary fractional excretion of phosphate (Fe(PO4)) were measured in 80 CKD patients. Multiple linear regression was used to test the hypotheses. FGF-23 and PTH were inversely associated with estimated GFR (eGFR), whereas calcitriol levels were linearly associated with eGFR. Hyperphosphatemia and hypocalcemia were present in only 12 and 6% of patients, respectively, all of whose eGFR was <30. Increased Fe(PO4) was associated with decreased eGFR, and both increased FGF-23 and PTH were independently associated with increased Fe(PO4). Increased FGF-23 and decreased 25(OH)D3 were independent predictors of decreased calcitriol, but the effects on calcitriol levels of renal function itself and hyperphosphatemia were completely extinguished by adjusting for FGF-23. It is concluded that FGF-23 levels increase early in CKD before the development of serum mineral abnormalities and are independently associated with serum phosphate, Fe(PO4), and calcitriol deficiency. Increased FGF-23 may contribute to maintaining normal serum phosphate levels in the face of advancing CKD but may worsen calcitriol deficiency and thus may be a central factor in the early pathogenesis of SHPT.

Adult↗

PubMed2005

Hyperphosphatemia and phosphate binders.

PURPOSE: The pathophysiology of hyperphosphatemia associated with end-stage renal disease and treatment with phosphate binders are discussed. SUMMARY: Phosphorus is an essential element necessary for the normal function of the human body, required for skeletal construction and synthesis of DNA, proteins, and adenosine triphosphate. In healthy individuals, serum phosphorus concentrations are maintained between 2.5 and 4.5 mg/dL through diet and renal excretion. In renal insufficiency, phosphorus excretion declines and hyperphosphatemia develops. The body's compensation mechanisms cause secondary hyperparathyroidism and renal osteodystrophy. Phosphate binders provide an effective means for managing serum phosphate. Commercially available phosphate binders include calcium carbonate, calcium acetate, sevelamer, lanthanum, and, rarely, aluminum hydroxide. Because of aluminum's known toxicities, aluminum-based phosphate binders have a limited place in therapy. Calcium carbonate's benefits are seen over a narrow gastric pH range, thereby limiting the drug's utility. Calcium acetate is effective over a wide pH range. Other phosphate binders, including sevelamer hydrochloride and lanthanum carbonate, have recently entered the market, but their use remains controversial. CONCLUSION: If left untreated, hyperphosphatemia can result in secondary hyperparathyroidism, renal osteodystrophy, and metastatic calcification of blood vessels and soft tissue. The treatment of hyperphosphatemia in patients with chronic renal failure includes dialysis, dietary phosphorus restrictions, phosphate-binding medications, and vitamin D analogs. Selection of phosphate binders should be based on patient characteristics, including serum phosphate, serum calcium, and intact parathyroid hormone concentrations, and patient tolerability.

Aluminum↗

PubMed2003

[Importance of the "adequate blood phosphorus" concept as a risk factor for hyperphosphatemia].

Hyperphosphatemia is an important risk factor of secondary hyperparathyroidism and extraosseous calcifications in chronic renal failure patients. In this study our hypothesis is that physicians misconception of adequate phosphatemia is a risk factor for hyperphosphatemia. In 1999 GEMOR sent a renal osteodystrophy inquiry to different hemodialysis centers in Argentina. It included 80 dialysis centers in 17 Argentinian provinces. The enquire had 33 questions about renal osteodystrophy. Here we report the section related to phosphorous metabolism. We obtained responses from 80 dialysis centers (4,512 dialysis patients), which represents about 24% of Argentinian dialysis centers. Physicians considered phosphorous levels between 4.5 to 5.5 mg/dl in 83.5% of centers as adequate, and between 5.5 to 6.5 mg/dl in 10.1%. Five out of 77 centers reported that they had no patients with hyperphosphatemia. The percentage of hemodialysis patients that had more than 6 mg/dl in each center was 28.8 +/- 15.9%. Those centers that aimed for phosphatemia between 5.5 and 6.5 mg/dl, had a higher percentage of patients with phosphatemia above 6 mg/dl than those aiming for between 4.5 and 5.5 mg/dl (42.8 +/- 16.7 vs 27.1 +/- 15.2% respectively, p = 0.007), and had higher mean of phosphatemia (6.4 +/- 0.7 vs 5.3 +/- 0.7 mg/dl respectively, p = 0.0001), than the last group. In conclusion, a higher mean phosphate level was obtained in hemodialysis centers where physicians considered higher pre-dialysis target levels. Some centers had no patients with hyperphosphatemia (neglect or good control?).

Argentina↗

PubMed2004

Dietary habits and counseling focused on phosphate intake in hemodialysis patients with hyperphosphatemia.

OBJECTIVE: To evaluate the dietary habits of hemodialysis patients with hyperphosphatemia and the effects of a dietetic intervention focused on limiting dietary phosphate load. DESIGN: Cross-sectional dietary evaluation and prospective intervention study. SETTING: Hospital hemodialysis units of Pisa and Pistoia, Italy. Subjects Forty-three stable adult hemodialysis patients, 20 of whom had phosphorus serum levels >5.5 mg/dL. INTERVENTION: Analysis of dietary composition and of the effects of individual dietetic counseling in an attempt to reduce phosphorus intake while preserving the same protein intake. MAIN OUTCOME MEASURES: Differences in nutrient intake between normophosphatemic and hyperphosphatemic patients, and changes in dietary phosphorus and phosphorus-protein ratio, serum phosphate, and calcium-phosphate product after dietetic intervention. RESULTS: No major differences in nutrient intake were detected between hyperphosphatemia and normophosphatemia patients, apart from a lower phosphorus-protein ratio (13.1 +/- 1.7 versus 14.1 +/- 2.1 mg/g, P < .05) in the former. After dietetic intervention in the hyperphosphatemia patients, phosphate and calcium intake decreased significantly (by 100 mg on average), whereas dietary protein did not change. A further decrease of the dietary phosphate-protein ratio (12.5 +/- 1.8 mg/g, P < .05) also occurred. Serum phosphate showed a trend to decrease in the intervention group, whereas the serum calcium-phosphate product decreased significantly (from 66.8 +/- 13.1 to 61.0 +/- 13.8 mg2 /dL2 , P < .05). CONCLUSIONS: In compliant and motivated patients, individual dietetic counseling may be useful in reducing phosphate load and in limiting the phosphate burden related to an adequate protein intake, with a potentially favorable impact on calcium-phosphate retention. A phosphate-controlled diet has a role in an integrated therapeutic approach to hyperphosphatemia and positive calcium-phosphorus balance in hemodialysis patients.

Aged↗

PubMedDate not supplied

The clinical management of hyperphosphatemia.

As renal function declines in patients with end-stage renal disease (ESRD), excess dietary phosphorus accumulates in the bloodstream. Routine dialysis removes up to 70% of absorbed phosphorus; therefore, hyperphosphatemia is found in the majority of patients with ESRD. The consequences of this imbalance include secondary hyperparathyroidism and osteodystrophy. Recent studies have also documented that hyperphosphatemia can lead to soft-tissue and vascular calcification; the latter is strongly associated with cardiovascular disease and, thus, increased mortality and morbidity. The reduction of phosphorus levels is, therefore, an important therapeutic target in this patient group. Management of hyperphosphatemia using conventional phosphate binders is not always successful. However, emerging therapies aim to reduce the incidence of hyperparathyroidism, bone disease, and calcification in this patient population. In this article, the consequences of hyperphosphatemia are reviewed, and recent developments in the treatment of the condition are discussed.

Aluminum Hydroxide↗

PubMed1986

Hyperphosphatemia after surgical correction of hypercortisolism in patients with Cushing's syndrome.

The change in phosphate metabolism after surgical correction of Cushing's syndrome was examined in 3 consecutive patients. During replacement therapy with hydrocortisone after successful operation, when serum cortisol levels were undetectable in the early morning, serum inorganic phosphate (PI) levels increased gradually with reduction of the replacement dose of hydrocortisone. Hyperphosphatemia developed 3-7 weeks after surgery when the patients was given 20-25 mg/day of hydrocortisone, and 2 patients demonstrated clinical manifestation of glucocorticoid deficiency. During these periods, there was a significant inverse relationship between serum Pi and the replacement dose of hydrocortisone in each patient. Thereafter, serum Pi started to decrease despite administration of the same amount of hydrocortisone and became normal by 26 weeks after surgery. Daily urinary Pi excretion was decreased compared to that before surgery, and the maximal tubular reabsorptive capacity for Pi (TmP/GFR) changed in parallel with serum Pi in all patients. Serum immunoreactive parathyroid hormone and urinary 3',5'-cyclic adenosine monophosphate excretion remained unchanged during the postoperative course. The serum concentrations of 1,25-dihydroxyvitamin D decreased from preoperatively normal values to subnormal levels after surgery with development of hyperphosphatemia and returned to normal with the fall of serum Pi. In summary, the present study demonstrates that surgical correction of hypercortisolism is accompanied by a transient hyperphosphatemia during the postoperative periods, probably due to increased renal Pi reabsorption, and that parameters of parathyroid function do not change during these periods. These results suggest that glucocorticoid has a direct action on Pi metabolism and that during the replacement therapy after surgical treatment of hypercortisolism hyperphosphatemia may develop due to relative glucocorticoid deficiency.

Cushing Syndrome↗

PubMed2026

Efficacy and safety of ferric citrate tablets in Chinese patients with hyperphosphatemia undergoing maintenance hemodialysis: a multicenter, randomized, open-label, active-controlled, phase III trial.

BACKGROUND: This study aimed to evaluate the efficacy and safety of ferric citrate tablets in Chinese patients with hyperphosphatemia undergoing maintenance hemodialysis (MHD). METHODS: In this phase III, multicenter, randomized, open-label, non-inferiority trial, patients with hyperphosphatemia on maintenance hemodialysis were randomly assigned to receive either ferric citrate or sevelamer carbonate tablets for 12 weeks. The primary endpoint was the change in serum phosphorus levels from baseline to week 12, with a non-inferiority margin of 0.32 mmol/L. Secondary endpoints included changes in serum calcium, intact parathyroid hormone, and safety assessments. RESULTS: A total of 239 patients were randomized to the ferric citrate group (n = 119) or the sevelamer carbonate group (n = 120). The mean change in serum phosphorus levels was -0.70 ± 0.50 mmol/L in the ferric citrate group and -0.61 ± 0.59 mmol/L in the sevelamer carbonate group (least squares mean difference, -0.09 mmol/L; 95% CI, -0.24 to 0.05 mmol/L; non-inferiority margin, 0.32 mmol/L). No significant inter-group differences were found in the percentage of patients achieving target phosphorus levels (49.09% vs. 48.28%, p = 0.902). Ferric citrate significantly improved iron-related parameters and hemoglobin levels. Most treatment-emergent adverse events were mild, with gastrointestinal disorders being the most common. CONCLUSIONS: Ferric citrate tablets were non-inferior to sevelamer carbonate in reducing serum phosphorus levels in hyperphosphatemia patients on maintenance hemodialysis, with the added benefit of improving iron-related anemia and a favorable safety profile.

Adult↗

PubMed1985

Elevated serum calcitriol concentrations do not fall in response to hyperphosphatemia in familial tumoral calcinosis.

Five affected members in two branches of a Druze Arab kindred presented with calcified deposits in or about the hips and knees, indicating the diagnosis of tumoral calcinosis. Serum vitamin D metabolite concentrations, immunoreactive parathyroid hormone, and the tubular reabsorption of phosphate were measured in three affected siblings, as well as in their parents and an unaffected sibling. Normocalcemia and hyperphosphatemia with an elevated tubular maximum for phosphate per glomerular filtration rate were found in the affected patients. Levels of serum immunoreactive parathyroid hormone were normal, and the calcitriol value (1,25-dihydroxyvitamin D) was normal or elevated in the three affected patients. A trial of a low-phosphorus diet and oral aluminum hydroxide gel did not lower serum phosphate levels or improve the calcified deposits. These findings suggest that serum calcitriol values do not decline in response to hyperphosphatemia in tumoral calcinosis and that hyperphosphatemia with elevated tubular reabsorption of phosphate is a constant feature of this disorder because the kidney fails to excrete the increased filtered load of phosphate.

Adult↗