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PubMed1994

Hyperphosphatemia in tumor lysis syndrome: the role of hemodialysis and continuous veno-venous hemofiltration.

We report a 4-year-old boy who developed tumor lysis syndrome complicated by severe hyperphosphatemia and acute renal failure, following chemotherapy for T-cell acute lymphoblastic leukemia. Despite successful treatment of hyperphosphatemia with hemodialysis, there was an immediate rebound in the high serum phosphorus level. The patient underwent a second treatment with hemodialysis which was then followed by continuous veno-venous hemofiltration (CVVH). CVVH maintained his serum phosphorus at a stable level until his renal function improved. CVVH can be used in conjunction with hemodialysis to successfully treat the hyperphosphatemia associated with tumor lysis syndrome.

Acute Kidney Injury↗

PubMed2005

Hyperphosphatemia due to fosphenytoin in a pediatric ESRD patient.

Fosphenytoin is indicated for the treatment of generalized convulsions and seizures occurring during neurosurgery. Metabolites of fosphenytoin include phenytoin, phosphate, and formaldehyde. The drug monograph recommends caution in administering fosphenytoin to patients in whom phosphate restriction is necessary. Additionally, fosphenytoin has altered pharmacokinetics in end-stage renal disease patients. We report a 17-year old African-American male with end-stage renal disease who developed acute hyperphosphatemia to 3.9 mmol/L (12.1 mg/dL) following the intravenous administration of 1000 mg of fosphenytoin for an idiopathic complex partial seizure. To our knowledge, this is the first report of acute hyperphosphatemia due to fosphenytoin administration. Due to this risk of hyperphosphatemia, we recommend that fosphenytoin should be used with caution in the end-stage renal disease population.

Adolescent↗

PubMed1999

A comparison of the calcium-free phosphate binder sevelamer hydrochloride with calcium acetate in the treatment of hyperphosphatemia in hemodialysis patients.

Current phosphate binders used in hemodialysis patients include calcium-based binders that result in frequent hypercalcemia and aluminum-based binders that result in total body aluminum accumulation over time. This investigation describes the use of a calcium- and aluminum-free phosphate-binding polymer in hemodialysis patients and compares it with a standard calcium-based phosphate binder. An open-label, randomized, crossover 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 administered either sevelamer or calcium acetate, and the dosages were titrated upward to achieve improved phosphate control over an 8-week period. After a 2-week washout period, patients crossed over to the alternate agent for 8 weeks. Eighty-four patients from eight centers participated in the study. There was a similar decrease in serum phosphate values over the course of the study with both sevelamer (-2.0 +/- 2.3 mg/dL) and calcium acetate (-2.1 +/- 1.9 mg/dL). Twenty-two percent of patients developed a serum calcium greater than 11.0 mg/dL while receiving calcium acetate, versus 5% of patients receiving sevelamer (P < 0.01). 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 24% mean decrease in serum low-density lipoprotein cholesterol levels. Sevelamer was effective in controlling hyperphosphatemia without resulting in an increase in the incidence of hypercalcemia seen with calcium acetate. 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.

Acetic Acid↗

PubMed2003

Hyperphosphatemia aggravates cardiac fibrosis and microvascular disease in experimental uremia.

BACKGROUND: Hyperphosphatemia is a known predictor of cardiovascular death and specifically of cardiac death in hemodialysis patients. The pathomechanisms involved have not been completely clarified. While a number of observations suggest an important role of hyperphosphatemia and positive calcium balance on atherosclerosis and calcification of the coronary conduit arteries, independent effects on postcoronary microvessels and on cardiac fibrosis have not been excluded. METHODS: Male Sprague-Dawley rats were sham operated (N = 14) or subtotally nephrectomized (SNX, N = 17) and subsequently placed on low phosphorus (0.08% w/w) and high phosphorus (1.2% w/w) diet under pair-feeding conditions. After 8 weeks, serum chemistry and inhibitory parathyroid hormone (iPTH) were measured, and the hearts were harvested using perfusion fixation. Arteriolar thickness and volume density of the interstitium (excluding vessels) were quantitated using stereologic techniques. RESULTS: In SNX animals with moderate renal failure serum phosphorus concentrations were higher than in sham-operated controls on low phosphorus diet (1.7 +/- 0.37 mmol/L) and were significantly higher in SNX + high phosphorus diet (2.33 +/- 0.23 mmol/L) compared to SNX + low phosphorus diet (1.95 +/- 0.32 mmol/L; P < 0.05). In sham-operated controls, dietary phosphorus content had no effect on cardiac morphologic indices. In contrast, in SNX + high phosphorus diet the index of interstitial cardiac fibrosis was significantly higher (3.22 +/- 0.44%) than in SNX + low phosphorus (2.75 +/- 0.46%) or in sham-operated controls (2.5 +/- 0.05% on high phosphorus and 2.4 +/- 0.89 on low phosphorus, respectively). In SNX + high phosphorus (14.0 +/- 9.0 microm), but not in SNX + low phosphorus (9.2 +/- 4.5 microm), arterial wall thickness was significantly higher compared to sham-operated controls (10.2 +/- 5.1 on high phosphorus and 9.8 +/- 5.0 micro;m on low phosphorus, respectively). The data were confirmed in an independent repeat experiment. CONCLUSION: High dietary phosphorus and hyperphosphatemia have significant effects on cardiac fibrosis and arterial wall thickening. Such abnormalities of cardiac architecture may be relevant for the increased cardiac risk in hyperphosphatemic uremic patients.

Animals↗

PubMed1998

Role of calcium carbonate administration timing in relation to food intake on its efficiency in controlling hyperphosphatemia in patients on maintenance dialysis.

A study has claimed that at an equal elemental calcium dose, CaCO3 was not less but equally as efficient in controlling predialysis hyperphosphatemia as calcium acetate, provided both calcium salts were ingested 5 min before meals instead of during meals because the higher acidity of the fasting gastric juice would allow for better dissociation of CaCO3. However, this study did not directly demonstrate that the efficiency of CaCO3 in controlling hyperphosphatemia was actually greater when it was administered before a meal than during a meal. To examine this point, we performed a 3 month randomized crossover trial in 12 reliable and stable patients maintained on chronic hemodialysis. Their plasma concentrations of calcium, protein, phosphate, bicarbonate, urea, and creatinine were measured before the first dialysis of each week and the amount of intact parathyroid hormone (PTH) at the beginning and at the end of each of the 3 months. Comparison of the plasma concentrations measured during the 2 modes of administration showed no significant differences in creatinine, urea, bicarbonate, or intact PTH. The mean (+/-SD) plasma concentration of PO4 was not significantly lower (1.88+/-0.50 vs. 1.74+/-0.41 mM) whereas the corrected level of plasma Ca was significantly lower (2.30+/-0.17 vs. 2.38+/-0.16 mM; p < 0.04) when CaCO3 was given before meals than during meals. In conclusion, the administration of CaCO3 before a meal does not increase its efficiency in controlling hyperphosphatemia because the level of plasma PO4 was actually slightly higher with this timing of administration whereas the comparison of the creatinine and urea levels suggested a stability of phosphate intake and the comparison of the PTH and bicarbonate levels suggested the stability of osteolysis and of the transcellular membrane shift of phosphate. Also, administration of CaCO3 before a meal is associated with significantly lower plasma corrected calcium, suggesting less absorption of calcium, which may be an advantage but only in hypercalcemic patients. There is no reason other than the prevention of its hypercalcemic effect to recommend the administration of CaCO3 just before meals rather than during meals.

Absorption↗

PubMed1998

Inhibition of gastric secretion by omeprazole and efficiency of calcium carbonate on the control of hyperphosphatemia in patients on chronic hemodialysis.

Contradictions exist in the literature regarding the effect of gastric secretion inhibition on phosphate absorption. In healthy controls, omeprazole would decrease the hyperphosphatemia or the hyperphosphaturia induced by an acute phosphate load, suggesting an inhibition of phosphate absorption. In chronic hemodialysis patients, gastric hypersecretion is associated with hyperphosphatemia, but inhibition of gastric hypersecretion by ranitidine in those receiving calcium carbonate (CaCO3) as a phosphate binder would paradoxically exacerbate their hyperphosphatemia. Because of these conflicting observations, we performed an open crossover study on 16 chronic stable hemodialyzed patients with a daily mean intake of 9.4+/-4 g of CaCO3, and we compared the plasmatic predialysis levels of phosphate, calcium, protides, bicarbonates, intact parathyroid hormone (PTH), urea, and creatininemia during 2 successive periods of 2 months, the first one without omeprazole and the second one with 20 mg omeprazole intake in the morning. Phosphatemia increased with omeprazole but not significantly from 1.80+/-0.38 to 1.89+/-0.42 mM whereas corrected calcemia decreased significantly (p = 0.04) from 2.41+/-0.18 to 2.36+/-0.16 mM as did bicarbonatemia from 26.7+/-3.5 to 25.7+/-3.1 mM (p < 0.05). No change in creatininemia or in blood urea was observed, suggesting the stable efficiency of dialysis as well as the stable intakes of protein and therefore of phosphate during the two study periods. In conclusion, inhibition of gastric secretion by omeprazole increases the plasmatic phosphate predialytic level but in a nonsignificant way. This increase may be explained by a slight but significant concomitant decrease of calcemia and bicarbonatemia. These results do not support the phosphate binding efficiency of CaCO3 being decreased by the inhibition of gastric acid secretion.

Absorption↗

PubMed2004

Calcium-enriched bread for treatment of uremic hyperphosphatemia.

OBJECTIVE: To assess phosphate-binding efficacy of a new food product, bread with unusually high calcium content (Ca-bread). DESIGN AND SETTING: A randomized parallel group trial in the university hospital outpatient dialysis unit. PATIENTS: Fifty-three randomly selected uremic patients who met the following inclusion criteria: (1) required maintenance hemodialysis treatment, (2) were not to receive vitamin D throughout the study, (3) were nondiabetic, and (4) were diagnosed with hyperphosphatemia. INTERVENTION: Fifty-three patients were randomized into 2 groups: control group (n = 26), which received calcium acetate as a phosphate binder throughout the study, and Ca-bread group (n = 27), which, after a 2-week washout period, received Ca-bread containing 2.5% of elemental calcium (by weight), which served as a phosphate binder. Bread was made using wheat flour, calcium carbonate, and fermented buttermilk. The amount of elemental calcium used as a phosphate binder was similar in both groups. Observation of both groups lasted 14 weeks. RESULTS: Mean serum phosphate concentration at randomization was 2.11 +/- 0.14 mmol/L in the control group and 2.20 +/- 0.13 mmol/L in the Ca-bread group. Mean serum calcium concentration at randomization was 2.12 +/- 0.21 mmol/L in the control group and 2.14 +/- 0.11 mmol/L in the Ca-bread group. The Ca-bread group patients' predialysis phosphate concentration decreased to a mean of 1.67 +/- 0.18 mmol/L (P <.05), and their mean calcium concentration increased to 2.27 +/- 0.11 mmol/L (P = NS). In the control group, neither value changed significantly from the original readings. After the hemodialysis session, the mean serum calcium concentration in the control group and the Ca-bread group increased by 7.5% and 7.9%, respectively (P = NS). Mean phosphate concentration simultaneously decreased to nearly 1/2 its original predialysis value in both groups. Ca-bread group patients saw a decrease in the mean phosphate concentration (from predialysis to postdialysis values) that was 13.8% greater than that of the control group (P = NS). CONCLUSION: A new form of calcium-containing phosphate binder was developed: Ca-bread with an elemental calcium content of 2.5%. Ca-bread allows for effective amelioration of hyperphosphatemia without inducing hypercalcemia. Furthermore, patient compliance may increase if hyperphosphatemia can be treated by consuming bread with an elevated calcium content.

Acetates↗

PubMed2002

Hyperphosphatemia in end-stage renal disease.

Hyperphosphatemia occurs universally in end-stage renal disease (ESRD) unless efforts are made to prevent positive phosphate balance. Positive phosphate balance results from the loss of renal elimination of phosphate and continued obligatory intestinal absorption of dietary phosphate. Increased efflux of phosphate from bone because of excess parathyroid hormone-mediated bone resorption can also contribute to increased serum phosphate concentrations in the setting of severe hyperparathyroidism. It is important to treat hyperphosphatemia because it contributes to the pathogenesis of hyperparathyroidism, vascular calcifications, and increased cardiovascular mortality in ESRD patients. Attaining a neutral phosphate balance, which is the key to the management of hyperphosphatemia in ESRD, is a challenge. Control of phosphorus depends on its removal during dialysis and the limitation of gastrointestinal absorption by dietary phosphate restriction and chelation of phosphate. Knowledge of the quantitative aspects of phosphate balance is useful in optimizing our use of phosphate binders, dialysis frequency, and vitamin D sterols. The development of new phosphate binders and efforts to find new ways to inhibit gastrointestinal absorption of phosphate will lead to improvements in the control of serum phosphate levels in ESRD.

Humans↗

PubMed1993

Methods of controlling hyperphosphatemia in patients with chronic renal failure.

The problem of hyperphosphatemia in patients with chronic renal failure is reviewed. The importance of high plasma phosphorus levels in the pathogenesis of hyperparathyroidism is concisely discussed. Basic concepts about phosphorus metabolism in normal persons and in patients with chronic renal failure are outlined. This is followed by a detailed discussion of the various therapeutic methods to control hyperphosphatemia. Dietary restriction, dialysance of phosphorus, and the use of the currently available phosphorus binders are comprehensively discussed. Finally, the various clinical situations associated with failure to control hyperphosphatemia are reviewed.

Animals↗

PubMed1993

Management of hyperphosphatemia in patients with renal failure.

Phosphate retention plays a major role in the pathogenesis of hyperparathyroidism at all stages of renal insufficiency. Dietary phosphate restriction is mandatory only for adults and is not advised for children because of the recommended diet allowance. Dietary restriction is usually not sufficient, and phosphate binders are almost always necessary when the glomerular filtration rate falls below 40 mL/min. Because long-term administration of aluminum phosphate binders is associated with risk of aluminum intoxication despite the use of so-called "safe doses", alternative phosphate binders should be used. Magnesium hydroxide and carbonate can be used only for dialysis patients because a low dialysate magnesium concentration is necessary to prevent the hazards of hypermagnesemia. Therefore, the major alternative is the use of alkaline salts of calcium. The most recently proposed salt, acetate, has a higher phosphate-binding capacity than carbonate but exposes patients to the same incidence of hypercalcemia despite the use of half the dose of elemental calcium. These salts should be taken with meals in order to complex more dietary phosphate and decrease calcium absorption and therefore the risk of hypercalcemia. Oral calcium alone, without 1 alpha OH-vitamin D3 derivatives, can prevent hyperphosphatemia and hyperparathyroidism in most uremic patients before dialysis and in about half of the patients dialyzed with a dialysate calcium of 1.5 to 1.65 mmol/L. 1 alpha OH-vitamin D3 derivatives, which increase intestinal absorption of phosphate, should be used only when hyperphosphatemia has been prevented by oral calcium and diet and when plasma parathyroid hormone levels increase above three times the upper limit of normal. To decrease hypercalcemic risk, patients should be given 1 alpha OH-vitamin D3 derivatives, preferably at night, as an intermittent bolus (intravenous or oral). In dialysis patients, the dialysate concentration of calcium may have to be further decreased in order to prevent hypercalcemia when high doses of oral calcium are necessary to control hyperphosphatemia.

Adult↗

PubMed2005

Treatment of hyperphosphatemia in patients with chronic kidney disease on maintenance hemodialysis.

Treatment of hyperphosphatemia in patients with chronic kidney disease on maintenance hemodialysis. Hyperphosphatemia in patients with ESRD leads to secondary hyperparathyroidism, renal osteodystrophy, and is independently associated with mortality risk. The exact mechanism by which hyperphosphatemia increases mortality risk is unknown, but it may relate to enhanced cardiovascular calcification. National Kidney Foundation K/DOQI bone metabolism and disease guidelines recommend maintenance of serum phosphorus (P) below 5.5 mg/dL, and Ca x P product less than 55 mg(2)/dL(2). Although calcium-based phosphate binders (CBPB) are cost effective, long-term safety concerns relate to their postulated role in progression of cardiovascular calcification. Sevelamer hydrochloride has been recommended as an alternative noncalcium phosphate binder. Results from the Calcium Acetate Renagel Evaluation (CARE study) indicate that calcium acetate is more effective than sevelamer in controlling serum phosphorous and Ca x P product in hemodialysis patients. In the Treat-to-Goal study, dialysis patients treated with sevelamer had slower progression of coronary and aortic calcification than patients treated with CBPB. The mechanism underlying the beneficial effect of sevelamer is unknown, but may relate to decreased calcium loading or to dramatic reductions in LDL cholesterol in sevelamer-treated patients. At present, evidence incriminating CBPB in the progression of cardiovascular calcification in ESRD remains largely circumstantial. As calcium acetate is more efficacious and cost effective than sevelamer, it remains an accepted first-line phosphate binder. In this review, we will examine these issues and provide rational guidelines for the use of calcium-based phosphate binders in patients on maintenance hemodialysis.

Acetates↗

PubMed2005

The role of daily dialysis in the control of hyperphosphatemia.

The role of daily dialysis in the control of hyperphosphatemia. In patients with end-stage renal disease (ESRD), hyperphosphatemia occurs in the vast majority of patients. The numerous clinical sequelae of hyperphosphatemia include secondary hyperparathyroidism and increased risk of cardiovascular death. Chronic hemodialysis as it is currently practiced in the United States does not remove sufficient phosphate to control serum levels within accepted guidelines. The inadequacy of conventional hemodialysis in removing phosphate mandates the use of phosphate binders in virtually all hemodialysis patients. Despite their proven efficacy, these medications fail to control phosphorous in 70% of hemodialysis patients. Additionally, these medications may have untoward side effects that must be considered since they are typically intended for lifetime use. Quotidian hemodialysis has in previous uncontrolled studies shown promise in reducing serum phosphorus while at the same time reducing or eliminating the need for phosphate binders. Recent results from our group demonstrate for the first time in a controlled fashion the efficacy of short daily dialysis in controlling serum phosphorus.

Hemodiafiltration↗

PubMed2005

Efficacy of combined sevelamer and calcium carbonate therapy for hyperphosphatemia in Japanese hemodialysis patients.

In Japan, calcimimetics and other phosphate binders such as lantanum carbonate are not available for patients on long-term hemodialysis (HD), so we prospectively evaluated the clinical efficacy of the combination of sevelamer hydrochloride and calcium carbonate (CaCO3) for hyperphosphatemia. The study group comprised 65 HD patients who had been administered CaCO3 (>or=1500 mg/day) for hyperphosphatemia [>or=6.0 mg/dL (>or=1.94 mmol/L)]. At the beginning of the study the dose of CaCO3 was reduced by 1500 mg/day and the patients divided into two groups according to the dose of additional sevelamer hydrochloride: group A 2250 mg/day; group B 3000 mg/day. Oral active vitamin D therapy was unchanged. Fourteen patients (21.5%) dropped out because of adverse effects and of the 51 remaining patients 35 (53.8%) suffered from gastrointestinal problems. Serum phosphate concentration decreased significantly [from 7.5+/-0.8 mg/dL (2.42+/-0.26 mmol/L) to 6.6+/-1.3 mg/dL (2.13+/-0.42 mmol/L), P<0.01] in group B only after the 8 weeks of combination therapy. The calcium-phosphate product (CaxPi) also decreased in group B only [from 74.4+/-13.4 mg2/dL2 (5.99+/-1.07 mmol2/l2) to 63.7+/-15.8 mg2/dL2 (5.13+/-1.27 mmol2/l2), P<0.001]. The combination of sevelamer hydrochloride and CaCO3 is a suitable regimen for hyperphosphatemia treatment in HD patients because it avoids both the hypercalcemia of CaCO3 and the adverse effects of sevelamer hydrochloride when each is used as single-drug therapy. The ability of sevelamer hydrochloride to decrease the serum phosphate concentration is 2/3 (2250/1500 mg) that of CaCO3.

Calcium Carbonate↗

PubMed1991

Spurious hyperphosphatemia in a dog with chronic lymphocytic leukemia and an IgM monoclonal gammopathy.

Spurious hyperphosphatemia was diagnosed in a 6-year-old, neutered female, mixed-breed dog with chronic lymphocytic leukemia associated with an IgM monoclonal gammopathy. The spurious hyperphosphatemia was probably caused by paraprotein precipitation which interfered with the ASTRA 8 automated analyzer measurements. Serial dilutions of the sample did not change the phosphorus value. Another analyzer system in which a protein-free sample was prepared prior to analysis gave a normal serum phosphorus concentration. There was a linear relationship between the amount of paraprotein and the measured total serum inorganic phosphate (r=0.75). A review of 700 chemistry profiles from dogs and cats and a review of 36 cases with polygonal gammopathy and 6 cases with monoclonal gammopathy did not reveal other cases of spurious hyperphosphatemia.

Journal Article↗

PubMed2005

Hyperphosphatemia in renal failure.

The recent recognition that hyperphosphatemia is a strong predictor of survival on dialysis has rekindled interest in the regulation and control of serum phosphate. In incipient renal failure hyperphosphatemia is prevented by increased fractional renal phosphate excretion mediated via an increase in parathyroid hormone and the novel phosphaturic hormone FGF-23 (and possibly others). At a glomerular filtration rate of approximately 30 ml/min this compensatory mechanism fails and hyperphosphatemia ensues. Pre-dialytic serum phosphate concentrations of >6 mg/dl increase cardiac mortality presumably to a large extent, but not exclusively, via promoting vascular calcification. It has recently been recognized that vascular calcification is not only a passive precipitation process following transgression of the critical Ca-x-P product, but is an active process accompanied by expression of osteoblastic bone markers in the vessel wall. Because of the recent recognition of the relation between vascular calcification and serum phosphate as well as serum calcium, there is a need for novel calcium-free phosphate binders. Currently sevelamer and lanthanum carbonate have been introduced and trivalent iron preparations are under development.

Animals↗

PubMed1992

Control of predialytic hyperphosphatemia by oral calcium acetate and calcium carbonate. Comparable efficacy for half the dose of elemental calcium given as acetate without lower incidence of hypercalcemia.

Since Mai et al. found, with the intestinal lavage technique, that the same dose of elemental calcium given as acetate (Ca Ac) complexed in the gut of uremic patients twice as much phosphate as calcium carbonate (CaCO3) while inducing a rather low calcium absorption, we wanted to see if half the dose of elemental calcium given as Ca Ac could control, on medium term, the predialysis plasma phosphate as well as 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 and Ca Ac, in 12 compliant patients on chronic dialysis previously treated by CaCO3. Because of poor tolerance of Ca Ac during the first period, 4 patients were excluded and the results were assessed only on the 8 patients who completed the study. For half the doses of elemental calcium (620 +/- 250 mg versus 1,310 +/- 560 mg versus 710 +/- 200 mg/day), Ca Ac allowed the same control of predialytic hyperphosphatemia (1.67 +/- 0.34; 1.74 +/- 0.32; 1.75 +/- 0.38) with paradoxically comparable normal mean plasma calcium concentration (2.61 +/- 0.14; 2.56 +/- 0.13; 2.55 +/- 0.14 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. In conclusion, Ca Ac controls predialytic hyperphosphatemia as efficiently as CaCO3 for half the dose of elemental calcium without, however, decreasing the frequency of hypercalcemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

PubMedDate not supplied

Hyperphosphatemia from lipid emulsion in a patient on total parenteral nutrition.

The clinical course of a patient is described in whom hyperphosphatemia occurred on total parenteral nutrition with lipid emulsion providing half of the nonnitrogenous caloric support. Renal insufficiency, hypoparathyroidism, pseudohypoparathyroidism, and severe catabolism are excluded as causes of this hyperphosphatemia. Changes in serum phosphate are attributed to metabolism of phospholipid present in the lipid emulsion, the sole phosphate source in this patient. These observations suggest that the phosphate of phospholipids can contribute significantly to the metabolic pool of inorganic phosphate. Lipid emulsion, most commonly thought of as a major caloric source, should not be neglected when one is confronted with hyperphosphatemia during total parenteral nutrition.

Fat Emulsions, Intravenous↗

PubMedDate not supplied

Skin necrosis: an unusual complication of hyperphosphatemia during total parenteral nutrition therapy.

BACKGROUND: Hyperphosphatemia complicated by calcification of subcutaneous arteries and skin infarcts are very rarely reported in the absence of chronic renal failure (CRF). We describe identical lesions in an obese woman with sepsis. Hyperphosphatemia resulted from an unintended excess of phosphate in her total parenteral nutrition (TPN) formulations. She did not have CRF or hyperparathyroidism. METHODS: The patient's records during 37 weeks of hospitalization 12 years ago and, subsequently, her outpatient records were reviewed. RESULTS: During a 7-week period, the total elemental phosphorus infused daily, as divalent phosphate, ranged from 1.8 to 4.2 g, median 3.1, over triple the normal daily requirement. This excess was unintended. This occurred before the current practice of pharmacist-monitoring of TPN formulations, and possibly resulted from misinterpretation of a revised formulation sheet, newly introduced to the nursing units at the start of that period. Serum phosphorus increased to 3.02 mmol/L (normal 0.76 to 1.46 mmol/L). She developed calcification of subcutaneous arteries, which was complicated by widespread infarcts of the anatomically related skin and subcutis, apparently the result of hypoperfusion of these vessels during an episode of septic shock. The infarcts were heralded by unusual, blotchy skin discolorations. CONCLUSIONS: This report, illustrating a startling cutaneous complication associated with apparent misinterpretation of TPN formulations, demonstrates a pathogenetic relationship between hyperphosphatemia, calcification of subcutaneous arteries, and necrosis of the skin and subcutis in the absence of CRF and hyperparathyroidism and introduces a new differential diagnosis for unusual skin lesions appearing during TPN therapy.

Adult↗