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)

A 5-month-old, male, Shih Tzu dog manifesting polyuria and polydipsia since 2-month-old was presented to our hospital with additional clinical complaints of vomiting and depression during recent a few days. Despite the symptomatic therapy for chronic renal failure, he died on the day after medication. Macroscopically, both kidneys were small in size with rough surface. Microscopical examination revealed bilateral renal fibrosis with dysplastic changes consisting of immature glomeruli and tubules, and foci of adenomatoid proliferation of tubular epithelium. In addition, incomplete lobulation of medulla with pelvic structures was also noticed in the right kidney. From these findings, the present case was diagnosed as renal dysplasia in Shih Tzu dog which was documented in the literatures.
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PMID:Renal dysplasia in a Shih Tzu dog in Japan. 1171 30

A geriatric domestic shorthair cat was presented for evaluation of chronic vomiting. Chronic renal failure was diagnosed on the basis of physical examination findings and results of a serum biochemical profile and urinalysis. Endoscopically obtained gastric biopsies were suggestive of a carcinoid tumor. Subsequently, an exploratory celiotomy with partial gastrectomy was performed. Histopathological and electron microscopic analysis of surgical biopsy specimens confirmed the diagnosis of a gastric carcinoid, which has not been previously reported in the cat. Following complete excision, the cat remained clinically stable and free of signs of gastrointestinal disease for 4 months before requiring treatment for progressive renal failure.
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PMID:Chronic vomiting associated with a gastric carcinoid in a cat. 1180 17

Protein energy malnutrition in dialysis patients has been well-described in the literature. Most malnourished patients with end stage renal disease (ESRD) suffer from a mixed marasmus-kwashiorkor type of malnutrition with loss of both somatic and visceral protein mass. Malnutrition is associated with increased risk of morbidity and mortality. Up to 50% of patients on dialysis have protein energy malnutrition (Mortelmans & Vanholder, 1999). Malnutrition may be under-recognized and under-reported in dialysis patients. Malnutrition may result from inadequate food intake secondary to the uremic condition, nausea, vomiting, loss of appetite, altered taste and other physiologic conditions that impede food intake or metabolism. The usual indices of nutritional assessment--body weight, body mass index (BMI), anthropometrics, etc., may be inaccurate in patients with ESRD, as the results are often skewed by fluid retention. Therefore, we often rely on weight loss, bloodwork, a pre-dialysis low serum potassium, phosphorus and urea, as early signs of a decreased food intake. When patients are malnourished, measures such as oral supplements and/or tube feedings may be used to augment protein and calorie intake. However, when these interventions are inadequate to reverse the malnutrition condition, intradialytic parenteral nutrition (IDPN) should be implemented. Although there is no definite supportive data to show that the use of IDPN improves morbidity and mortality of dialysis patients, there are data to support that IDPN has positive effects on numerous nutritional parameters (Acchiardo, 2000; Capelli et al., 1994; Foulks, 1999; Hiroshige et al., 1998; Ikizler et al., 1995; Korzets et al., 1999; Mortelmans & Vanholder, 1999; Saunders et al., 1999; Smolle et al., 1995). In this article, we will discuss the causes of malnutrition in dialysis patients, the use of IDPN on one of our patients, and the potential complications associated with IDPN.
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PMID:The use of intradialytic parenteral nutrition to treat malnutrition: a case study. 1453 27

Ferric gluconate complex in sucrose (Ferrlecit) has been associated with less side-effects than iron dextran; however, the recommended dose of 62.5-125 mg per treatment is only suitable for haemodialysis (HD) patients. We retrospectively analysed the incidence of the side-effects associated with a high dose of Ferrlecit infusion (20 treatments in 13 patients; 10 treatments of 250 mg/3-4 h, and 10 treatments of 500 mg/5 h infusion). The patients were in the age range of 32-75 years old, seven with chronic renal failure (CRF), and six on dialysis treatment. One (10%) of the 10 treatments using a 250 mg dose was complicated with severe nausea/vomiting, diarrhoea and a burning sensation in the feet. Three (30%) of the 10 treatments using a 500 mg dose were complicated with: chills, severe nausea/vomiting, hypotension and syncope in one; severe nausea/vomiting, diarrhoea and hypotension in one; and an episode of vomiting in one patient. A single treatment with a 250 mg dose resulted in no significant change in haematological parameters. A single treatment with a 500 mg dose resulted in a significant increase in haemoglobin (Hgb) and haematocrit (Hct), but only a rising trend in serum iron,% transferrin saturation and ferritin pre versus 1-2 months postinfusion. In conclusion, Ferrlecit doses of 250 or 500 mg are complicated with significant untoward reactions in 10-30% of patients, in a dose-dependent fashion.
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PMID:Incidence of side-effects associated with high-dose ferric gluconate in patients with severe chronic renal failure. 1499 10

Hyperparathyroidism is a disease characterized by hypercalcemia with hypophosphoremia resulting from increased secretion of parathyroid hormone (PTH). The disease may be divided into 3 forms: a) primary, b) secondary, c) tertiary (secondary refractory form). Primary hyperparathyroidism is rare in children; hyperplasia is more frequent during the early years of life (neonates and infants) and is difficult to distinguish from adenoma in children. The disease may be asymptomatic; elevated calcemia levels (>12 <13.5 mg/dl) are accompanied by anorexia, asthenia and persistent stipsis; severely elevated concentrations (>13.5 mg/dl) are accompanied by nausea, vomiting, polyuria due to osmosis, with dehydration and progressive onset of lethargy, stupor and coma. Osteopenia or osteitis fibrosa cystica may be present due to augmented bone resorption. Height and weight increases are altered due to anorexia and dehydration. Differential diagnosis includes iatrogenic causes of hypercalcemia (excessive vitamin D intake, prolonged immobilization, etc.) and idiopathic familial hypercalcemia. Emergency treatment is required in cases of extremely elevated hypercalcemia (Ca >13.5-14 mg/dl), due to risk of injury to the heart, the central nervous system, the gastrointestinal tract and the kidneys. The 4 cardinal points of treatment are: hydration, calciuresis, inhibition of bone calcium resorption, treatment of the cause underlying hyperparathyroidism. Secondary hyperparathyroidism is found in cases where chronic hypocalcemia is present, particularly in chronic renal failure, untreated deficiency rickets, chronic intestinal malabsorption, hepatobiliary disease, types I and II vitamin D-dependent rickets, tubular acidosis or Fanconi's syndrome. The tertiary form is distinguished by the autonomous nature of the parathyroid glands which have become hypertrophic/hyperplastic due to uncontrollable, chronic severe renal failure. It can also be of iatrogenic origin due to excessive intake of inorganic phosphates in familial hypophosphatemic rickets or chronic vitamin D deficiency.
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PMID:Hyperparathyroidism. 1524 24

Renal failure remains a serious cause of mortality in Yemen. Our region has 1.25 million population and our hospital is the central hospital, which has a nephrology department and performs dialysis for the region. Between January 1998 and December 2002, we admitted 547 patients; including children, with acute renal failure (ARF) and chronic renal failure (CRF). CRF was observed in 400 patients, an incidence of 64 per million per year and a prevalence of 320 per million. ARF occurred in 147 persons with an incidence of 23.5 per million per year and a prevalence of 117.5 patients per million. Of all patients, 72% were adults (age range, 20-60 years) with a male preponderance. As a tropical country, malaria (27.9%), diarrhea (13.6%), and other infectious diseases were the main causes. Next most common were obstructive diseases causing CRF and ARF (26.8% and 12.9%, respectively), mainly urolithiasis, Schistosomiasis, and prostatic enlargement. However the cause of CRF in 57.5% of patients was unknown as most persons presented late with end-stage disease (64.7%), requiring immediate intervention. Other causes, such as hepatorenal syndrome, snake bite, diabetes mellitus, and hypertension, showed low occurrence rates. Patients presented to the hospital mostly in severe uremia and without a clear history of prior medications. The major findings were vomiting, acidosis, and hypertension with serum creatinine values ranging between 2.8-45 mg/dL (mean value, 13.4 mg/dL). Anemia was observed in 80.4% of CRF versus 62.6% of ARF patients. Hypertension prevalence was 65.5% among CRF patients, of whom 25% were in hypertensive crisis, whereas among ARF the prevalence was only 26.5%.
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PMID:Renal failure in Yemen. 1535 Apr 75

Uncorrected hypercalcemia can cause clinical signs such as polyuria, polydipsia, vomiting, diarrhea, lethargy, and depression and contributes to the development of primary renal failure and soft tissue mineralization. Treatment of hypercalcemia includes diagnosis and treatment of the underlying disease process and some combination of excracellular fluid volume expansion by administration of fluids intravenously and administration of glococorticosteroids, salmon calcitonin, and furosemide. Bisphosphonates such as pamidronate disodium also may be safe and effective in the treatment of hypercalcemia. The purpose of our study was to characterize the efficacy and safety of pamidronate in the treatment of hypercalcemia attritutable to several different disease processes in the dog and cat. Seven dogs and 2 cats were administered pamidronate at a dose of 1.05-2.0 mg/kg IV for a variety of disease processes, including neoplasia (n = 4), calcipotriene toxicity (n = 3), nocardiosis (n = 1), and idiopathic hypercalcemia with chronic renal failure (n = 1). In all the animals, IV pamidronate administration rapidly decreased serum calcium concentrations without evident toxicosis. Two animals received pamidronate several times without obvious toxicosis. On the basis of the findings in our retrospective study, pamidronate may be a safe and effective drug with which to lower both serum total and ionized calcium concentrations in patients with hypercalcemia arising from a wide variety of underlying disease processes.
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PMID:Uses and effectiveness of pamidronate disodium for treatment of dogs and cats with hypercalcemia. 1571 44

Glomerulocystic kidney was diagnosed in a 5-year-old female Shiba dog, which died from chronic renal failure with convulsions, vomiting and diarrhoea. Haematological examination revealed non-regenerating anaemia, azotaemia and high serum creatinine. Grossly, both kidneys were mildly atrophic with multiple small cysts in the cortex. Histopathological examination revealed marked dilatation of Bowman's space, often with glomerular atrophy or loss, and mild interstitial fibrosis. Bowman's basement membranes (BMs) were tortuous and thickened, with patchy calcification. Glomerulo-tubular junctions in the urinary pole side of the kidneys had a stenotic appearance associated with thickening of Bowman's BMs and calcification. Focal interstitial fibrosis around the glomerulo-tubular junction was also found. Continuity with the proximal tubule was evident in cystic glomeruli. Ultrastructurally, marked thickening of Bowman's BMs with many granular deposits in the urinary pole side was observed. The findings indicate that glomerular cystic changes may have developed as a consequence of glomerulo-tubular junctional stenosis due to thickened Bowman's BMs and focal periglomerular fibrosis in the urinary pole side of the kidneys.
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PMID:Glomerulocystic kidney in a domestic dog. 1602 37

Coxsackie virus infection may be life-threatening, although in most cases, it is asymptomatic. Coxsackie virus infection can cause rhabdomyolysis. This study reports a 39-year-old female patient with chronic renal failure who presented with fever, myalgia, anuria, edema, vomiting, diarrhea, exacerbation of renal function, elevation of serum CK, CK-MB, CK-MM, myoglobin, and liver function abnormality. Serology for Coxsackie virus IgM antibody was positive at first, and IgG antibody became positive 4 weeks later. Muscle biopsy showed skeletal muscle denaturalization and necrosis. She underwent hemodialysis three times per week and then kidney transplantation. No evidence suggests relapse of Coxsackie virus infection 5 months after transplantation. As illustrated with the present case, serological testing may reveal an early, quick, and simple diagnosis in a case of rhabdomyolysis after a viral illness.
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PMID:Rhabdomyolysis following recent severe coxsackie virus infection in patient with chronic renal failure: one case report and a review of the literature. 1652 25

(1) Patients who require dialysis for chronic renal failure develop phosphocalcium metabolic disorders that often lead to secondary hyperparathyroidism. Standard treatment consists of a phosphate chelator and vitamin D, along with the use of an appropriate calcium concentration in the dialysis bath, but is difficult to manage. (2) Parathyroid cancer is a rare malignancy frequently associated with hypercalcaemia. (3) Cinacalcet is a calcimimetic agent that reduces the parathormone level. Clinical evaluation includes more than a dozen dose-finding studies and clinical trials. The optimal dose seems to range from 30 to 180 mg/day and varies widely from one patient to another. (4) 3 double-blind placebo-controlled trials, lasting for a maximum of one year and involving a total of 1136 dialysis patients with chronic renal failure, showed no improvement in quality of life with cinacalcet. The target parathormone level was reached by 40% of patients on cinacalcet versus 5% of patients on placebo, while the effects of cinacalcet on calcium levels (-7%) and phosphate levels (-8%) were modest. No impact on bone complications is mentioned in available reports. (5) The assessment of treatment of parathyroid cancer is limited to one ongoing non comparative trial involving 21 patients. (6) During clinical trials, 11% of dialysis patients had low parathormone levels, creating a risk of adynamic bone disease and fractures, but available data are sparse. (7) Two-thirds of patients receiving cinacalcet have episodes of hypocalcaemia, which may in part account for reports of seizures (1.4% of patients), nausea (31%) and vomiting (27%). Many adverse effects seen in animal studies have not been adequately investigated in the clinical setting, such as an increase in the QT interval, thyroid disorders, and sexual dysfunction. Cinacalcet is a powerful CYP 2D6 inhibitor and is also metabolised by isoenzymes CYP 3A4 and CYP 1A2, creating an increased risk of drug interactions. (8) In practice, treatment with cinacalcet seems difficult to manage and to provide only limited benefits. Available assessment reports leave many questions unanswered, and this is a further reason not to use this product outside of clinical trials, either after failure of phosphate chelator and vitamin D therapy (especially as an alternative to surgery) or in parathyroid cancer.
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PMID:Cinacalcet: new drug. Secondary hyperparathyroidism: where are the clinical data? 1676 95


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