Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The starting point of cardiogenic shock is an extensive myocardial infarction. Through a backward and forward failure of the left ventricle a shock-specific disturbance of the microcirculation occurs with a reduction of the circulation in the periphery of the body and development of a tissue acidosis (metabolic acidosis). Fall in blood pressure and cardiac volume, congestion of blood in the region of the pulmonary vessels and signs of reduced circulation in the body periphery (severe physical weakness, apathy, cold and clammy skin, oliguria) determine the clinical picture of cardiogenic shock. Therapeutically, intra-aortal balloon counter-pulsation, possibly combined with a cardiosurgical intervention, has reduced the mortality of cardiogenic shock after acute myocardial infarction from 90--100% to 60--70%.
MMW Munch Med Wochenschr 1978 Dec 08
PMID:[Cardiogenic shock following acute myocardial infarction. Pathophysiology and clinical aspects (author's transl)]. 10 80

The acute intravenous and oral toxicity of single doses of paraquat dichloride was studied in the cynomolgus monkey. Renal handling and effects upon renal function were also investigated following an oral dose of [14C]paraquat. Clinical signs consisted of vomiting, anorexia and dyspnoea. By 48 h all animals showed signs of acute renal failure with oliguria, high plasma urea and SGPT levels and metabolic acidosis. Animals dosed orally showed similar, though less severe, signs to those dosed intravenously. The oral LD50 was approx. 70 mg paraquat cation/kg. Following an oral dose plasma levels peaked by 2 h, but were constant from 12 h to 24 h. Paraquat clearance was high initially and exceeded the creatinine and urea clearance, but fell off markedly after 14 h as renal failure developed. By 18 h urine production had ceased. It is concluded that acute renal failure and acute pulmonary damage are the main causes of death, with interstitial pulmonary fibrosis being a factor in animals surviving the acute phase.
Toxicology 1979 Dec
PMID:The toxicity and renal handling of paraquat in cynomolgus monkeys. 12 Jun 23

Lithium intoxication was induced in rats by intraperitoneal administration of lithium chloride in a daily dose of 200 mg/kg (0.22 LD50) for 6 days. Polyuria connected with pathological changes in the epithelium of the convoluted tubules and depression of the antidiuretic hormone--acid mucopolysaccharides system in the area of the straight kidney tubules was observed on the 6th day of the experiments. Oligouria and death of some of the animals on the 7th experimental day was caused by severe lesions the kidney structure. Further observation (30 days) demonstrated that, along with the regeneration processes, there developed a marked sclerosing ofthe kidney tissue. A conclusion was drawn that severe lithium intoxication was associated with the development of acute renal insufficiency. Functional reserves of the kidneys after the cessation of lithium chloride administration remained lowered for a long period.
Biull Eksp Biol Med 1976 Dec
PMID:[Role of the kidneys in the pathogenesis of lithium poisoning]. 13 80

Fifty-nine patients were seen with oliguria in 1975. Forty had acute renal failure (ARF) and 19 rapidly reversible oliguria (RR). The causes of the oliguria were medical (64%), surgical (27%) and obstetrical (9%). The following were valuable in the assessment of patients with oliguria: urine sodium concentration (UNa) and osmolality, coagulation studies and high dose intravenous urography. Patients presenting with a high UNa or a coagulation abnormality were more likely to have ARF. Central venous pressure monitoring was helpful in the initial management but the administration of diuretics was not. Twenty patients with ARF were treated conservatively and the remainder by dialysis. Infection was both the commonest complication of ARF and the most frequent cause of death. Seventy percent of those with ARF died. Death was more common in the elderly or patients with a medical aetiology. The mortality of ARF remains high in spite of advances in the management of its metabolic and infective complications because of the acceptance of more high risk patients. An improved awareness of the preventable causes of oliguria is apparent.
N Z Med J 1977 Dec 28
PMID:Oliguria and its sequelae. 27 81

Urinary N-acetyl-beta-D-glucosaminidase (NAG) activities were measured in 181 patients with renal allografts during a 15-month period. Activities were high immediately after transplantation but decreased rapidly in the absences of complication. Urinary NAG activities increased by 50% or more in relation to 33 of 36 (92%) episodes of acute rejection diagnosed and treated by clinicians during the first 90 days after transplantation. The increase preceded clinical diagnosis in 70% of the cases, the median interval being 1.5 days. NAG activities decreased after treatment of rejection in 90% of the cases. Chronic rejection, renal vein thrombosis, renal artery stenosis, oliguria, hypotension, and the administraion of gentamicin may also cause increased NAG activity. Urinary NAG assay is simple and inexpensive, and is a useful aid to the early diagnosis of rejection of renal transplants. Results must, however, be interpreted by the clinician, bearing in mind other causes for increased activity.
Transplantation 1978 Dec
PMID:Urinary N-acetyl-beta-D-glucosaminidase assay in renal transplant recipients. 36 24

A 62-year-old man spread maneb on about 200 sq m of garden and subsequently was taken to the emergency clinic with complaints of oliguria, diarrhea, and hoarseness. Based on the clinicobiochemical data, he was found to have acute renal failure; the serum levels of BUN, creatinine, and potassium were 144.3 mg/dL, 14 mg/dL, and 5.8 mEq/L, respectively. The ST segment depression in V4-6, reciprocal ST segment elevation in V1-3, and inverted T waves in V5 and V6 were recorded on ECGs. Both the renal failure and the ECG abnormalities disappeared after hemodialysis. The possibility exists that the maneb caused the acute renal failure.
JAMA 1979 Dec 07
PMID:Acute renal failure and maneb (manganous ethylenebis[dithiocarbamate]) exposure. 49 Aug 86

Possible relation between the changes in the penicillin pharmacokinetics and coagulograms under the effect of trypsin in rats and man was analysed. It was found that parenteral administration of the enzyme was accompanied by a simultaneous increase in the penicillin blood level, oliguria, a decrease in the antibiotic amount excreted with urine and drop of the fibrinogen level in plasma. The latter is consequent on intravascular coagulation which results in temporary impairment of the excretion function of the kidneys defining the changes in the penicillin pharmacokinetics under the effect of trypsin.
Antibiotiki 1979 Dec
PMID:[Mechanism of the effect of proteolytic enzymes on antibiotic pharmacokinetics]. 51 51

Twenty infants and young children with hereditary fructose intolerance (HFI) were admitted to hospital. None was diagnosed at admission. Referals were for vomiting of unknown aetiology (16X), pyloric stenosis or hiatus hernia (5X), toxic condition (3X), and hepatomegaly of unknown origin (5X). Feeding difficulties (20X), vomiting (18X), and failure to thrive (16X) were leading symptoms. The most frequent clinical findings were hepatomegaly (18X), pallor (14X), haemorrhages (13X). Ascites, oliguria, tachypnoea, fever, splenomegaly and rickets were less frequent. Laboratory findings were indicative of disturbed hepatic and renal tubular function and also of disturbed intermediary metabolism (hypokaliaemia, hypophosphataemia). However, hypoglycaemia was found in only 4 out of 15 patients tested. Differential diagnosis after hospital admission centered on metabolic disorders such as glycogenoses, galactosaemia, tyrosinosis, or Wilson's disease. Hepatitis, toxic hepatosis, liver tumour, intrauterine infection and sepsis were also considered. Eleven children had first ingested fructose within the first 6 weeks of life. The diagnosis was usually established only many weeks or months after first fructose intake and appearance of symptoms. This documents how difficult the diagnosis of this disease can be both in practice and in hospital. The course was severe in 11 children and lethal in 4. In only 5 patients was the course mild. The 16 survivors are doing well under fructose-exclusion diet. Irreversible visual impairment after intraocular haemorrhage occurred once. In each case HFI could have been suspected immediately, had a detailed nutritional history been taken. Practising paediatricians should know the composition of commonly used infant formulae. They should never prescribe sugared condensed milk for intractable vomiting prior to excluding HFI. Solution for intravenous infusion containing fructose and sorbitol are life-threatening for undiagnosed HFI patients.
Helv Paediatr Acta 1978 Dec
PMID:Hereditary fructose intolerance in early childhood: a major diagnostic challenge. Survey of 20 symptomatic cases. 73

Described are six patients with acute renal insufficiency due to histologically proven massive lymphomatous infiltration of the kidneys. All patients were admitted to a renal intensive care unit over a period of six years. Oliguria was the presenting symptom in two of the patients. This complication of lymphoma is suggested by enlargement of the kidneys and mild proteinuria in the absence of other causes of uremia and can be demonstrated by renal biopsy. Local radiation therapy performed in two patients produced improvement of renal function.
Cancer 1976 Dec
PMID:Acute renal insufficiency due to lymphomatous infiltration of the kidneys: report of six cases. 79 11

Renal ischemia of 90 min duration provokes initial oliguria and hyperazotemia; however, in rats with high diuresis, with or without renal renin depletion, protection against acute renal failure is observed in this model. The protection is directly proportional to the diuresis.
Schweiz Med Wochenschr 1977 Dec 10
PMID:[Protection against acute renal insufficiency by means of forced diuresis in an ischemic rat model]. 92 53


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