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)

Glucosylthiazolidine-4-carbonic acid, an intermediate of the Maillard reaction between D-glucose and L-cysteine, was given in doses of 0, 25, 50 or 100 mg/kg b.w. by oral intubation to male and female rats for 21 days. General appearance, growth, food consumption, haematology, urine analysis and serum chemistry including determinations of enzyme activities, organ weights and macroscopic and microscopic pathology were used as criteria for adverse effects. Effects on the kidneys were indicated by oliguria and decreased specific gravity of the urine in males and histopathological changes of the proximal tubules in females. The no-effect dose established from this study is 25 mg/kg b.w.
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PMID:[The subacute toxicity of glucosylthiazolidine-4-carbonic acid in rats]. 208 62

Lithium salts, in particular the carbonate and citrate, were formerly in widespread use, forming part of alkaline salt mixtures which were used for treatment of the many disorders belonging to the uric acid diathesis. Among these disorders were mania, depression, acute mania, acute melancholia and periodic depression. Satisfactory prophylactic effects on periodic depression were directly claimed. Daily doses of 3 to 26 mmol of lithium were recommended as standards. Only slight or moderate symptoms of poisoning were reported in a very few cases during the period in question (1860 to 1930), when the popularity of these lithium-containing prophylactic drugs with a favourable therapeutic index was at its peak. Lithium intoxication was not a serious clinical problem until 1949 when Cade introduced his fortuitously effective, but nevertheless high, dosage regimen which was continued until signs of recovery from mania appeared. For the maintenance dose, Cade in principle recommended, but seldom adhered to, 17 mmol/day. Chronic lithium intoxication starts insidiously with silent affliction of the kidneys followed by 'prodromal' symptoms, and when moderate severity has been reached, an accelerating renal vicious circle with decreasing kidney function is imminent. After this point the chronic intoxication resembles acute intoxication. Active detoxification at this, or an earlier stage, leaves the patient with a good chance of recovery. At a later stage, with the occurrence of oliguria, semi-coma or coma, and latent convulsive movement, recovery is less certain. There is no specific antidote for the toxic effects of lithium. Haemodialysis is the most effective treatment for acute lithium poisoning. For patients with impaired, or potentially impaired renal function, peritoneal dialysis may be an alternative, but less effective, treatment. Forced diuresis demands unimpaired renal function, and is little more effective than withdrawal of treatment, supplemented with correction of water and electrolyte balance. Sodium overloading is not recommended. Patients on lithium prophylaxis are treated on an outpatient basis. Prevention of intoxication depends on cooperation between patient and clinician, and possibly on the use of smaller, low risk dosages in most patients.
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PMID:Clinical features and management of lithium poisoning. 328 25

Patients with severe lactic acidosis and oliguria who receive large amounts of sodium bicarbonate may develop fluid overload and hyperosmolarity. We infused massive amounts of isotonic sodium bicarbonate and simultaneously removed the excess sodium and water with ultrafiltration if 2 patients with lactic acidosis. The first patient received 1,125 mmol of bicarbonate over 4.5 h with a rise in pH from 7.00 to 7.36 and in HCO3 from 3.5 to 15.7 mmol/l. The second received 968 mmol of bicarbonate over 5.25 h with a rise in pH from 7.00 to 7.27 and in HCO3 from 5.3 to 14 mmol/l. Blood pressure remained stable or rose, electrolytes normalized, excess fluid was removed, and a higher pH was maintained. Isotonic bicarbonate infusion with simultaneous ultrafiltration is a safe and rapid method of correcting the metabolic status of patients with severe lactic acidosis who have not responded to standard therapy.
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PMID:Rapid correction of severe lactic acidosis with massive isotonic bicarbonate infusion and simultaneous ultrafiltration. 630 Jul 14

A schizophrenic woman, aged 45, was admitted complaining of high fever, oliguria, blackish urine, muscle swelling and pain. She had been treated for the past 3 years with haloperidol (8 mg), levomepromazine (150 mg), chlorpromazine (75 mg), lithium carbonate (600 mg), bromocriptine mesilate (7.5 mg), etizolam (1 mg), and flunitrazepam (2 mg), Physical examination revealed her to be an obese and uncommunicatable woman with swelling and weakness of the extremities and abdominal distension without borborygmus. Urine was dark brown and (+) for protein and occult blood. Blood chemistry analysis revealed BUN 71 mg/dl, creatinine 6.8 mg/dl, CPK 143,850 IU and myoglobin 3,980 ng/ml. PRA on the 11th hospital day was 96 ng/ml/hour. This patient fulfilled the Levenson's diagnostic criteria for manifestations of neuroleptic malignant syndrome (NMS). High PRA did not decrease after cessation of the diuretics. After treatment with dantrolene sodium and 10 treatments with hemodialysis, azotemia disappeared with the start of diuresis. The PRA also decreased to the normal level. Characteristic acceleration of the central sympathetic stimuli in NMS seemed to have induced hyperreninemia, which together with rhabdomyolysis, might have contributed to the development of acute renal failure.
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PMID:[A case of acute renal failure in neuroleptic malignant syndrome associated with rhabdomyolysis--possible contributing role of hyperreninemia]. 781 49

Rhabdomyolysis is associated with infectious diseases in approximately 5% of cases and acute kidney injury occurs in 33-50% of cases. Gangrenous myositis is a deep seated infection of the subcutaneous and muscular tissues. We report the case of an 18 year-old man who was admitted to the emergency room with leg pain, fever, nausea, vomiting and oliguria. Physical examination showed moderate dehydration, peripheral cyanosis and skin necrosis with severe myalgia and no subcutaneous gas. Laboratory findings at admission were: serum urea 111 mg/dL, creatinine 1.3 mg/dL, potassium 6.3 mEq/L, creatine kinase (CK) 112,452 IU/L, aspartate amino transaminase (AST) 1116 IU/L, alanine amino transaminase (ALT) 1841 IU/L, pH 7.31, bicarbonate (HCO3) 11 mEq/L and lactate 4.3 mmol/L. Emergency hemodyalisis was started, and antibiotics were given due to high suspicion for bacterial infection. The patient developed respiratory insufficiency and septic shock needing mechanical ventilation and vasoactive drugs. He presented spontaneous gangrenous myositis in both legs and in his left arm. After 26 sessions of hemodialysis, partial recovery of renal function was observed. He was discharged from the ICU after 38 days, still with leg pain. Acute kidney injury due to rhabdomyolysis should be considered as a possible complication of gangrenous myositis.
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PMID:Acute kidney injury due to rhabdomyolysis-associated gangrenous myositis. 1926 Mar 87

Acute lithium intoxication may cause serious neurologic and cardiac manifestations, up to the patient's death. Owing to its low molecular weight, relatively small volume of distribution close to that of total body water, and its negligible protein binding, lithium can be efficiently removed by any extracorporeal modality of renal replacement therapy (RRT). However, the shift from the intracellular to the extracellular compartment, with the inherent rebound phenomenon after the end of RRT, might limit the efficacy of the conventional, short-lasting haemodialysis. There have been no published studies up to now concerning the use of sustained low-efficiency dialysis (SLED) in lithium intoxication. This report describes a woman with a voluntary acute lithium ingestion of 40 tablets of lithium carbonate (8.12 mEq lithium each). The lithium concentration increased up to 4.18 mEq/l about 24 h after admission, notwithstanding treatment with intravenous crystalloids and gastric lavage. She developed mental status changes, oliguria, hypotension and bradycardia. We started SLED (8 h) with a blood flow of 200 ml/min and countercurrent dialysate flow of 300 ml/min. Lithium serum levels decreased by 86% during treatment, and the patient fully awoke recovering a normal mental status within the first 4 h of treatment. SLED was completed safely within the prescribed time. After the end of treatment, the rebound of lithium concentration was unremarkable. Renal function fully recovered, and the patient was transferred into a psychiatric facility 3 days after admission.
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PMID:Sustained low-efficiency dialysis (SLED) for acute lithium intoxication. 2598 26