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Clinicopathologic findings were retrospectively evaluated in 26 cats and 24 dogs with ethylene glycol intoxication. Common clinical signs were ataxia, depression, vomiting, and hypothermia. Characteristic alterations in the hemogram and serum chemical profile included neutrophilia, lymphopenia, azotemia, hyperphosphatemia, hypocalcemia, hyperglycemia, and decreased whole blood bicarbonate. Common urinalysis findings included isosthenuria, proteinuria, glucosuria, hematuria, calcium oxalate and hippurate crystalluria, and the presence of renal epithelial cells, white blood cells, and granular and cellular casts in the urine sediment. The high death rate (78%) was attributed to delays in presentation, diagnosis, and therapy.
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PMID:Clinicopathologic findings in dogs and cats with ethylene glycol intoxication. 669 34

Lethargy, anorexia and vomiting suggest azotemia in cats with FUS. Clinicopathologic findings may include azotemia, hyperphosphatemia, hyperglycemia, hyperkalemia, and signs of urinary tract inflammation on urinalysis. Treatment of FUS depends on the degree of illness but generally includes removal of the urethral obstruction, bladder lavage, fluid and antibiotic therapy, and subsequent feeding of a canned, low-Mg diet with added table salt.
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PMID:Management of acute illness in cats. Feline urologic syndrome. 673 7

Renal failure was diagnosed in 22 young Doberman Pinscher dogs. The clinical findings were anorexia, weight loss, vomiting, lethargy, polydipsia, polyuria, and dehydration. Laboratory findings were azotemia, hyperphosphatemia, lymphopenia, nonregenerative anemia, hypercholesterolemia, and proteinuria. The kidneys were characterized pathologically by glomerular sclerosis, cystic glomerular atrophy, tubular dilatation, tubular atrophy, mononuclear interstitial inflammation, interstitial fibrosis, interstitial mineralization, and hyperplasia of the collecting duct epithelium.
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PMID:Juvenile renal disease in Doberman Pinscher dogs. 683 84

Phosphorus abnormalities among patients suffering from eating disorders, although cited, have received relatively little attention. Studies generally report decreased concentrations of phosphorus for both bulimia and anorexia nervosa. We have recently noted hyperphosphatemia in several consecutive hospitalized bulimic patients who appeared to have normal renal function and calcium levels. Case files of 30 inpatient and outpatient female bulimic patients and 30 sex- and age-matched physically healthy psychiatric inpatients and outpatients were reviewed. Phosphorus and electrolytes related to phosphorus metabolism were compared between the two groups. Twenty-four of 30 bulimic patients (80%) were found to have at least one elevated serum phosphorus concentration, whereas all but one of 30 age-matched controls had values within normal limits. Elevated phosphorus levels were generally in the mild to moderate range. No correlation was found between phosphorus levels and any of the other electrolytes examined in both patients and controls. No correlation was found between phosphorus levels and the reported frequency of bingeing and vomiting or the number of laxatives ingested. Since bulimic patients are generally of normal weight and tend to deny their disturbed eating habits, diagnosis is often delayed. However, bulimia may be suspected from biochemical abnormalities such as hypokalemia, hypochloremia, elevated amylase, and acid-base disturbances. This preliminary study indicates that elevated serum phosphorus levels may serve as an additional objective marker for the presence of bulimia nervosa.
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PMID:Hyperphosphatemia: an objective marker for bulimia nervosa? 764 49

Tetracyclines have been used as in vivo indicators of new bone formation because they form complexes with mineral at bone-forming surfaces. Four of 12 dogs in a bone-labeling study developed clinical signs of renal disease (vomiting, diarrhea, dehydration, and azotemia) within 1 to 2 days of receiving oxytetracycline at a bone-labeling dose of 25 mg/kg of body weight, once daily for 2 consecutive days. To delineate the relationship between oxytetracycline administration and renal damage, six dogs were given the bone-labeling dose intravenously and were subsequently evaluated by determination of clinical signs, serum biochemical analysis, urinalysis, and histologic examination (experiment 1). Drug administration was modified in the five dogs remaining in the bone-labeling orthopedic study. These dogs received the oxytetracycline dose as a slow intravenous infusion diluted with 250 ml of lactated Ringer's solution (experiment 2). All six dogs of experiment 1 developed persistent isosthenuria within 2 days of receiving the bone-labeling dose of oxytetracycline. Clinical illness (three of six dogs) was associated with azotemia, creatinemia, and hyperphosphatemia. All dogs had multifocal, mild to moderate flattening of renal tubular epithelium, characteristic of nephrosis. None of the dogs of experiment 2 developed any clinical indications of renal disease, and the only biochemical abnormality was isosthenuria in two of the five dogs. Thus the development of clinical signs and biochemical abnormalities associated with the intravenous administration of oxytetracycline was obviated by the slow administration of a dilution of the calculated bone-labeling dose of the antibiotic.
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PMID:Oxytetracycline-induced nephrotoxicosis in dogs after intravenous administration for experimental bone labeling. 890 81

Thirty-four patients, aged 3 to 17 years, were randomized to receive oral sodium phosphate solution or a polyethylene glycol-based solution in preparation for elective colonoscopy. Nineteen patients received two doses of oral sodium phosphate solution (45 mL/1.7 m2/ dose) and 15 received polyethylene glycol-based solution (4 L/1.7 m2). Compliance with oral sodium phosphate solution was judged as easy or tolerable in 15 of 19 patients, but only in 5 of 15 who were given polyethylene glycol-based solution. The quality of colon cleansing was rated by an endoscopist who was blinded to the colon preparation method used. The bowel preparation was excellent or good (only liquid remaining in the colonic lumen) in 18 of 19 patients who received oral sodium phosphate solution and in 6 of 15 who received polyethylene glycol-based solution. The incidence of vomiting was similar in both groups, but abdominal pain occurred more frequently in the polyethylene glycol-based solution group. Hyperphosphatemia developed in patients who received oral sodium phosphate solution (serum phosphorus = 2.3 +/- 0.7 mmol/L (7.2 +/- 2.2 mg/dL; mean +/- SD), but only in 1 of 15 patients in the polyethylene glycol-based solution group. Patients did not exhibit symptoms of hyperphosphatemia and serum calcium concentrations were similar in both groups. In summary, oral sodium phosphate solution is better tolerated than polyethylene glycol-based solution for bowel preparation in children. However, hyperphosphatemia occurred frequently in patients who received oral sodium phosphate solution. Further studies are needed to determine the optimal dose for safety and efficacy for the use of these solutions in children.
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PMID:Comparison of oral sodium phosphate to polyethylene glycol-based solution for bowel preparation for colonoscopy in children. 898 50

Forty-six patients were randomized to receive either 45 or 90-ml oral sodium phosphate (NaP) (Fleet Phospho-Soda), or X-Prep (a Senna preparation) before elective colonoscopy to compare the quality of colon cleansing, ease of preparation, and gastrointestinal intolerance. Before colonoscopy, one of us administered a questionnaire to the patient to assess how well the preparation was tolerated (scale from 1 to 5: 1 = easy, to 5 = unable to finish) and about the presence of four symptoms:abdominal pain, nausea, vomiting, and dizziness. The quality of colon cleansing was graded by two gastroenterologists (1 = excellent, 2 = good, 3 = fair, 4 = poor), who were unaware of how the patient was prepared or tolerated the preparation. The overall quality of bowel preparation with 90-ml oral NaP was better than with X-Prep and 45-ml NaP (p < 0.01). Patients found preparation with NaP to be easier than X-Prep (p < 0.002). No difference was seen in the incidence of abdominal pain, nausea, vomiting or dizziness. In the 90-ml NaP group, a significant rise in sodium and chloride occurred. However, increments were not greater than 5%. Hyperphosphatemia was noted with NaP, but was transient, and no concomitant decrease in calcium was seen. We conclude that, in the groups of patients studied, 90-ml NaP is a safe colonic cleansing agent that is better tolerated and more effective than others.
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PMID:A randomized prospective trial comparing 45 and 90-ml oral sodium phosphate with X-Prep in the preparation of patients for colonoscopy. 979 53

Patients with end-stage renal disease commonly develop secondary hyperparathyroidism. Calcitriol may be administered to such patients to decrease the synthesis and secretion of parathyroid hormone (PTH) and to help maintain calcium and phosphorus homeostasis. However, the doses of calcitriol required to suppress serum PTH concentrations can lead to hypercalcemia or hyperphosphatemia in many patients undergoing hemodialysis. Paricalcitol is a new vitamin D analogue that is safe and effective in suppressing elevated concentrations of PTH in patients with established hyperparathyroidism who are maintained on chronic hemodialysis. As with vitamin D, the biologic action of paricalcitol is mediated through activation of the vitamin D receptor (VDR). The VDR functions as a ligand-induced transcription factor regulating the rate of expression of genes that are involved in controlling not only calcium homeostasis and bone remodeling but also hormone secretion, inhibition of cell growth, and induction of cell differentiation. In vitro studies have shown that paricalcitol inhibits PTH secretion from bovine parathyroid cells in a dose-dependent manner. Studies in renally insufficient rats demonstrated that paricalcitol caused approximately 10 times less elevation of serum calcium concentrations than calcitriol. In clinical studies, paricalcitol effectively decreased PTH by about 60% over a 12-week period. Mean serum concentrations of calcium were significantly increased but remained within the normal range. There were occasional (5/414 determinations) transient elevations in serum calcium above the upper limit of normal in some (5/401) patients. Serum phosphorus values did not change significantly compared with baseline, although they tended to be slightly higher in the paricalcitol-treated group than in the group receiving placebo. Elevations of the calcium-times-phosphorus product were relatively few but occurred more often in the paricalcitol than in the placebo group. The terminal half-life of paricalcitol was 5 to 7 hours in healthy subjects; in patients undergoing hemodialysis, it was 14 hours. Adverse events associated with paricalcitol use included, among others, chills, feeling unwell, fever, sepsis, palpitations, dry mouth, gastrointestinal bleeding, nausea, vomiting, edema, light-headedness, and pneumonia. Paricalcitol should be considered as an alternative to calcitriol in the treatment of patients who are undergoing maintenance hemodialysis for end-stage renal disease, as it has a decreased potential to induce hypercalcemia and hyperphosphatemia. Additional studies are required to determine the long-term effects of therapy.
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PMID:Paricalcitol, a new agent for the management of secondary hyperparathyroidism in patients undergoing chronic renal dialysis. 1032 13

A 42-year-old man came to our emergency room hyperthermic (oral temperature, 42.4 degrees C), diaphoretic, and delirious. Other findings included labile blood pressure, sinus tachycardia (heart rate, 138/min), tachypnea (respiratory rate 34/min), muscle rigidity, and incontinence. Two days earlier, he had gone to a local clinic with complaints of abdominal pain, nausea, and vomiting. Promethazine was prescribed, and this was the patient's only medication on admission. Laboratory studies showed leukocytosis, hypernatremia, metabolic acidosis, elevated creatinine phosphokinase level, elevated transaminase levels, azotemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and myoglobulinuria. The clinical and laboratory findings were characteristic of the neuroleptic malignant syndrome, with promethazine as the offending agent.
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PMID:Neuroleptic malignant syndrome due to promethazine. 1054 78

The acute tumor lysis syndrome (ATLS) is characterized by the rapid development of hyperuricemia, hyperkalemia, hyperphosphatemia, and acute renal failure (ARF). Hematologic malignancies are responsible for most cases of ATLS. Control of hyperuricemia and the achievement of a high urine flow are the mainstays of prevention. Urinary alkalinization should be performed only when hyperuricemia is present. Hypercalcemia occurs in 10% to 20% of patients with cancer at some time during the disease course. Parathyroid hormone-related protein (PTHrP) is the most common mediator of humoral hypercalcemia of malignancy (HHM), while local osteolysis is the principal mechanism in patients with bone metastasis. Hydration with saline and administration of pamidronate control hypercalcemia in most patients. Hyponatremia with an increase in total-body salt and water content, manifested as edema and/or ascites, is the most common electrolyte abnormality in cancer patients. Hyponatremia due to salt depletion may occur in patients who receive cisplatin. The syndrome of inappropriate antidiuretic hormone secretion (SIADH) may occur in association with cancer of the lung, after high-dose cyclophosphamide, and during vigorous fluid administration in patients with chemotherapy-associated emesis. Lactic acidosis without tissue hypoperfusion may be seen in patients with extensive liver metastasis or with certain hematologic malignancies. In the latter cases, lactate levels parallel disease activity and chemotherapy often leads to resolution of the lactic acidosis. Idiopathic hyperammonemia has been described after intensive chemotherapy for hematological malignancies and following bone marrow transplantation.
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PMID:Metabolic emergencies in the cancer patient. 1086 20


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