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)

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.
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PMID:Acid-base balance and plasma composition in the aestivating lungfish (Protopterus). 1 65

We report epidemiologic, clinical, laboratory, and biopsy findings in 14 cases of nephropathia epidemica. The patients were between 19 and 49 years of age. The onset of the disease was characterized by high fever, nausea, headache, backache, abdominal pain, proteinuria, oliguria, hematuria, and uremia. The symptoms subsided rapidly during the polyuria phase, which followed the oliguria stage. Because of renal failure, hemodialysis was required in eight cases. Edema of eyelids, conjunctival injection and hemorrhages, transitory myopia, and acute glaucoma were the most common eye abnormalities. Renal biopsy specimens showed glomerular changes, with mild swelling of the epithelial cells of Bowman's capsule, thickening of the basement membrane of glomerular capillaries, glomerular adhesions, inflammatory cell infiltration, leukocytoclasis and hemorrhages in the interstitium, and eosinophilic hyaline degeneration and vacuolization of the epithelial cells of the proximal tubuli.
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PMID:Nephropathia epidemica. The Scandinavian form of hemorrhagic fever with renal syndrome. 1 20

The spectrum of kidney and urinary tract disorders related to purines comprises acute hyperuricosuric nephropathy, chronic urate nephropathy and urolithiasis. Two factors in the development of acute hyperuricosuric nephropathy are increased uric acid concentration and low pH in the tubular fluid. Chronic urate nephropathy still possess several problems: incidence (although this seems to be decreasing, presumably owing to effective prevention), the source of interstitial urate, the cause of the interstitial deposition of urate, and the role of urate deposits in the pathogenesis of the interstitial nephropathy. The relation of the experimental nephropathy to the pathogenesis of chronic urate nephropathy in the human is not yet clear but a model is proposed according to which interstitial urate derives from two sources: hyperuricaemic plasma and hyperuricosuric tubular fluid. Urolithiasis related to purines leads to uric acid-urate stones, xanthine stones, 2,8-dihydroxyadenine stones, iatrogenic xanthine and oxipurinol stones, and possibly calcium stones. Pathogenetic factors in uric acid lithiasis are hyperuricosuria (whether due to an inborn enzyme abnormality or of unknown aetiology) and low urinary pH; oliguria is a contributory factor. There remain several open questions about uric acid lithiasis: incidence, the shift of its location from lower to upper urinary tract, the interplay of pathogenetic factors, and the role of compounds which inhibit crystallization.
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PMID:Implications of disorders of purine metabolism for the kidney and the urinary tract. 2 29

The single drug therapy of diazepam can be introduced to effectively control convulsions in eclampsia. This treatment will have particular application in rural obstetrics where eclampsia is seen in severe form. The dose schedule of diazepam, as described in this study, shows the therapy to have a stabilizing effect on hypertension and pulse rate. It causes neither respiratory depression nor oliguria. Diazepam is an effective muscle relaxant. Its depressive effect on the newborn is in no way inferior to that of lytic cocktail therapy. The drug is readily available at low cost, even in the remote rural areas, and can be easily administered by any doctor or midwife.
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PMID:Diazepam therapy in eclampsia. 4 87

The role of raised plasma renin and angiotensin-II concentrations in the development of acute renal failure in man was examined in patients in shock from various causes and in patients in whom hypotension was used to promote haemostasis. Ten of the thirteen patients in shock had raised angiotensin-II concentrations in peripheral blood and acute renal failure manifested by oliguria, increasing serum-creatinine, a urine osmolality of less than 400 mos-mol/kg and a urine/plasma osmolality ratio of less than 1-5. Although patients who were hypotensive for periods of 1 h 45 min to 4 h to promote haemostasis during surgery had similarly raised plasma-renin activity and angiotensin-II concentrations in peripheral venous blood, they did not have acute renal failure. It is concluded that high plasma-angiotensin-II concentrations do not explain the pathogenesis of acute renal failure in patients in shock.
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PMID:Plasma renin and angiotensin II in acute renal failure. 6 36

Seven children (aged 8--17 years) presented with a high fever, headache, confusion, conjunctival hyperaemia, a scarlatiniform rash, subcutaneous oedema, vomiting, watery diarrhoea, oliguria, and a propensity to acute renal failure, hepatic abnormalities, disseminated intravascular coagulation, and severe prolonged shock. One patient died, one had gangrene of the toes, and all have had fine desquamation of affected skin and peeling of palms and soles during convalescence. Five patients were studied prospectively. Staphylococcus aureus related to phage-group I was isolated from mucosal (nasopharyngeal, vaginal, tracheal), or sequestered (empyema, abscess) sites, but not from blood. This organism produces an exotoxin which causes a positive Nikolsky sign in the newborn mouse and which is biochemically, pathologically, and immunologically distinct from phage-group-II stapphylococcal exfoliatin.
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PMID:Toxic-shock syndrome associated with phage-group-I Staphylococci. 8 81

50 episodes of renal allograft rejection were treated by oral prednisolone and 49 by intravenous methylprednisolone. Both treatments achieved reversal of rejection in approximately 60% of episodes. Morbidity-rates, as assessed by hypertension, oliguria, fluid retention, and infection, tended to be greater after oral treatment. When the results were reexamined for accelerated, acute, and chronic rejection episodes the only difference demonstrated was an increased frequency of fluid retention in patients treated by oral prednisolone for an acute rejection episode. There was no evidence that intravenous methylprednisolone was nephrotoxic.
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PMID:Oral versus intravenous high-dose steroid treatment of renal allograft rejection. The big shot or not? 8 51

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%.
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PMID:[Cardiogenic shock following acute myocardial infarction. Pathophysiology and clinical aspects (author's transl)]. 10 80

A 72-year-old man with a peptic ulcer received seven units of apparently compatible red blood cells. Six days after the last unit, he had a hemolytic transfusion reaction manifested by high fever, marked fall in hematocrit, hemoglobinemia, hemoglobinuria, severe bilirubinemia and oliguria. He went on to become uremic, hyperkalemic, anuric and died five days later. Serologic studies showed that the donor and recipient bloods were completely compatible prior to the transfusions and that unexpected antibodies were not detected. The anamnestic response from donor antigens was precipitous even after a latent period of six days.
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PMID:Fatal delayed hemolytic transfusion reaction due to anti-c + E. 11 99

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.
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PMID:The toxicity and renal handling of paraquat in cynomolgus monkeys. 12 Jun 23


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