Mild Hyperphosphatemia Research Articles

Alteraciones electrolíticas inducidas por la preparación para los estudios de imagen del colon

An adequate bowel cleansing is needed prior to radiologic and endoscopic procedures. However, it may have a number of adverse effects, including abnormalities of calcium-phosphorus homeostasis. This was an observational prospective study in a hospital practice setting. We included consecutive inpatients (n = 47) subjected to a barium enema or colon endoscopy. Prior cleansing was done as indicated by the attending physician by using a low-salt oral poliethylenglicol (PEG) solution, oral sodium phosphate or a phosphate-containing enema. PEG solution frequently caused mild increases in serum sodium, and decreases in serum potassium. Oral phosphate caused a significant increase in serum phosphorus and parathormone concentrations, whereas it decreased serum calcium. Mild hyperphosphatemia was found in 57% of cases, and hypocalcemia in 36%. Phosphate enema also increased serum phosphate, causing mild hyperphosphatemia (33% cases). Although in the whole subgroup of enema-treated patients there were no significant changes in serum calcium, mild hypocalcemia was found in 27% cases. Bowel cleansing procedures, particularly those using oral phosphate salts, frequently induce hyperphosphatemia and other abnormalities in serum electrolytes. Although usually transitory and without overt clinical consequences, clinicians should be aware of this potential risk, especially in elderly patients and those with impaired renal function.

Mild Hyperphosphatemia and Mortality in Hemodialysis Patients

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. 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). 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). 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.

Failure to gain weight on long-term parenteral nutrition attributed to tri-iodothyronine thyrotoxicosis

We describe the case of a 49-y-old female patient on long-term parenteral nutrition after abdominal surgery who failed to gain weight despite nutritional provision in excess of theoretical requirements. On investigation, she was found to have a negative nitrogen balance (−5.9 g) and to have a tri-iodothyronine thyrotoxicosis but without many of the typical clinical features of hyperthyroidism. The patient also had mild hypercalcemia and hyperphosphatemia, which resolved fully after mobilization and treatment of the thyrotoxicosis. A derangement of the liver function tests was observed, which worsened progressively during parenteral nutrition but resolved promptly at its discontinuation. This case illustrates the importance of carrying out appropriate investigations including all thyroid function tests on patients who fail to gain weight on nutritional support.

Clinical manifestations of VX poisoning following percutaneous exposure in the domestic white pig.

Nerve agents are a class of organophosphorus chemicals that inhibit certain cholinesterase enzymes (ChE). If untreated, percutaneous exposure to nerve agents, such as VX (O-ethyl-S-[2(diisopropylamino)ethyl] methylphosphonothioate) can cause paralysis, apnoea and death. Much of the information concerning the percutaneous absorption and subsequent toxicity of nerve agents has been obtained using various rodent models. However, the most relevant 'skin model' is arguably the pig. Therefore, the purpose of this study was to examine the clinical manifestations of VX intoxication in the domestic white pig following a 2 LD50 (120 microg/kg) percutaneous challenge. There was a consistent onset of signs (where present) in each animal: mastication was followed by miosis, salivation, fasciculations and apnoea. Whilst ChE activity did not correlate with the onset of signs, there was a qualitative relationship in that mastication preceded substantial ChE inhibition, miosis lagged behind the linear decrease in acetylcholinesterase (AChE) activity and fasciculations and apnoea occurred after maximum ChE inhibition had been attained (5-10% of normal). These observations may be of use for the triage of patients exposed to VX. In comparison with similar studies with GD, VX did not affect glucose utilization. However, VX was similar to GD in that it caused a mild hyperkalaemia and hyperphosphataemia, although the significance of this observation was not clear. There was substantial lateral diffusion of the initial droplet of VX over the application site, indicating that, when decontaminating exposed skin, attention should also be directed to areas peripheral to the original site of exposure.

Refeeding syndrome: effective and safe treatment with Phosphates Polyfusor.

Severe hypophosphataemia associated with refeeding syndrome requires treatment with intravenous phosphate to prevent potentially life-threatening complications. However, evidence for replacement regimens is limited and current regimens are complex and replace phosphate inadequately. To assess the effectiveness and safety of 50 mmol intravenous phosphate infusion, given as a 'Phosphates Polyfusor', for the treatment of severe hypophosphataemia in refeeding syndrome. Patients with refeeding syndrome and normal renal function received a Phosphates Polyfusor infusion for the treatment of severe hypophosphataemia (< 0.50 mmol/L). The outcome measures were serial serum phosphate, creatinine and calcium concentrations for 4 days following phosphate infusion and adverse events. Over 2 years, 30 patients were treated. Following treatment, 37% of cases had a normal serum phosphate concentration and 73% had a serum phosphate concentration of > 0.5 mmol/L within 24 h. Ten patients required more than one Phosphates Polyfusor infusion. Within 72 h, 93% of cases had achieved a serum phosphate concentration of > or = 0.50 mmol/L. No patient developed renal failure. Three episodes of transient mild hyperphosphataemia were recorded. Four patients developed mild hypocalcaemia. This is the largest published series of the use of intravenous phosphate for the treatment of severe hypophosphataemia (< 0.50 mmol/L), and is the most effective regimen described. All patients had refeeding syndrome and were managed on general wards.

Serum phosphate abnormalities in the emergency department

Abnormalities in serum phosphate levels are more prevalent in certain subsets of Emergency Department patients than in the general population. Patients with diabetic ketoacidosis, chronic obstructive pulmonary disease, alcoholism, malignancy, and renal failure are at increased risk. Multiple factors, including nutritional intake, medications, renal or intestinal excretion, and cellular redistribution, are potential etiologies. The clinical manifestations of mild hypophosphatemia or hyperphosphatemia are typically minor and nonspecific (myalgias, weakness, anorexia). When the imbalance is severe, critical complications may occur (tetany, seizures, coma, rhabdomyolysis, respiratory failure, ventricular tachycardia). Mild asymptomatic hypophosphatemia can be treated with oral phosphate supplementation (15 mg/kg daily) on an outpatient basis. Patients with severe or symptomatic hypophosphatemia should be treated with IV phosphate therapy (0.08-0.16 mg/kg over 6 h) and admitted for monitoring and subsequent serum electrolyte testing. Mild asymptomatic hyperphosphatemia is commonly managed in renal failure by limiting dietary intake and reducing absorption with phosphate-binding salts. Hemodialysis may be required for severe hyperphosphatemia with symptomatic hypocalcemia.

A controlled trial of intermittent enteral nutrient supplementation in maintenance hemodialysis patients

Objective: This controlled trial was undertaken to evaluate the benefits of short-term enteral nutrient supplementation in maintenance hemodialysis (MHD) patients using a high-calorie and high-protein blend formula (low-cost home-prepared [HP] blend or a commercially available supplement) and to study its effect on selected parameters of nutritional status. The acceptability and palatability of the HP blend formula, ease of use, and cost were also assessed in comparison with the commercial nutritional supplement (CNS). Design: Randomized controlled trial. Setting: Hemodialysis (HD) unit of a tertiary referral care hospital in Southern India. Patients: Nondiabetic adult MHD patients with no intercurrent illness, on regular thrice weekly MHD for at least 1 month before recruitment, with a body mass index (BMI) <20 and a serum albumin level of <4.0 g/dL. Patients were randomized into control group and experimental group, the latter in turn to recieve either CNS or HP blend. Intervention: The control group received appropriate monitoring, including dietary recall and counselling for the prescribed diet (protein intake of 1.2 g/kgIBW/d and energy of 35 to 45 kcal/kgIBW/d) but no specific post-HD supplement. Patients in the supplement group received the respective supplement post-HD (providing 500 kcal and 15 g protein) for 1 month in addition to the monitored diet prescription. Main Outcome Measures: (1) Nutritional status parameters, BMI and serum albumin; (2) functional status on a 10-point Karnofsky scale; (3) adverse metabolic effects, hyperphosphatemia at start and end of study; and (4) subjective scoring for appetite, and acceptability of and tolerance to supplement. Results: Both groups showed an improvement in dry weight and BMI. In addition, the supplement group showed a significant increase in serum albumin level and functional scoring. Mild hyperphosphatemia occurred in the supplement group. An increase in baseline food intake was seen in the control group, but not in the supplemented group. No intolerance was reported to either supplement. Conclusion: Enteral nutrient supplementation was shown to bring about a significant improvement in serum albumin level even in a short-term study. Use of an HP supplement was beneficial, acceptable, and inexpensive. © 2002 by the National Kidney Foundation, Inc.

Intermittent doxercalciferol (1α-Hydroxyvitamin D2) therapy for secondary hyperparathyroidism

Hypercalcemia and hyperphosphatemia frequently necessitate vitamin D withdrawal in hemodialysis patients with secondary hyperparathyroidism. In short-term trials, doxercalciferol (1α-hydroxyvitamin D2 [1αD2 ]) suppressed intact parathyroid hormone (iPTH) effectively with minimal increases in serum calcium and phosphorus (P) levels. This modified, double-blinded, controlled trial examined the efficacy and safety of 1αD2 use in 138 hemodialysis patients with moderate to severe secondary hyperparathyroidism by using novel dose titration; 99 patients completed the study. Hemodialysis patients with secondary hyperparathyroidism were enrolled onto this study, consisting of washout (8 weeks), open-label 1αD2 treatment (16 weeks), and randomized, double-blinded treatment with 1αD2 or placebo (8 weeks). Oral 1αD2 was administered at each hemodialysis session, with doses titrated to achieve target iPTH levels of 150 to 300 pg/mL. Baseline iPTH levels (897 ± 52 [SE] pg/mL) decreased by 20% ± 3.4% by week 1 (P < 0.001) and by 55% ± 2.9% at week 16; iPTH levels returned to baseline during placebo treatment but remained suppressed with 1αD2 treatment. In 80% of the patients, iPTH level decreased by 70%, reaching the target level in 83% of the patients. Grouping patients by entry iPTH level (<600, 600 to 1,200, and >1,200 pg/mL) showed rapid iPTH suppression in the group with the lowest level; greater doses and longer treatment were required in the group with the highest level. During open-label treatment, serum calcium and P levels were 9.2 ± 0.84 (SD) to 9.7 ± 1.05 mg/dL and 5.4 ± 1.10 to 5.9 ± 1.55 mg/dL, respectively. During double-blinded treatment, serum calcium levels were slightly greater with 1αD2 than placebo, but P levels did not differ. During double-blinded treatment, 3.26% and 0.46% of serum calcium measurements exceeded 11.2 mg/dL with 1αD2 and placebo, respectively (P < 0.01); median level was 11.6 mg/dL during hypercalcemia. Intermittent oral 1αD2 therapy effectively suppresses iPTH in hemodialysis patients with secondary hyperparathyroidism, with acceptable mild hypercalcemia and hyperphosphatemia.

Alterations in growth, haematopoiesis and serum chemistry profiles infitness 1 4226SB mutant mice

We investigated patterns of growth, haematopoiesis and alterations in serum chemistry profiles that were associated with anN-ethyl-N-nitrosourea-induced mutation in thefitness 1 locus in chromosome 7 in mice. Mice hemizygous for thefit 1 mutation [c fit 14226SB/Df(c Mod2 sh1)VT] had growth retardation characterised by decreased body weights, shorter body lengths and tail lengths at 40 and 60 days of age compared to normal homozygous control mice [cch+/cch+]. Haemograms revealed that mice hemizygous for thefit 1226SB mutation that were killed at 40 days had microcytic, hypochromic anaemia that was mildly regenerative in nature. No significant differences were detected in total leucocyte counts, differential leucocyte counts and platelet counts between hemizygous mutant mice and control mice. Haemograms from the surviving mice hemizygous for thefit 14226SB mutation that were killed at 60 days indicated that the haemoglobin concentrations, mean corpuscular volumes and mean corpuscular haemoglobin concentrations were significantly decreased compared to normal controls. The reticulocyte counts and the platelet counts from the mice hemizygous for thefit 14226SB mutation were mildly increased compared to normal controls killed at 60 days. Serum chemistry analyses at 40 days of age indicated that the hemizygousfit 1 mutant mice had hypoproteinaemia characterised by hypoalbuminaemia and hypoglobulinaemia. They also developed hypoglycaemia, mild hyperphosphataemia and moderate elevation in the activity of alkaline phosphatase in serum. Quantitative isozyme analysis indicated that the increase in total serum alkaline phosphatase activity in the hemizygous mutant mice was due to an increase in the bone isozyme. In addition to those alterations in the serum chemistry profile noted above, hemizygous mutant mice killed at 60 days had an extremely mild increase in urea nitrogen concentration and mildly increased activities of alanine aminotransferase and aspartate aminotransferase in serum. From these data, it was concluded that thefit 14226sb mutation m mice causes growth retardation, microcytic, hypochromic anaemia, and alterations in serum chemistry profiles that suggest lesions in one or more organ system(s). The exact mechanism(s) by which thefit 14226SB mutation mediates these lesions remains to be elucidated.

老年者慢性腎不全における代謝性アシドーシスの特徴について

The present study was designed to clarify the characteristics of metabolic acidosis in aged patients with chronic renal failure. The subjects consisted of ambulatory cooperative patients (19 males and 18 females). Their values of creatinine clearance (Ccr) varied from 6.8 to 107.5 ml/min/1.73 m2. The relationship of Ccr to acid-base and electrolyte disturbances was investigated. The estimations of normal values in acid-base and electrolyte composition were based on the method of Hoffmann. The results are summarized as follows: 1. A high incidence of metabolic acidosis was demonstrated in patients whose Ccr values were below 20 ml/min/1.73 m2. 2. A significant positive correlation of Ccr values and plasma levels of bicarbonate (p less than 0.001) and a significant inverse correlation of Ccr values and serum levels of chloride (p less than 0.01) were observed. 3. The values of the anion gap did not change, irrespective of Ccr values. 4. Serum concentrations of potassium were inversely correlated with plasma levels of bicarbonate (p less than 0.01). Hyperchloremic normal anion gap acidosis with hyperpotassemia was the characteristic feature of metabolic acidosis in aged patients with chronic renal failure. The normal anion gap could be explained by normophosphatemia or mild hyperphosphatemia, even in the patients with advanced renal failure.

Renal Abnormalities in Sickle Cell Disease

Many renal structural and functional abnormalities have been associated with sickle cell disease. The patients have an impaired urinary concentrating ability but an intact diluting capacity. There are defects in both urinary acidification and potassium excretion, although overt metabolic acidosis and hyperkalemia occur infrequently. Proximal tubular function is supranormal, as manifested by increased reabsorption of phosphate and increased secretion of creatinine. The former results in mild hyperphosphatemia, while the latter causes substantial overestimation of the glomerular filtration rate (GFR) by creatinine clearance. Both GFR and renal plasma flow are increased in young patients with sickle cell disease, but prostaglandin inhibitors decrease the GFR. The GFR progressively decreases with increasing age. Proteinuria, and even nephrotic syndrome, are relatively frequent; the most common renal lesion in children is focal glomerular sclerosis, which may be associated with progressive deterioration in renal function. Glomerular hyperfiltration has been implicated in the pathogenesis of the glomerular lesions, as well as in the development of renal failure. In patients with end-stage renal disease, both hemodialysis and kidney transplantation have been successful. Recurrent hematuria is a relatively common problem in patients with sickle cell disease. The bleeding usually remits spontaneously, but occasionally requires therapy with aminocaproic acid. Papillary necrosis may occur, and is thought to result from medullary ischemia.

Primary hypoparathyroidism in the dog. Report of 15 cases and review of 13 previously reported cases.

Fifteen dogs with primary hypoparathyroidism diagnosed at the University of California Veterinary Medical Teaching Hospital were compared with 13 previously reported cases. Age, sex, breed, and historical and physical findings were similar in both groups of dogs. Middle-aged females were affected primarily. A history of neurologic or neuromuscular disease was present in all 28 dogs, with 18 dogs having seizures. Posterior lenticular cataract formation secondary to hypocalcemia was suspected in six dogs. The most characteristic biochemical finding in all dogs was profound hypocalcemia (less than 6.5 mg/dl) and mild hyperphosphatemia. Serum magnesium concentrations were decreased in two dogs. Serum parathyroid hormone concentrations were consistent with the diagnosis of primary hypoparathyroidism in eight of nine dogs. Lymphocytic parathyroiditis was diagnosed in the 12 dogs from which tissue was submitted for histopathology. Successful management of the patient depended on frequent monitoring of the serum calcium concentration during initial and maintenance therapy.

Exogenous Hyperthyroidism With Osteoporosis

Symptomatic osteopenia accompanied by subclinical hyperthyroidism developed in three women who were receiving excess thyroid hormone medication. Excessive thyroid replacement therapy resulted in mild hypercalcemia, hyperphosphatemia, and hyperphosphatasemia associated with diffuse skeletal demineralization and multiple fractures. Nondecalcified sections of double tetracycline-labeled iliac crest bone showed an accelerated rate of bone turnover with marked osteoclastosis and resorption of the cortical as well as the trabecular bone, typical of endogenous hyperthyroidism. Since thyroid hormones are among the most frequently prescribed medications, bone loss caused by exogenous hyperthyroidism may be more common than previously recognized.

Clinical Study of Pseudohypoparathyroidism Type I &amp; Type II

Pseudohypoparathyroidism (PHP) is a disorder characterized by renal and/or skeletal refractoriness to the effect of parathyroid hormone (PTH). In 1973, it was first proposed by Drezner et al that PHP could be divided into two types, e.g., PHP Type I and PHP Type II. PHP Type I is a disorder which fails to show the increase of urinary c-AMP and phosphaturia by the administration of PTH, but PHP Type II is that which responds to the administration of PTH with a marked rise of urinary c-AMP, but no increase of phosphate excretion, In 1974 Rodriguez et al demonstrated a patient with PHP Type II who restored normal renal responsiveness to PTH by calcium administration. Here we present two patients who fitted in the categories of PHP Type I & II, respectively, and restored normal renal responsiveness by the combined Ca-PTH administration or dibutyryl-cAMP infusion. Case I (PHP Type I) was a 31 yr old male with marked hypocalcemia and hyperphosphatemia, who showed neither increase of urinary c-AMP nor phosphate excretion in response to PTH infusion. Case II (PHP Type II), also diagnosed as Sjögren syndrome was a 22 yr old female with relatively mild hypocalcemia and hyperphosphatemia, who showed a marked rise of ordinary c-AMP, but no increase of phosphate excretion by PTH administration. Acute infusion of calcium, followed by PTH administration restored renal responsiveness to PTH in both types, though calcium infusion showed only little effects. The patient of PHP Type I received calcium gluconate and Vitamin D therapy and serum Ca improved, when PTH or DBc-AMP was given with the reappearance of PTH-like action. Thus in PHP Type I, the lack of c-AMP response to PTH, coupled with the ability of infused DBc-AMP to evoke a normal renal response suggests that the metabolic defect in this disorder may exist in hormone receptor-adenyl cyclase complex. Calcium infusion followed by PTH administration probably might evoke calcium influx and c-AMP production, resulting in the reappearance of hormone action. In PHP Type II, as c-AMP generation system is intact, the metabolic defect can be thought to exist in the rather poorly defined process beyond c-AMP generation. The combined Ca-PTH administration also restored normal renal response, probably partly due to the improved calcium environment of renal tubular cells. Though it is difficult to explain why endogenously generated c-AMP had no effect, but DBc-AMP had on reappearance of PTH-like action, it is speculated that DBc-AMP may have much more stronger effects for intracellular receptor site of c-AMP in PHP Type II. Conclusively these results clearly suggest that the nature of the metabolic defects in PHP is not a genetically determined inrreversible disorder, but rather a functional one which can be reversibly restored by special conditioning.