Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Classic renal tubular acidosis is characterized by a primary defect in establishment of a large hydrogen ion gradient across the distal renal tubule. Thus the development of hyperchlorenic metabolic acidosis follows. In addition, hypokalemia results from renal potassium wasting secondary hyperaldosteronism from sodium wasting and contraction of the extracellular fluid. The presenting signs and symptoms are growth retardation, fatigue, periodic paralysis, polyuria, polydipsia, vomiting and constipation as well as nephrocalcinosis and nephrolithiasis. It is suggested that effective treatment with alkali therapy requires markedly higher doses than formerly recommended, and may related to a higher rate of endogenous acid production from (1) intermediary metabolism of sulfur amino acids and organic acids, (2) impaired tubular reabsorption of bicarbonate and (3) hydrogen ion release from hydroxyapatite formation. It is also suggested that acidosis may interfere with vitamin D metabolism and thus play an important role in the pathoetiology of the growth failure in children with this disorder.
Nephron 1979
PMID:Acid-base, calcium, potassium and aldosterone metabolism in renal tubular acidosis. 3 60

The effects of synthetic salmon CT, administered subcutaneously and intermittently (1 MRC U/kg/day for 15 days/month over 6 months) were investigated in 15 uremic patients on regular dialysis treatment (RDT), all presenting various degrees of osteodystrophy. Clinically, osteoarticular pain disappeared in 8 out of 10 cases; 1 patient with rib fractures had a rapid calcification of the bone fracture repair tissue. No significant changes were found in serum calcium and PTH levels. Phosphotemia showed a significant decrease within the first 20 days. The varying individual hypophosphatemic response proved to be related to the initial level of phosphatemia. The alkaline phosphatase, when increased, showed a decrease to the normal range. A significant decrease in osteoclastic hyperactivity (active resorption surface, osteoclast index) and a slight increase in osteoblastic pool (active osteoid surface) were documented. No change was noted when osteomalacia predominated. Side effects included: anorexia, nausea, vomiting, face flushing. Our data suggest that salmon CT may be usefully employed in chronic uremic patients on RDT, when secondary hyperparathyroidism predominates.
Nephron 1979
PMID:Effect of calcitonin on bone lesions in chronic dialysis patients. 49 16

The effect of acute ethanol administration into the cerebral ventricles on the unanesthetized cat upon emesis produced by norepinephrine and clonidine injected similarly as well as upon emesis evoked by copper sulfate given orally was compared and investigated. Ethanol inhibited the norepinephrine- and clonidine-induced emesis. The inhibitory effect of ethanol occurred after a transient and inconsistent emetic action of the drug. Norepinephrine-induced emesis was about 12 times more sensitive than clonidine-induced emesis to the inhibitory effect of ethanol. In addition, norepinephrine-, but not clonidine-induced emesis was abolished after ablation of the area postrema. On the contrary, intracerebroventricular ethanol had virtually no effect on emesis caused by intragastric copper sulfate. The inhibitory effect of ethanol is ascribed to an action on alpha-2 adrenoceptors within the area postrema and on imidazoline-preferring sites and/or muscarinic cholinoceptors outside the area postrema, but not on the emetic region of the brainstem reticular formation. It follows then that ethanol can differentiate alpha-2 adrenoceptors from imidazoline-preferring sites and/or muscarinic cholinoceptors in the brain of the cat.
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PMID:Differential inhibition by ethanol of norepinephrine- and clonidine-induced emesis in cats. 141 63

Symptoms were evaluated in 13 haemodialysis patients at dialysate temperatures between 37 and 35 degrees C. After a control period at 37 degrees C (stage 1) dialysate flow rate was increased from 300 ml/min in half the patients but no change in temperature was made (stage 2). In stage 3 dialysate temperature was reduced to 36.5 degrees C and in stage 4 to 35 degrees C. Blood pressure and temperature were measured pre- and post dialysis and patient completed a questionnaire indicating if they experienced any of nine specified symptoms: itch, restless legs, nausea, vomiting, headache, cramp, lethargy, hypotension and change in temperature. Trial stages were compared with chi 2 analysis using Yates correction. Symptoms per dialysis fell from 1.11 to 0.71 between stage 1 and 2 (p less than 0.0005). This was considered to be a trial effect. There was no further significant improvement in symptoms overall as the temperature was reduced to 35 degrees C. However, if complaints of coldness are excluded, there was a progressive reduction in symptoms from stage 1 to stage 4. Dialysate flow rate did not affect symptom reporting. There was no effect on body core temperature or blood pressure due to cool dialysate. Our results suggest there may be some benefit in lowering the dialysate temperature but this is small in relation to the placebo effect. Caution must be used in assessing similar studies using small numbers of dialyses.
Nephron 1989
PMID:Assessment of the symptomatic benefit of cool dialysate. 266 42

Nonspecific symptoms are common in dialysis patients but few methods are available to measure their severity and their response to alteration in dialysis therapy. To determine the clinical features and measure the severity of the most important symptoms in end-stage renal disease (ESRD) patients, 97 dialysis patients were interviewed, 63 of whom were reinterviewed 1 year later. For comparison 82 transplant recipients were also interviewed. The six most important symptoms in dialysis patients (using the product of the patient's perception of severity and prevalence) were tiredness, cramps, pruritus, dyspnea, headaches and joint pain. The symptoms were long-standing, occurred frequently, with little difference in prevalence between hemo- and peritoneal dialysis patients, and were often unrelated to a hemodialysis session. For each symptom, several dimensions of severity were assessed including frequency, duration, effect on sleep, daily living, activity, subjective quality of life and necessity for drug therapy. Often these dimensions did not correlate with patient's perception of severity. For each symptom these items were combined to give an aggregate score with a range 0-10. Interobserver reproducibility for each symptom score was greater than or equal to 0.7 but intraobserver reproducibility was poor for 3 symptoms, because of the fluctuating nature of the symptoms. Construct validity was demonstrated by finding a significantly worse distribution of aggregate scores for tiredness, cramps, pruritus, dyspnea and nausea/vomiting in dialysis compared to transplant patients. Aggregate scores changed little after 1 year's follow-up in stable dialysis patients but significant improvement in the aggregate scores for tiredness, dyspnea and nausea/vomiting were observed in 14 patients after successful transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1988
PMID:Clinical features and severity of nonspecific symptoms in dialysis patients. 306 60

The first case of spontaneous perforation of the esophagus during hemodialysis is reported. This occurred in a 73-year-old patient, following vomiting, which he frequently experienced during dialysis.
Nephron 1985
PMID:Perforation of the esophagus (Boerhaave's syndrome) during hemodialysis. 401 Aug 54

The effects of high sodium 144 mmol/l (mEq/l) dialysate were studied in normotensive, hypertensive and anephric chronic hemodialysis patients. Comparisons of blood pressures, weights and side effects associated with the hemodialysis procedure were made between two 6-month periods using dialysate sodium concentration of 133 mmol/l (mEq/l), followed by a high dialysate sodium of 144 mmol/l (mEq/l), each patient acting as his own control. No difference was found in the frequency of cramps or 'disequilibrium' side effects (nausea, vomiting, headache, restlessness). High sodium dialysate is beneficial for normotensive and anephric patients in reducing dialysis-induced hypotension and was not associated with any deleterious effects on long-term blood pressure control. In hypertensive patients, the benefit is less clear, and hypertension may increase.
Nephron 1985
PMID:Effects of high sodium dialysate during maintenance hemodialysis. 403 43

The purpose of the present study was to develop a controllable experimental model in the dog that would consistently and predictably produce a malignant hypertensive crisis, and to determine the sequential changes in renal function, salt and water balance, and hormones that are involved in the transition from benign to accelerated hypertension. Norepinephrine (NE) was infused continuously into the renal artery of unilaterally nephrectomized dogs that were maintained on 50 mEq sodium/day. The infusion rate of NE was increased each day according to the following schedule: 0.05, 0.1, 0.2, 0.3, 0.4, and 0.5 microgram/kg/min. During the first 4 to 5 days of intrarenal NE infusion, there was a progressive decrease in glomerular filtration rate (GFR) and effective renal plasma flow (ERPF), and increases in plasma renin activity (PRA), mean arterial pressure (MAP), and filtration fraction. At the end of this period of benign hypertension, MAP had risen from a control value of 91 +/- 4 to 132 +/- 8 mm Hg, in association with approximately a 10-fold increase in PRA and a 40% reduction in renal function. Then, suddenly, during the subsequent 24-hour infusion period, the MAP increased abruptly in all animals (MAP = 156 +/- 8 mm Hg), and a hypertensive crisis occurred. This crisis was associated with the following: salt and water depletion, hyponatremia, hypovolemia and hemoconcentration, polydipsia, marked activation of the renin-angiotensin-aldosterone system, increased plasma cortisol concentration, hemolysis, marked impairment in renal function, lethargy, and vomiting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Malignant hypertensive crisis induced by chronic intrarenal norepinephrine infusion. 637 96

A 6-year and 8-month-old boy on chronic intermittent peritoneal dialysis for end stage kidney disease presented with severe diarrhea, abdominal distension, cramps, tenesmus and vomiting. Barium enema showed rigidity and irregularity of the mucosa of the sigmoid and distal descending colon, with 'thumb print like' appearance, findings compatible with ischemic colitis. The institution of hemodialysis and discontinuation of the peritoneal dialysis resulted in a marked clinical and radiological improvement. Kidney transplantation performed a month later was associated with a complete cure of his intestinal disease.
Nephron 1984
PMID:Ischemic colitis in chronic intermittent peritoneal dialysis. 670 19

We have encountered a sporadic form of aseptic peritonitis, not previously described, that we refer to as acute sterile peritonitis (ASP). This syndrome, which occurs with a frequency of 0.1% of dialyses, begins abruptly during peritoneal dialysis with abdominal pain, fever, and occasionally chills and vomiting. Coincident with the onset of symptoms, the dialysate return becomes cloudy with many white blood cells. Cultures are negative and resolution occurs within hours with continued dialysis. In this report we detail the clinical features of this new syndrome.
Nephron 1982
PMID:Acute sterile peritonitis. 709 27


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