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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of acetate and bicarbonate dialysates on tolerance to dialysis have been examined in 30 patients with chronic renal failure (CRF). Symptomatic homeostatic impairment (nausea, vomiting, headache) and cardiovascular instability (tachycardia, arrhythmia, dyspnea) were less common (p less than 0.05) in bicarbonate dialysis. The cardiovascular symptoms correlated with antihypertensive effects of acetate (p = +0.48). Tolerance to ultrafiltration was better with bicarbonate dialysis. Gas chromatographic measurement of blood acetate concentrations in 7 patients on bicarbonate dialysis showed them to be 1.4 +/- 0.31 mmol/l at the beginning of dialysis treatment and 1.7 +/- 0.24 mmol/l at its end (normal, 1.7 +/- 0.14 mmol/l). Of 26 patients on acetate dialysis, 9 patients showed initial and late acetate concentrations of 1.7 +/- 0.26 and 2.5 +/- 0.23 mmol/l, respectively, while in 17 patients an initial concentration of 4.8 +/- 0.32 mmol/l rose to 9.0 +/- 1.1 mmol/l at the end of the treatment (p less than less than 0.01). Dialysis-induced complications had a higher incidence in the latter group (p less than 0.02). Acetate dialysis was poorly tolerated by 65% of the patients. The intolerance was aggravated by myocardial lesions and slow acetate turnover indicated by blood acetate concentrations above 7-8 mmol/l.
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PMID:[The effect of acetate and bicarbonate on the tolerance for hemodialysis therapy in chronic kidney failure]. 208 65

Intracranial pressure (ICP) was continuously monitored in a thirty-two-year-old female of acoustic neurinoma complicated with chronic renal failure. Severe headache with vomiting has begun to appear during hemodialysis for several months, prompting a diagnosis of an obstructive hydrocephalus. Continuous ventricular drainage was placed after admission and changes of ICP were monitored during hemodialysis. Dynamic changes of electrolytes, protein, sugar, urea nitrogen, and creatinine levels in the cerebrospinal fluid (CSF) as well as osmolarity were measured every one hour during the hemodialysis. An increment of ICP started to occur gradually after initiation of hemodialysis reaching the maximum value 23 minutes later. It was spontaneously decreased to the initial level 8 minutes later followed by fluctuations thereafter consisting of the changes of 20 to 30 mmHg. A remarkable rise in osmotic pressure in CSF has been observed corresponding to the rise of ICP which created a large difference from the blood osmotic pressure that consistently decreased following the onset of hemodialysis. Whereas, the absolute values of all measured factors including electrolytes and urea nitrogen in CSF have decreased consistently which did not seem to contribute intermittent increment of osmotic pressure of CSF. The cause of ICP increment in our case was considered mainly due to increase of water content in the brain tissue caused by the widening of osmotic gradient between the CSF and blood, although the substances responsible to the actual increase of CSF osmotic pressure remained unclear.
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PMID:[Elevation of intracranial pressure during hemodialysis--continuous measurement of cerebrospinal fluid pressure in a patient with acoustic neurinoma]. 220 42

Twenty-two infants (mean age 7.5 months) with chronic renal failure (CRF) were studied for their nutrition, growth, and upper gastrointestinal function. Most infants had a history of poor caloric intake and 7 had received supplemental feeding (SF) prior to the investigation. All infants were undergrown, underweight, and malnourished. The infants were characterized as having only a fair interest in food, refusing feedings, and vomiting excessively. Sixteen of 22 infants (73%) had significant gastroesophageal (GE) reflux demonstrated by 24-h esophageal pH monitoring. Gastroesophageal scintiscans were less sensitive and specific in detecting the reflux. Infants with GE reflux were significantly younger and more often required SF than those without GE reflux. There were no significant differences in the degree of renal failure, growth failure, caloric intake, protein intake, or nutritional status between the infants with and without GE reflux. From these studies we conclude that GE reflux should be considered as one of the factors contributing to the feeding problems of infants with CRF.
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PMID:Feeding disorders and gastroesophageal reflux in infants with chronic renal failure. 264 12

Animals with renal failure have a number of fairly predictable metabolic abnormalities. They are commonly presented to the veterinarian in a state of negative water balance, although prior fluid therapy in an oliguric patient may result in overhydration. Animals with oliguric ARF have sodium retention; those with polyuric ARF have increased urinary sodium loss. Chronic renal failure does not necessarily affect the ability of the renal tubule to conserve or excrete sodium, although the response to changes in sodium load is much slower than in the normal animal. Potassium retention occurs in oliguric ARF and potassium wasting in polyuric ARF; potassium balance is approximately normal in animals with CRF. Both ARF and CRF cause metabolic acidosis, although the acid-base status in a given animal will be affected by respiratory compensation, as well as other problems such as vomiting. Calcium levels are usually normal to slightly decreased in renal failure, whereas phosphorus levels are generally increased. The basic principles of fluid therapy should be used when constructing a plan for such therapy in an animal with renal failure. Intravenous administration of fluids is almost always necessary. The choice of the type of fluid, solutes, and electrolytes to be administered is based on the predicted abnormalities associated with renal failure as well as the laboratory abnormalities in the animal. Careful monitoring of the patient and periodic assessment of various laboratory parameters are necessary in order to make appropriate adjustments in fluid therapy.
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PMID:Fluid therapy for acute and chronic renal failure. 264 69

A 48-year-old man was admitted for treatment of Cushing's syndrome due to right adrenal adenoma, associated with chronic renal failure (CRF) with a blood urea nitrogen level of 64.2 and serum creatinine level of 3.9 mg/dl. After removal of the adrenal adenoma, the CRF deteriorated with progressive symptoms of anorexia, vomiting and hypertension, and the patient was placed on hemodialysis. Prior to adrenalectomy, the 17 OHCS and 17 KGS in the urine were not so high. However, the urinary 17 KS was high with an elevated 11-oxy fraction. In comparison with 2 patients suffering from adrenal Cushing's syndrome with normal renal function, there were no large accumulated quantities of glucuronic conjugated and unconjugated metabolites in the plasma of the CRF Cushing's syndrome, with confirmation ascribable to the radioimmunoassayable cross-reactivity of the cortisol antiserum used in the radioimmunoassay kit. In the Cushing's syndrome with CRF, almost all the cortisol, which was hypersecreted from the adenoma, was presumed to be converted to the 11-oxy fraction of 17 KS, possibly by activation of hepatic enzymes.
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PMID:Cortisol and its metabolites in the plasma and urine in Cushing's syndrome with chronic renal failure (CRF), compared to Cushing's syndrome without CRF. 279 94

A number of factors affect the concentration and distribution of magnesium in patients with chronic renal failure (CRF). Poor nutritional intake, impaired absorption from the intestine, vomiting, diarrhea, the use of diuretics and acidosis may result in a negative balance. More commonly, accumulation of magnesium may be the consequence of reduced renal excretion. Magnesium concentrations are increased in serum and red cells in CRF patients. Bone concentrations and total body magnesium also appear to be increased; muscle magnesium does not appear to be increased. Use of magnesium hydroxide-containing antacids as phosphate binders in patients with CRF was largely discontinued 2 decades ago after reports described increases in serum magnesium concentrations to toxic levels. More recently, the undesirable effects of aluminum-containing phosphate binders (encephalopathy, osteomalacia) have led several investigators to report favorable experiences using low concentrations of magnesium in dialysate and a combination of magnesium and aluminum-containing antacids, as phosphate binders, while closely monitoring serum magnesium concentrations.
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PMID:Chronic renal failure and magnesium metabolism. 380 22

A case of intramural esophageal hemorrhage in a hemodialysis patient is described. The hemorrhage followed an episode of vomiting and violent retching. Spontaneous resolution occurred with conservative management. The clinical course resembled that of previous case reports of intramural esophageal hemorrhage, whether or not associated with chronic renal failure and intermittent hemodialysis.
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PMID:Intramural esophageal bleeding in a hemodialysis patient. 443 94

Prostaglandin E2 is known to stimulate erythropoiesis by different mechanisms. A clinical trial of prostaglandin E2 to stimulate erythropoiesis in four patients with anemia of end stage renal disease resulted in an increment in peripheral blood Burst Forming Units-Erythroid (BFU-E). This increase in erythroid progenitors returned to baseline with cessation of therapy. A significant increase in serum erythropoietin (EPO) activity was demonstrated in one patient and was noticeable in another. Side effects mainly consisted of local pain at the site of the infusion and vomiting.
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PMID:A clinical trial of prostaglandin E2 to increase erythropoiesis in anemia of end stage renal disease. A preliminary report. 637 77

Chronic renal failure was diagnosed in 6 young Standard Poodles from 2 related litters. Clinically, the disease was characterized by polydipsia, polyuria, anorexia, lethargy, vomiting, and bony deformities suggestive of fibrous osteodystrophy. Laboratory evaluation revealed azotemia and hypercholesterolemia in all 6 dogs and nonregenerative anemia in 3 dogs. Two dogs had hyperphosphatemia and another 2 were hypercalcemic. Isosthenuria and proteinuria were found in both dogs for which urinalyses were available. The kidneys were characterized pathologically by interstitial fibrosis, variable interstitial infiltrates of lymphocytes and plasma cells, tubular atrophy, tubular dilatation, tubular basement membrane mineralization, cystic glomerular atrophy, and immaturity of glomeruli, with inconspicuous capillary lumens.
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PMID:Juvenile renal disease in related Standard Poodles. 662 80

The effects of sequential prostacyclin infusions at 2, 4, and 8 ng/kg/min for 1 hr were determined in six patients with chronic renal failure. Diastolic blood pressure decreased in a dose-dependent fashion from 74 +/- 4 mm Hg (mean +/- SEM) to 70 +/- 4, 66 +/- 5, and 55 +/- 5 during the 2, 4, and 8 ng/kg/min infusions, respectively; systolic blood pressure was not affected by prostacyclin. The fall in diastolic blood pressure was associated with a progressive rise in heart rate from 77 +/- 3 to 91 +/- 4 bpm and lowering of body temperature from 36.7 +/- 0.1 to 36 +/- 0.2 degrees. The threshold concentration of adenosine diphosphate that evoked reversible and irreversible platelet aggregation increased progressively from 1.2 to 2.8 and from 2.8 to 6 microM, respectively, during the prostacyclin infusions. Prostacyclin infusions had no effect on prothrombin time, activated partial thromboplastin time, or platelet count, but template bleeding time increased (not statistically significantly) from 5.8 to 12.3 min. In three of six patients, the 8 ng/kg/min infusion was terminated prematurely due to nausea, vomiting, and/or hypotension. We conclude that platelet aggregability can be inhibited in patients with chronic uremia by infusing 4 ng/kg/min prostacyclin without causing untoward side effects. When infused at hemodynamically tolerable doses, prostacyclin might serve as an in vivo inhibitor of platelet aggregation during hemodialysis or cardiopulmonary bypass.
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PMID:Effects of prostacyclin infusion in uremic patients: hematologic and hemodynamic responses. 701 91


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