Pathophysiology of X-linked hypophosphatemia, tumor-induced osteomalacia, and autosomal dominant hypophosphatemia: a perPHEXing problem.
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Animals↗
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[Clinical manifestations of hypophosphatemia--with special reference to physiopathology of hypophosphatemia caused by an antacid].
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Adult↗
Reversible depression of myocardial performance in hypophosphatemia.
Studies of myocardial function in patients with hypophosphatemia have yielded conflicting results. Systolic time intervals were performed in 19 patients during and after the correction of hypophosphatemia; 11 had severe (0.9 +/- 0.15 mg/dL) and eight had moderate (1.4 +/- 0.11 mg/dL) hypophosphatemia. Controls were 14 patients with normal serum phosphorus levels. No patient with hypophosphatemia had clinical congestive heart failure. When hypophosphatemia was corrected, improvement in left ventricular performance was seen only in patients with severe hypophosphatemia (p less than 0.001); in eight patients left ventricular performance was normal during hypophosphatemia but showed significant improvement with its correction (p less than 0.01). Patients with moderate hypophosphatemia showed no significant change. Our results confirm the findings of O'Conner et al, whose study is the only previous one to demonstrate hypophosphatemia-induced myocardial depression in humans. Contradictory results from other studies may be explained by the inclusion of patients with moderate hypophosphatemia and failure to repeat measurements after the correction of hypophosphatemia. We conclude that reversible depression of myocardial performance is seen in hypophosphatemia only when it is severe. In some cases, normal left ventricular performance improves when hypophosphatemia is corrected.
Heart Ventricles↗
[Hypophosphatemia in the hospitalized patient].
BACKGROUND: Phosphate is an obligatory component of cellular function. Serum, levels are maintained within narrow levels by regulatory mechanisms. The normal range of phosphate concentration is 2.5-4.5 mg/dL. In certain clinical situations these mechanisms are insufficient and hypophosphatemia ensues. AIM: This study aimed to compare hospitalization course and clinical outcome of patients with moderate hypophosphatemia (1.0-2.0 mg/dl) with patients with extreme hypophosphatemia (< 1.0 mg/dL). METHODS: Patients who had at least one measurement of serum phosphate level of 1.0 mg/dL or less comprised the extreme hypophosphatemic group. Patients with at least one serum, phosphate level of between 1.0 and 2.0 mg./dL, but never had a phosphate level of less than 1.0 mg/dL comprised the moderate hypophosphatemic group. Files of 50 consecutive patients who had extreme hypophosphatemia and 100 consecutive patients with moderate hypophosphatemia were retrieved and analyzed. RESULTS: The two groups of patients were similar with reference to age, gender ratio, background disease and indication for hospitalization. There was a higher proportion of obese patients in the moderate hypophosphatemia group. There was a higher proportion of patients who consumed alcohol on a regular basis before hospitalization in the extreme hypophosphatemic group. Patients suffering from extreme hypophosphatemia were more likely to be hospitalized in the intensive care unit and ventilated on hospitalization. Length of hospitalization was longer for the extreme hypophosphatemia group than for the moderate hypophosphatemia group. When comparing the group outcomes it was found that more patients with severe hypophosphatemia died. CONCLUSION: Severe hypophosphatemia is a severe metabolic derangement. It appears in critically sick patients, who should be followed closely and treated properly. The clinical relevance of moderate hypophosphatemia was not checked in this study.
Adult↗
Hypophosphatemia in living liver donors.
BACKGROUND AND AIM: Some patients who undergo donor hepatectomy for adult living donor liver transplantation develop hypophosphatemia postoperatively. Since this imbalance appears to be a factor in postoperative complications, some authors advocate routine supratherapeutic phosphorus repletion. The purpose of this study was to determine the frequency of hypophosphatemia after elective donor lobectomy for liver transplantation and to assess whether phosphorus repletion is necessary in this patient group. METHODS: The cases of 26 patients who donated 19 right lobe and seven left lateral lobe grafts between August 2004 and March 2005 were evaluated. Postoperative phosphorus levels and other relevant data were obtained from our institution's transplant database. Presence/severity of hypophosphatemia was categorized as follows: normal (>2.5 mg/dL), mild (1.5 to 2.5 mg/dL), moderate (1.1 to 1.5 mg/dL), and profound (<1.0 mg/dL). RESULTS: No patients undergoing donor hepatectomy suffered profound or life-threatening hypophosphatemia and no donor required hyperalimentation for phosphate repletion. Twenty one donors (80.7%) did not have postoperative hypophosphatemia. In addition there appears to be no increased morbidity related to hypophosphatemia. A left lateral segment donor (3.8%) had moderate hypophosphatemia that alleviated with oral intake gradually. Four patients (15.5%; three of right lobe donor, one of left lateral segment donor) had mild hypophosphatemia. We also appropriately corrected the hypophosphatemia with encouragement of normal oral intake. By postoperative day 5, essentially all donor phosphorus levels were corrected to normal range. CONCLUSIONS: The results suggest that hypophosphatemia after donor hepatectomy is not as common as previously reported. We find that appropriate early oral intake postoperatively effectively prevents/minimizes hypophosphatemia in patients who undergo donor hepatectomy.
Adult↗
Life-threatening hypophosphatemia after right hepatic lobectomy for live donor adult liver transplantation.
Life-threatening hypophosphatemia (phosphorus < 1.0 mg/dL) has been reported only once after liver resection for tumor and was associated with a significant increase in postoperative complications. Hypophosphatemia is associated with reversible cardiac dysfunction, hypoventilation, and impaired immunity. The purpose of this study was to determine the incidence of hypophosphatemia after elective right hepatic lobectomy for live donor adult liver transplantation (LDALT), investigate the associated complication rate and surgical outcome of live liver donors, and determine the efficacy of prospective treatment with phosphate repletion as part of total parenteral nutrition (TPN). Evaluation of 30 donors who provided 30 right-lobe grafts between December 1998 and January 2000 was performed. Of the initial 18 live liver donors (group 1), 10 donors were treated with TPN that contained slightly more (35 +/- 8 mmol/d) than the recommended daily allowance (RDA) of phosphorus (30 mmol/d) starting on postoperative day 1. The last 12 donors (group 2) were prospectively studied and administered similar TPN with 2 times the RDA for phosphorus (60 mmol/d). All donors in group 1 developed hypophosphatemia that was either life threatening (phosphorus < 1.0 mg/dL) in 70% or severely depleted (phosphorus, 1.5 to 1.1 mg/dL) in 30%. With more aggressive phosphate repletion (group 2), only 8% developed life-threatening (phosphorus < 1.0 mg/dL) hypophosphatemia and 30% developed severe (phosphorus, 1.1 to 1.5 mg/dL) hypophosphatemia. Results suggest that hypophosphatemia is a universal event after LDALT and may have contributed to the observed complications in this study. Repletion of phosphorus at twice the RDA abrogates the incidence of hypophosphatemia and may reduce donor morbidity. Institutions performing LDALT should carefully monitor live liver donors for hypophosphatemia and correct abnormal phosphate levels. Additional studies are needed to determine whether more aggressive parenteral repletion can prevent postoperative hypophosphatemia and thus improve outcomes.
Adult↗
Refeeding hypophosphatemia in critically ill patients in an intensive care unit. A prospective study.
BACKGROUND: Hypophosphatemia has been reported after refeeding of malnourished patients. Nutritional support is often delayed in patients in the intensive care unit (ICU) as a consequence of enteral intolerance and bowel hypomotility. OBJECTIVE: To determine the incidence, risk factors, and clinical impact of refeeding hypophosphatemia in a heterogeneous group of patients in an ICU. DESIGN: Prospective, noninterventional study. SETTINGS: Surgical and medical ICUs of a university-affiliated community hospital. PATIENTS: Sixty-two patients in the ICU who were refed after being starved for at least 48 hours were prospectively followed up. INTERVENTIONS: None. MAIN OUTCOME MEASURES: Each patient had a nutritional assessment prior to the initiation of nutritional support. Serum phosphate, magnesium, and calcium levels were measured at baseline, and these measurements were repeated daily. Refeeding hypophosphatemia was considered to have developed in patients whose serum phosphorus level fell by more than 0.16 mmol/L to below 0.65 mmol/L. RESULTS: Twenty-one patients (34%) experienced refeeding hypophosphatemia. In 6 patients, the serum phosphorus level fell below 0.32 mmol/L. The only risk factor studied that could predict the development of hypophosphatemia was the serum prealbumin concentration (mean +/- SD, 127 +/- 34 vs 79 +/- 40 g/L, P < .001). Seventeen (81%) of these 21 patients in whom hypophosphatemia developed had a prealbumin concentration less than 110 g/L compared with that in 12 (30%) of the patients who did not experience this complication (P < .001). In those patients in whom refeeding hypophosphatemia developed, the serum phosphorus level reached a mean +/- SD nadir of 1.9 +/- 1.1 days after feeding was started. Although the Acute Physiology and Chronic Health Evaluation II score was similar (mean +/- SD, 19 +/- 6 vs 18 +/- 7), the length of mechanical ventilation (mean +/- SD, 10.5 +/- 5.2 vs 7.1 +/- 2.8 days; P = .04) and the length of hospital stay (mean +/- SD, 12.1 +/- 7.1 vs 8.2 +/- 4.6 days; P = .01) were significantly longer in those patients who experienced hypophosphatemia compared with those patients who did not experience this complication. CONCLUSIONS: Refeeding hypophosphatemia occurs commonly in critically ill patients in the ICU. Starvation for a period as short as 48 hours and poor nutritional status predispose to this syndrome. Patients at risk should be refed slowly, and the serum phosphorus level should be closely monitored and supplemented as required.
Aged↗
Severe hypophosphatemia. Pathophysiologic implications, clinical presentations, and treatment.
We conducted this review to heighten the awareness and describe pathologic manifestations of hypophosphatemia. We present 3 cases of varied manifestations of hypophosphatemia where recognition was delayed. In certain settings, severe hypophosphatemia has significant morbidity and potential mortality. Appreciation of the pathophysiologic basis for organ dysfunction in severe hypophosphatemia should result in early recognition and treatment. We reviewed the English-language literature for reported cases and research studies dealing with pathophysiologic mechanisms subserving clinical manifestations. We observed that depletion of adenosine triphosphate (ATP) would explain most of the derangement noted in cellular functions. Phosphate plays a key role in the delivery of oxygen to the tissue. Lack of phosphate, therefore, leads to tissue hypoxia and hence disruption of cellular function. Severe hypophosphatemia becomes clinically significant when there is underlying phosphate depletion. Otherwise, short-term acute hypophosphatemia is not usually associated with any specific disorder. Chronic hypophosphatemia, on the other hand, results in hematologic, neuromuscular, and cardiovascular dysfunction, and unless corrected, the consequences can be grave. Most of the time hypophosphatemia results from renal loss of phosphate, diagnosed by a fractional secretion of phosphate > 5%. It is hard to provide precise estimates of how many patients are seen with hypophosphatemia annually at academic medical centers. This is complicated by use of chemistry panels that do not measure inorganic phosphate unless specifically ordered. This often leads to delay in correct diagnosis, and, therefore, additional delay in providing appropriate management. A high index of suspicion alone avoids the unnecessary withholding of treatment that can be life saving.
Acute Disease↗
Prevalence of hypophosphatemia in sepsis and infection: the role of cytokines.
BACKGROUND: Sepsis occurs following the presence of bacteria in the circulation and is associated with fever, hyperthermia, and hypotension. Hypophosphatemia develops in the early stages of sepsis. High levels of inflammatory cytokines also characterize early sepsis. AIM: The aim of the present study was to correlate hypophosphatemia with cytokines and cytokine receptor levels during early sepsis. We aimed to reestablish the results obtained from patients in an in vivo experimental model, in order to understand the mechanism of hypophosphatemia induction in early sepsis. METHODS: Ninety-nine patients were enrolled in this study and their clinical condition was classified as the presence of infection, sepsis, and bacterial growth in blood cultures. Phosphate levels and cytokine levels were recorded. In order to determine whether hypophosphatemia is correlated to the increased inflammatory cytokines, we injected normal mice with recombinant cytokines and studied their effect on phosphate levels. RESULTS: Our results revealed that 80% of the septic patients had hypophosphatemia associated with very high levels of tumor necrosis factor (TNF)alpha and interleukin (IL)-6 and of soluble IL receptor (sIL)-2R and IL-6R, especially in those patients with positive blood cultures. Injection of IL-6, TNFalpha and IL-1beta in mice markedly decreased the phosphate serum levels. CONCLUSIONS: Significant associations were demonstrated between high levels of inflammatory cytokines and their receptors and between serum phosphate levels, especially in patients with positive blood culture. Our results point to a correlation between the high inflammatory cytokines levels and hypophosphatemia during early sepsis. Cytokine levels and hypophosphatemia may be included in sepsis evaluation and prognosis. Anticytokine strategies might, therefore, reverse hypophosphatemia and other parameters of sepsis.
Cytokines↗
Post-transplant hypophosphatemia: Tertiary 'Hyper-Phosphatoninism'?
Hypophosphatemia is a common complication of kidney transplantation. Tertiary hyperparathyroidism has long been thought to be the etiology, but hypophosphatemia can occur despite low parathyroid hormone (PTH) levels and can persist after high PTH levels normalize. Furthermore, even in the setting of normal allograft function, hypophosphatemia, and hyperparathyroidism, calcitriol levels remain inappropriately low following transplantation, suggesting that mechanisms other than PTH contribute. Fibroblast growth factor-23 (FGF-23) induces phosphaturia, inhibits calcitriol synthesis, and accumulates in chronic kidney disease. We performed a prospective, longitudinal study of 27 living donor transplant recipients to test the hypotheses that excessive FGF-23 accounts for hypophosphatemia and decreased calcitriol levels following kidney transplantation. Hypophosphatemia <2.5 mg/dl developed in 85% of subjects, including one who had previously undergone parathyroidectomy; 37% developed phosphate < or =1.5 mg/dl. The mean pre-transplant FGF-23 level was 1,218+/-542 RU/ml. Within the first week following transplantation, mean levels decreased to 557+/-579 RU/ml, which were still above normal. FGF-23 was independently associated with serum phosphate (P < 0.01), urinary excretion of phosphate (P < 0.01), and calcitriol levels (P < 0.01); PTH was not independently associated with any of these parameters. We calculated area under the curve for FGF-23 and PTH between the pre- and first post-transplant levels as a summary measure of early exposure to these phosphaturic hormones. An area under the FGF-23 curve greater than the median was associated with a relative risk of developing hypophosphatemia < or =1.5 mg/dl of 5.3 (P = 0.02) compared with lower levels. Increased area under the PTH curve was not associated with greater risk of hypophosphatemia. Excessive FGF-23 exposure in the early post-transplant period appears to be more strongly associated with post-transplant hypophosphatemia than PTH.
Adult↗
Treatment of hypophosphatemia in patients receiving specialized nutrition support using a graduated dosing scheme: results from a prospective clinical trial.
OBJECTIVE: To determine the safety and efficacy of a graduated dosing scheme of phosphorus replacement therapy in patients with hypophosphatemia receiving specialized nutrition support. DESIGN: Prospective clinical trial. SETTING: A 455-bed tertiary care institution, with Level I trauma designation. PATIENTS: Seventy-eight adult patients, followed and co-managed by a multidisciplinary Nutrition Support Service, with a serum phosphorus concentration of < 3 mg/dL (< 0.97 mmol/L) and no evidence of renal insufficiency, calcium or parathyroid disorders, or obesity. INTERVENTIONS: Patients were enrolled into one of three categories based on their serum phosphorus concentration: mild hypophosphatemia (2.3 to 3 mg/dL [0.74 to 0.97 mmol/L]), moderate hypophosphatemia (1.6 to 2.2 mg/dL [0.52 to 0.71 mmol/L]), or severe hypophosphatemia (< 1.5 mg/dL [< 0.48 mmol/L]). Each patient received one intravenous phosphorus bolus dose, based on the assigned category of hypophosphatemia, according to a graduated dosing scheme: 0.16 mM/kg (mild), 0.32 mM/kg (moderate), or 0.64 mM/kg (severe). Serum/blood concentrations of phosphorus, calcium, albumin, magnesium, urea nitrogen, and creatinine were measured for three consecutive days. MEASUREMENTS AND MAIN RESULTS: Sixty-seven patients completed the protocol. There were 31 patients with mild hypophosphatemia, 22 patients with moderate hypophosphatemia, and 14 patients with severe hypophosphatemia. Serum phosphorus concentrations increased significantly (p < .001) in all groups after the phosphorus bolus: 2.6 +/- 0.6 to 3.3 +/- 0.6 mg/dL (0.84 +/- 0.19 to 1.1 +/- 0.19 mmol/L) for the mild group; 1.9 +/- 0.6 to 2.7 +/- 0.6 mg/dL (0.61 +/- 0.19 to 0.87 +/- 0.19 mmol/L) for the moderate group; 1.3 +/- 0.8 to 2.3 +/- 0.8 mg/dL (0.42 +/- 0.26 to 0.74 +/- 0.26 mmol/L) for the severe group. There were no clinically significant changes in serum/blood calcium, albumin, urea nitrogen, or creatinine concentrations and no adverse reactions to the phosphorus regimens throughout the 3-day study period. CONCLUSION: The graduated dosing scheme of phosphorus replacement therapy is both safe and efficacious in patients receiving specialized nutrition support.
Adult↗
Hypophosphatemia after right hepatectomy for living donor liver transplantation.
Hypophosphatemia has been described in patients undergoing right hepatectomy for liver cancer and in living donors for liver transplantation who also received total parenteral nutrition. At the study centre, significant hypophosphatemia (0.36 mmol/L or less) requiring intravenous replacement was seen in two of the first nine living donors for adult-to-adult liver transplantation. To determine the frequency of hypophosphatemia in living donors, the authors obtained phosphate levels on stored serum samples from postoperative days 0, 1, 3 and 7 in all nine patients, none of whom were on total parenteral nutrition. Within the first week, hypophosphatemia developed in 55.6% of patients and phosphate levels returned to normal by day 7 in all nine patients. One patient had normal phosphate levels during the first week, but had profound hypophosphatemia (0.32 mmol/L) on day 14 when he presented with a Staphylococcus aureus infection of a bile collection and significant hypoxemia. The extent of hepatectomy and the rate of liver regeneration, estimated by baseline and postoperative day 7 volumetric computed tomography scans, did not correlate with the development of hypophosphatemia. In conclusion, hypophosphatemia is common in living donors undergoing right hepatectomy and may be associated with complications. All living donors should be monitored for the development of hypophosphatemia during the first two postoperative weeks.
Adult↗
The clinical implications of hypophosphatemia following major hepatic resection or cryosurgery.
OBJECTIVES: To determine the incidence and predisposing factors leading to postoperative hypophosphatemia after major hepatic surgery and the consequences of this electrolyte abnormality. DESIGN: A retrospective study. SETTING: A university tertiary care referral center. PATIENTS AND METHODS: Thirty-five consecutive patients undergoing either major hepatic resections or cryosurgery from July 1994 through January 1997 were retrospectively reviewed for the occurrence of hypophosphatemia and postoperative complications. MAIN OUTCOME MEASURES: Prolonged ventilatory support, intensive care unit and hospital stays, and the incidence of postoperative complications. RESULTS: The overall incidence of hypophosphatemia in our series was 21 (67%) of 35 with a mortality rate of 1 (2.8%) in 35. Mean operative time, estimated blood loss, partial vascular occlusion time, and transfusion requirements were similar between the hypophosphatemic and the nonhypophosphatemic groups. The presence of postoperative complications was significantly greater in the hypophosphatemic group (17 [80%] of 21) vs the nonhypophosphatemic group (4 [28%] of 14) (P<.05). The incidence of antacid use in the hypophosphatemic group (14 [66%] of 21) was significantly higher than the use in the nonhypophosphatemic group (2 [14%] of 14) (P<.05). CONCLUSIONS: Hypophosphatemia commonly occurs in major hepatic procedures. The presence of moderate hypophosphatemia is associated with the use of antacid therapy but no other perioperative or operative variables. The occurrence of hypophosphatemia correlates with an increased incidence of postoperative complications. Awareness of this entity can direct aggressive replacement of phosphates and avert the occurrence of severe hypophosphatemia and associated complications.
Adult↗
Treatment of hypophosphatemia using a protocol based on patient weight and serum phosphorus level in a surgical intensive care unit.
BACKGROUND: Hypophosphatemia may cause organ derangements in the surgical intensive care unit. The purpose of this study was to determine the impact of a repletion protocol for hypophosphatemia based on admission weight and phosphorus level. STUDY DESIGN: All patients who presented to an 18-bed surgical intensive care unit with a serum phosphorus level of 2.2 mg/dL or less or who received phosphorus supplementation despite having normal levels were identified. In the preintervention phase between January and June 2001, 137 patients were retrospectively identified who met these criteria. A protocol was then designed giving a single intravenous dose of phosphorus based on weight and serum phosphorus. Repletion was given with sodium or potassium phosphorus based on presupplementation levels. After protocol implementation 141 patients met these criteria between September 2001 and February 2002, and treatment and postrepletion levels were followed prospectively. RESULTS: A total of 47 patients were repleted before the intervention with adequate followup and 22 (47%) attained a normal level. Supplementation success was 53% in moderate hypophosphatemia (2.2 mg/dL or less) and 27% in severe hypophosphatemia (less than 1.5 mg/dL). After protocol implementation, 111 patients were repleted with 84 (76%) correcting to a normal level (p = 0.002 compared with retrospective patients). Success was 78% in moderate hypophosphatemia and 62% in severe hypophosphatemia. Inappropriate supplementation of normal phosphorus levels decreased from 51 to 16 patients after protocol implementation. CONCLUSIONS: A protocol based on weight and serum levels successfully treated both moderate and severe hypophosphatemia in the majority of critically ill patients. Protocol implementation also decreased unnecessary supplementation of normal phosphorus levels.
Adult↗
Hypophosphatemia and hemolytic anemia associated with diabetes mellitus and hepatic lipidosis in cats.
Hypophosphatemia associated with hemolytic anemia was diagnosed in five cats with diabetes mellitus and in one cat with idiopathic hepatic lipidosis. The hematocrit began decreasing within 24 to 48 hours after documented hypophosphatemia in each case. The anemia resolved in all five surviving cats. Because of the temporal relationship and lack of other detectable causes, hemolytic anemia was presumed to be caused by hypophosphatemia. There were increased Heinz bodies in three of six hypophosphatemic cats during episodes of hemolysis. Intravenous potassium phosphate administration corrected the hypophosphatemia in four of five cats. The effective dosages of intravenous phosphate ranged from 0.011 to 0.017 mmol of phosphate/kg/h for 6 to 12 hours. Hypocalcemia (5.4 to 8.7 mg/dL) occurred in four of five cats treated with intravenous phosphate; however, only one cat developed clinical signs attributable to hypocalcemia. Based on this retrospective study, we recommend monitoring serum phosphorus concentration every 6 to 12 hours in cats likely to become hypophosphatemic. Treatment of hypophosphatemia in cats is warranted because of the apparent increased susceptibility of cats to hypophosphatemia-induced hemolysis. Cats with severe hypophosphatemia (< or = 1.5 mg/dL) should be given oral or parenteral phosphate if contraindications do not exist.
Anemia, Hemolytic↗
Severe hypophosphatemia in sepsis as a mortality predictor.
Hypophosphatemia has long been reported to be associated with sepsis and has been correlated with sepsis severity. This retrospective study was undertaken at a university hospital to determine whether severe hypophosphatemia could serve as a mortality predictor in septic patients. Charts of 6,190 septic patients who were hospitalized during one year (2001-02) were examined. Fifty-five patients were selected and were divided into 2 groups: group 1 comprised 26 patients with severe hypophosphatemia (serum inorganic phosphate (Pi) <1 mg/dl); group 2 comprised 29 patients without severe hypophosphatemia (Pi >1 mg/dl. The patients' charts were reviewed and information was collected regarding medical anamnesis, physical examination, hematological and biochemical analyses, chest x-ray, and cultures of blood and urine. The results demonstrated that 80.8% of the patients with severe hypophosphatemia died, vs 34.5% of the patients without severe hypophosphatemia (p = 0.001). Being in the severe hypophosphatemic group increased the risk of death by nearly 8-fold (odds ratio = 7.98; 95% CI = 2.3 to 27.6). These findings indicate that severe hypophosphatemia can serve as an independent mortality predictor in sepsis.
Adult↗
Hypophosphatemia in postoperative patients with total parenteral nutrition: influence of nutritional support teams.
UNLABELLED: PURPOSE, SETTING AND SUBJECTS: We conducted a prospective, descriptive study of postoperative patients under total parenteral nutrition controlled by a Multidisciplinary Nutritional Support Team in a tertiary care hospital. Between january 2002 and november 2003. Data of nutritional status, nutritional support, hypophosphatemia, electrolyte and metabolic complications were reviewed. RESULTS: 215 postoperative patients (63.3% male, 68 +/- 13.9 years old, 47.4% neoplasia). were included. Nutritional support according nutritional needs was made during fasting 14.2 +/- 18.4 days. Mild-moderate initial malnutrition was present in 58% of patients. 18.1% developed postoperative hypophosphatemia 96 hours after starting total parenteral nutrition containing phosphate. 37.7% patients showed moderated and 6.5% severe hypophosphatemia. Nutritional intervention corrected hypophosphatemia (p < 0.001). Factors related to hypophosphatemia were hypokalemia, hypomagnesemia, hypercalcemia, female sex, neoplasia, 96-hour postoperative period and duration of nutrition. CONCLUSIONS: Prevalence of hypophosphatemia in postoperative patients with total parenteral nutrition is high and needs timely monitoring. The intervention of Multidisciplinary Nutritional Support Team is effective detecting and correcting postoperative hypophosphatemia.
Aged↗
Nephrocalcinosis is associated with renal tubular acidosis in children with X-linked hypophosphatemia.
BACKGROUND: X-linked hypophosphatemia is characterized clinically by rickets and growth retardation. Therapy of this disorder with phosphate and vitamin D often produces nephrocalcinosis. The long-term effects of nephrocalcinosis on renal function in patients with X-linked hypophosphatemia are unknown. The purpose of this study was to evaluate the prevalence of glomerular and tubular disorders in patients with X-linked hypophosphatemia who developed nephrocalcinosis. METHODS: The creatinine clearance and the prevalence of renal tubular acidosis were compared in 19 patients with X-linked hypophosphatemia and nephrocalcinosis with 15 patients with X-linked hypophosphatemia without nephrocalcinosis. RESULTS: Sixteen of the 19 patients (84%) with nephrocalcinosis had a hyperchloremic metabolic acidosis compared with one of the 13 patients without nephrocalcinosis (P < .01). The serum bicarbonate of patients with nephrocalcinosis was 20.0 +/- 0.7 as compared to 24.5 +/- 0.6 mmol/L in patients without nephrocalcinosis (P < .01). The urinary anion gap was positive in all patients with acidosis (+62.1 +/- 13.3 mmol/L). The creatinine clearance was 125 +/- 6 mL/min/1.73 m2 in patients with nephrocalcinosis and 124 +/- 7 mL/min/1.73 m2 in those without nephrocalcinosis. CONCLUSION: Therapy of X-linked hypophosphatemia is often associated with nephrocalcinosis. Nephrocalcinosis is associated with renal tubular acidosis in patients with X-linked hypophosphatemia.
Acidosis, Renal Tubular↗