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PubMed2000

Calcium acetate versus calcium carbonate in the control of hyperphosphatemia in hemodialysis patients.

CONTEXT: Hyperphosphatemia has an important role in the development of bone and mineral abnormalities in end-stage renal disease (ESRD). OBJECTIVE: To compare the phosphorus binding power and the hypercalcemic effect of calcium acetate and calcium carbonate in hemodialysis patients. TYPE OF STUDY: Crossover, randomized, double-blind study. PLACE: A private hospital dialysis center. PARTICIPANTS: Fifty-two patients who were undergoing regular hemodialysis three times a week ([Ca++] dialysate = 3.5 mEq/L). PROCEDURES: Half of the patients were started on 5.6 g/day of calcium acetate and, after a 2 week washout period, received 6.2 g/day of calcium carbonate. The other half followed an inverse protocol. MAIN MEASUREMENTS: Clinical interviews were conducted 3 times a week to monitor for side effects. Determinations of serum urea, calcium, phosphorus, hematocrit, Kt/V and blood gas analysis were obtained before and after each treatment. RESULTS: Twenty-three patients completed the study. A significant increase in calcium plasma levels was only observed after treatment with calcium carbonate [9.34 mg/dl (SD 0.91) vs. 9.91 mg/dl (SD 0.79), P < 0.01]. The drop in phosphorus levels was substantial and significant for both salts [5.64 mg/dl (SD 1.54) vs. 4.60 mg/dl (SD 1.32), P < 0.01 and 5.89 mg/dl (SD 1.71) vs. 4.56 mg/dl (SD 1.57), P < 0.01, for calcium acetate and calcium carbonate respectively]. The percentage reduction in serum phosphorus (at the end of the study) per milliequivalent of salt administered per day tended to be higher with calcium acetate but statistical significance was not found. CONCLUSION: Calcium acetate can be a good alternative to calcium carbonate in the handling of hyperphosphatemia in ESRD patients. When calcium acetate is used, control of hyperphosphatemia can be achieved with a lower administration of calcium, perhaps with a lower risk of hypercalcemia.

Acetates↗

PubMed2000

Hyperphosphatemia: pharmacologic intervention yesterday, today and tomorrow.

Control of serum phosphorus continues to be of utmost importance in renal replacement therapy, due to the high prevalence of hyperphosphatemia in the dialysis population. Hyperphosphatemia has traditionally been associated with secondary hyperparathyroidism, soft tissue calcification, and renal osteodystrophy. Recent evidence implicates poor phosphorus control as an important factor in the development of cardiovascular calcification, cardiac disease, and death in patients with chronic renal failure. Dietary restriction of phosphorus, while an important factor in the control of serum phosphorus, has practical problems that limit its success in most patients. Aluminum was used in the past to inhibit phosphorus absorption, but its accumulation has serious, toxic effects on bone. Calcium-based binders have largely replaced aluminum; however, these binders are limited by the excessive amounts of calcium absorbed, which can frequently lead to positive calcium balance, suppression of bone turnover, and hypercalcemia. Calcium overloading is also associated with soft tissue and cardiovascular calcification. More recent strategies for managing hyperphosphatemia and renal bone disease include the use of nonabsorbed phosphate binders that are aluminum- and calcium-free and the development of vitamin D analogs that control parathyroid hormone activity with less calcemic effects. Future goals include defining optimal target levels of phosphorus, calcium, and parathyroid hormone and developing clinical approaches that will promote parathyroid glands, bone, and cardiac health.

Chronic Kidney Disease-Mineral and Bone Disorder↗

PubMed1975

Hyperphosphatemia and hypocalcemia in Burkitt lymophoma. Complications of chemotherapy.

In two patients, metabolic complications, previously unreported to our knowledge, of severe hyperphosphatemia and hypocalcemia in addition to hyperkalemia nad hyperuricemia were demonstrated after treatment with cyclophosphamide. In one patient, elevated blood and ascites lactate levels were measured. The levels decreased rapidly to normal following chemotherapy. The hyperphosphatemia and hyperkalemia may have been due to rapid tumor lysis and the hypocalcemia may have been caused by the hyperphosphatemia. The reduction in blood and aseties lactate levels may reflect the lysis of anaerobically metabolising tumor cells. Renal dialysis was required in the management of both cases. Because of the potential for cardiac arrythmias related to electrolyte imbalance, it is recommended that whenever possible reanl dialysis be available before treating cases of Burkitt lymphoma with large tumor burden.

Abdominal Neoplasms↗

PubMed2004

Hyperphosphatemia in Chinese peritoneal dialysis patients with and without residual kidney function: what are the implications?

BACKGROUND: Hyperphosphatemia is an important predictor for mortality in hemodialysis patients. This study evaluated significant factors associated with hyperphosphatemia in peritoneal dialysis (PD) patients. METHODS: We estimated residual renal function (RRF), dialysis adequacy, and normalized protein equivalent nitrogen appearance (nPNA), together with simultaneous measurement of serum phosphorus levels in 252 prevalent Chinese continuous ambulatory peritoneal dialysis (CAPD) patients. RESULTS: Average serum phosphorus level was 5.2 +/- 1.5 mg/dL (1.68 +/- 0.48 mmol/L). Serum phosphorus levels were 5.6 mg/dL or greater (> or =1.81 mmol/L) in 44.0% of anuric patients (n = 116) versus 28.7% of patients with RRF (n = 136; P = 0.012). Patients with RRF maintained serum phosphorus levels at or less than the median value (< or =5.1 mg/dL [< or=1.65 mmol/L]), with a total creatinine clearance (CCr) of 72 +/- 25 L/wk/1.73 m2 and nPNA of 0.94 +/- 0.19 g/kg/d in contrast to a total CCr of 63 +/- 22 L/wk/1.73 m2 (P = 0.031) and nPNA of 1.03 +/- 0.22 g/kg/d (P = 0.011) in patients with serum phosphorus levels greater than the median value. Among anuric patients, total CCrs were 46 +/- 9 and 42 +/- 7 L/wk/1.73 m2 (P = 0.005) and nPNA values were 0.89 +/- 0.17 and 0.98 +/- 0.18 g/kg/d (P = 0.010) for patients with serum phosphorus levels at the median value or less and greater than the median value, respectively. Multiple regression analysis showed that residual glomerular filtration, despite an average of less than 2 mL/min/1.73 m2, was independently associated with phosphorus control in PD patients. nPNA, PD CCr or urea clearance, body mass index, and parathyroid hormone level were other important correlates of serum phosphorus levels in patients with and without RRF. CONCLUSION: Hyperphosphatemia is a frequent complication in Chinese CAPD patients. Our study not only shows the importance of RRF in maintaining serum phosphorus levels in PD patients, but also the limitations of PD alone to achieve adequate phosphorus control in anuric patients.

Adult↗

PubMed2004

Efficacy and safety of sevelamer. Comparison with calcium carbonate in the treatment of hyperphosphatemia in hemodialysis patients.

OBJECTIVE: Current phosphate binders used in hemodialysis patients include calcium-based binders that result in frequent hypercalcemia. The use of a calcium- and aluminum-free phosphate-binding polymer in hemodialysis (sevelamer) disclosed efficacy in the short and long-term studies. However, due to race differences we performed a short-term study on the Saudi hemodialysis patients and compared sevelamer with a standard calcium-based phosphate binder. METHODS: An open-label, randomized, cross-over study was performed to evaluate the safety and effectiveness of sevelamer hydrochloride in controlling hyperphosphatemia in hemodialysis patients. After a 2-week phosphate binder washout period, stable hemodialysis patients were given either sevelamer or calcium carbonate, and the dosages were titrated to achieve phosphate control over an 8-week period. After a 2-week washout period, patients crossed over to the alternate agent for 8 weeks. Twenty patients from the Dialysis Unit of King Fahd Hospital, Jeddah, Kingdom of Saudi Arabia, were recruited for the study between March 2003 and June 2003. RESULTS: There was a similar decrease in serum phosphate values over the course of the study with both sevelamer (-3.3 +/-2.2 mg/dL) and calcium carbonate (-3.9 +/-2.8 mg/dL). Fifty-two percent of patients developed serum calcium greater than 2.75 mmol/L (11.0 mg/dL) while receiving calcium carbonate versus 26% of patients receiving sevelamer (p<0.05). The incidence of hypercalcemia for sevelamer was not different from the incidence of hypercalcemia during the washout period. Patients treated with sevelamer also sustained a 13% mean decrease in serum cholesterol levels. CONCLUSION: Sevelamer was effective in controlling hyperphosphatemia without resulting in an increase in the incidence of hypercalcemia seen with calcium carbonate. This agent appears quite effective in the treatment of hyperphosphatemia in hemodialysis patients, and its usage may be advantageous in the treatment of dialysis patients.

Adult↗

PubMed2001

[Hyperphosphatemia and hypoparathyroidism].

There are great differences in causes and treatments of hypoparathyroidism between patients with normal renal function and those with impaired renal function (dialysis patient). In patients with normal renal function, hypocalcemia and hyperphosphatemia develop because of the decrease in PTH synthesis or PTH function, and major target for treatment is hypocalcemia. In dialysis patients, hyperphosphatemia inevitably develops by the decrease in urinary excretion of phosphate and about three to six times greater concentration of PTH is required to maintain the normal bone metabolism. Hyperphosphatemia should be strictly treated, but it remains still unsure what is the real pathogenesis of hypoparathyroidism, and whether hypoparathyroidism should be treated or not in dialysis patient.

English Abstract↗

PubMed1991

[Comparison of calcium acetate and calcium carbonate for the control of predialysis hyperphosphatemia].

The present study was conducted to determine whether half the dose of elemental calcium given as acetate (Ca Ac) could control on medium term the predialysis plasma phosphate as well as calcium carbonate (CaCO3) while inducing less frequent hypercalcemia. This was evaluated in a cross-over study of 3 periods of 10 weeks according to the sequence Ca Ac, CaCO3, Ca Ac, in 12 compliant patients on chronic dialysis previously treated by Ca CO3. Because of poor tolerance of Ca Ac during the first period 4 patients were excluded and the results have been assessed only on the 8 patients who completed the study. For half the doses of elemental calcium (620 +/- 250 mg versus 1310 +/- 560 mg versus 710 +/- 200 mg/day) Ca acetate allowed the same control of predialytic hyperphosphatemia (1.67 +/- .34; 1.74 +/- .32; 1.75 +/- .38) with paradoxically comparable normal mean plasma calcium concentration (2.61 +/- .14; 2.56 +/- .13; 2.55 +/- .14 mmol/l). Plasma alkaline phosphatases and intact PTH concentrations remained also stable during the 3 periods. The frequency of hypercalcemia greater than 2.75 mmol/l (12; 9; 20%) and of hyperphosphatemia greater than 2 mmol/l (17; 22; 27%) were comparable with the 2 treatments. We conclude that calcium acetate controls predialytic hyperphosphatemia as efficiently as CaCO3 for half the dose of elemental calcium without however decreasing the frequency of hypercalcemia.

Acetates↗

PubMed1991

Endocrine crises. Hypophosphatemia and hyperphosphatemia.

Pathophysiology, clinical sequelae, and treatment for hypophosphatemia and hyperphosphatemia are discussed. Hypophosphatemia results from a variety of conditions including malnutrition, carbohydrate refeeding, acid-base disorders, and hormonal and drug effects. Patients suffering from severe hypophosphatemia may present with a variety of syndromes that can become detrimental and even life-threatening if this electrolyte depletion goes untreated. Hyperphosphatemia occurs because of increased extracellular phosphate load from either endogenous or exogenous sources or from a decrease in renal phosphate excretion. Left untreated, hyperphosphatemia can result in dangerous calciumphosphate precipitation into vital organs and tissues.

Aged↗

PubMed1986

Hyperphosphatemia as a detectable laboratory manifestation of glucocorticoid withdrawal syndrome.

We found hyperphosphatemia in five patients who had undergone unilateral adrenalectomy (ADX) for resection of cortisol-producing adenomas. The mean (+/- SEM) serum inorganic phosphorus level, theoretical renal phosphorus threshold and percent tubular phosphorus reabsorption rose from the preoperative level of 3.3 +/- 0.2 mg/dl, 2.6 +/- 0.2 mg/dl and 82.1 +/- 0.6%, to 6.0 +/- 0.2 mg/gl, 7.4 +/- 0.4 mg/dl and 95.9 +/- 1.0%, respectively, after ADX (P less than 0.001, P less than 0.001, P less than 0.001). Urinary phosphorus excretion decreased from 549 +/- 40 to 294 +/- 108 mg/day after ADX (P less than 0.05). Changes in serum calcium, serum sodium, serum potassium, serum chloride and creatinine clearance were not significant after ADX. Hyperphosphatemia may be the only abnormality found in serum electrolytes in glucocorticoid deficiency. It thus seems that hyperphosphatemia may be regarded as one of the clinical manifestations of the glucocorticoid withdrawal syndrome.

Adenoma↗

PubMed1982

Hyperphosphatemia: a factor that provokes severe experimental acute renal failure.

UNLABELLED: The purpose of this study was to determine whether pre-existent hyperphosphatemia potentiates the severity of evolving ARF. Normal rats were subjected to graded phosphate infusions (0 to 0.07 mmol/kg/hr) in order to induce differing degrees of hyperphosphatemia (6.8 to 10.3 mg/dl). After a 40 min control period, ARF was induced either by HgCl2 administration (12 mg/kg) or by bilateral renal pedicle cross-clamping (25 min). GFRs before and after renal injury were determined by measuring the Cioth. The percent decrease of GFR after renal injury strongly correlated with the degree of phosphate loading (r = 0.71, HgCl2; r = 0.82, ischemia) (p less than 0.001). In addition, phosphate-treated ARF rats showed striking histologic changes not seen in their non-phosphate-treated counterparts, i.e., marked vacuolization of the proximal tubules and variable degrees of glomerular capillary collapse. Renal calcium/phosphate deposition could not be demonstrated in any kidney by the Von Kossa or the alizarin red histochemical techniques. Terminal serum phosphate concentrations ranged from 7.5 to 19.1 mg/dl. Phosphate-infused control rats had stable GFRs and normal renal histology. CONCLUSION: Hyperphosphatemia may significantly exacerbate the functional and histologic correlates of acute renal failure. The pathogenesis of this response remains unknown.

Acute Kidney Injury↗

PubMed1993

Assessment of hyperphosphatemia and hypophosphatemia.

Methodologic aspects including causes of factitious hyperphosphatemia and hypophosphatemia are summarized. The differential diagnosis of hyperphosphatemia is reviewed under its three broad causes: decreased glomerular filtration rate, increased exogenous or endogenous phosphate load, and increased renal tubular phosphate reabsorption. The differential diagnosis of hypophosphatemia is reviewed under its three broad causes: inadequate gastrointestinal input, excess phosphate losses, and transcellular shifts. The consequences of hyperphosphatemia and hypophosphatemia are outlined with a focus on pathophysiologic and clinicochemical sequelae. A laboratory perspective is emphasized in outlining management strategies.

Diagnosis, Differential↗

PubMed1996

Severe hyperphosphatemia and hypocalcemia: a dilemma in patient management.

In the following report, a case of severe hyperphosphatemia and tetanic hypocalcemia resulting from the inadvertent oral ingestion of a phosphate enema is described. The physiology of serum phosphate regulation and the mechanism by which the elevation of serum phosphate is thought to induce hypocalcemia is discussed, and the treatment of hyperphosphatemia is reviewed. Finally, the potential consequences of the administration of calcium to treat tetany in a patient with severe hyperphosphatemia are considered.

Aged↗

PubMed1994

Hyperphosphatemia in multiple myeloma.

We report three cases of IgG kappa multiple myeloma with pseudohyperphosphatemia. The patients' serum calcium levels were normal, and the hyperphosphatemia was not related to impaired renal function. No hypoparathyroidism was found, and no exogenous phosphate preparation had been given. Since the hyperphosphatemia was of no obvious clinical or physiological significance, as evidenced by normal serum levels of 1,25 dihydroxy vitamin D3, it was diagnosed as spurious and was connected to interference of the paraprotein with the chromogenic assay. In two of the patients major fluctuations in serum phosphate levels were seen, induced by the changes in globulin and paraprotein levels that occurred during therapy and relapse.

Aged↗

PubMed1977

Mechanism of induction of hypercalcemia and hyperphosphatemia by lead acetate in the rat.

The present study is an investigation of the mechanism of hypercalcemia and hyperphosphatemia induced by the intravenous injection of lead acetate (Pb-Ac). A total of 118 male rats were injected with 30 mg/kg of Pb-Ac, or with 16.5 mg/kg of sodium acetate as the control. The levels of serum calcium, phosphorus and lead were then determined at various time periods after the injections. Serum calcium and phosphorus levels increased with time after Pb-Ac injection and the maximum values of calcium (17 mg%) were found after 1 h and of phosphorus (13.5 mg%) after 30 min. Both calcium and phosphorus levels reverted to the normal range after 12 h. The maximum net rates of increase of calcium and phosphorus were found immediately after Pb-Ac injection. At that time, deposition of lead at the calcifying sites of bone and incisor dentin was demonstrated by a histochemical examination. In other experiments the changes in the calcium and phosphorus contents in the medium after shaking bone powder in serum with Pb-Ac in an in vitro system were studied. It was confirmed that the calcium and phosphorus were displaced from the bone mineral, the extent of the displacement being correlated with the concentration of the Pb-Ac added to the medium, and that these displacements were very rapid reactions. These results suggest that hypercalcemia and hyperphosphatemia following Pb-Ac injection results from a direct action of lead on the bone mineral.

Animals↗

PubMed1992

Severe hyperphosphatemia associated with hemorrhagic shock.

Hyperphosphatemia is an electrolyte abnormality that most frequently results from renal insufficiency and the attendant inability to excrete phosphorus (PO4) efficiently. A case is presented in which a young man with hemorrhagic shock developed severe hyperphosphatemia in the absence of renal failure. This is the first such case documented to the authors' knowledge. The prompt correction of the primary cause (ie, hypoperfusion and acidosis) resulted in a rapid return of PO4 levels to normal. This was probably related to the intracellular shift of PO4. Physicians should be aware of this electrolyte disturbance because it is not a well-recognized complication and because, in most cases, proper treatment of shock will also correct the elevated PO4.

Adult↗

PubMed1986

Histamine-induced hyperphosphatemia and hypocalcemia in the laying hen.

The effects of histamine on plasma inorganic phosphorus (Pi) and total calcium values were studied in laying hens during egg formation and in non-laying hens. Histamine induced hyperphosphatemia and slight hypocalcemia during eggshell calcification, whereas the most pronounced hypocalcemia was observed during the early stages of egg formation. The histamine-induced hyperphosphatemia was completely inhibited by cimetidine but only partly by promethazine. However, the histamine-induced hypocalcemia was totally inhibited by cimetidine and promethazine.

Animals↗

PubMed2004

Homozygous ablation of fibroblast growth factor-23 results in hyperphosphatemia and impaired skeletogenesis, and reverses hypophosphatemia in Phex-deficient mice.

Fibroblast growth factor-23 (FGF-23), a recently identified molecule that is mutated in patients with autosomal dominant hypophosphatemic rickets (ADHR), appears to be involved in the regulation of phosphate homeostasis. Although increased levels of circulating FGF-23 were detected in patients with different phosphate-wasting disorders such as oncogenic osteomalacia (OOM) and X-linked hypophosphatemia (XLH), it is not yet clear whether FGF-23 is directly responsible for the abnormal regulation of mineral ion homeostasis and consequently bone development. To address some of these unresolved questions, we generated a mouse model, in which the entire Fgf-23 gene was replaced with the lacZ gene. Fgf-23 null (Fgf-23-/-) mice showed signs of growth retardation by day 17, developed severe hyperphosphatemia with elevated serum 1,25(OH)2D3 levels, and died by 13 weeks of age. Hyperphosphatemia in Fgf-23-/- mice was accompanied by skeletal abnormalities, as demonstrated by histological, molecular, and various other morphometric analyses. Fgf-23-/-) mice had increased total-body bone mineral content (BMC) but decreased bone mineral density (BMD) of the limbs. Overall, Fgf-23-/- mice exhibited increased mineralization, but also accumulation of unmineralized osteoid leading to marked limb deformities. Moreover, Fgf-23-/- mice showed excessive mineralization in soft tissues, including heart and kidney. To further expand our understanding regarding the role of Fgf-23 in phosphate homeostasis and skeletal mineralization, we crossed Fgf-23-/- animals with Hyp mice, the murine equivalent of XLH. Interestingly, Hyp males lacking both Fgf-23 alleles were indistinguishable from Fgf-23/-/ mice, both in terms of serum phosphate levels and skeletal changes, suggesting that Fgf-23 is upstream of the phosphate regulating gene with homologies to endopeptidases on the X chromosome (Phex) and that the increased plasma Fgf-23 levels in Hyp mice (and in XLH patients) may be at least partially responsible for the phosphate imbalance in this disorder.

Alleles↗

PubMed2004

Factors for increased morbidity and mortality in uremia: hyperphosphatemia.

Hyperphosphatemia is a metabolic abnormality present in the majority of patients treated by dialysis. Inorganic phosphorus (iP) can be categorized as a true uremic toxin given its known in vivo and in vitro effects and the ability to reduce these effects by normalizing iP levels. However, despite regular and adequate dialysis treatment, the goal of normalization of phosphorus levels rarely is achieved. This article briefly evaluates the significance of hyperphosphatemia in hemodialysis patients, current therapeutic approaches, and describes a new model for evaluating the dialysis prescription for iP balance.

Humans↗