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Query: UMLS:C0028961 (oliguria)
 1,847 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Administration of a single oral dose of 60 mg/kg O,O,S-trimethyl phosphorothioate (OOS-Me), a malathion impurity, resulted in a substantial increase in the amounts of amino acids along with a change in the nature of proteins excreted in the urine of treated rats. In contrast to control rats, a small increase in albumin and a small decrease in alpha 1-globulin were observed. However, alpha2-, beta- and gamma 1-globulin, which were not detected in the urine of control rats, were found in substantial amounts in the urine of OOS-Me-treated rats. These findings, coupled with observed increases in urinary glucose levels and consistent specific gravity readings of 1.01 even though treated rats were experiencing oliguria, provide evidence for OOS-Me-induced kidney tubule damage.
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PMID:Dysproteinuria induced in rats by O,O,S-trimethyl phosphorothioate. 359 Feb 28

(+/-)alpha-Chlorohydrin (80 mg kg-1) given by mouth to group-housed adult male Sprague Dawley rats produced an increase in the weight of the kidneys which persisted for at least 7 days, but there were no deaths. This dose administered to Sprague Dawley rats caged singly killed 3 out of 8 animals. The toxicity was studied in more detail using Wistar rats caged singly in metabolic cages. 4 out of 9 animals died with oliguria and anuria after 120 mg kg-1 (+/-)alpha-chorohydrin, 100 and 120 mg kg-1 (in the surviving animals), produced a loss in appetite and body weight, proteinuria, a dose-related diuresis and an increased water intake. Urinary glucose was dramatically elevated after 100 mg kg-1 but after 120 mg kg-1 the glucosuria was not as marked. By day 7 all parameters were returning to their pre-injection values. A dose of 80 mg kg-1 had no effect upon any of the parameters studied. The results are discussed in relation to the basic biochemical mechanism by which the drug exerts its antifertility action, which is achieved at much lower doses.
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PMID:Some preliminary observations of the nephrotoxicity of the male antifertility drug (+/-)alpha-chlorohydrin. 610 24

It has been demonstrated that the sensitivity to HgCl2 nephrotoxicity increases with maturity in the rat, and that neonates are largely unaffected by a dose of 5 mg/kg. In the present study, immature rat pups were exposed to higher doses of HgCl2 to determine whether this effect was attributable to a quantitative or qualitative difference in the renal sensitivity to HgCl2. Sprague-Dawley rats were injected with a single dose of 5, 7.5, 10, 12.5, 20, or 30 mg/kg on Postnatal Day 1; 5, 7.5, 10, 12.5, 15, or 20 mg/kg on Day 8; or 6.25, 7.5, 10, or 12.5 mg/kg on Day 15. Renal function was evaluated at 24, 48, and 120 hr after treatment by measuring urine volume, osmolality, urinary pH, and chloride content, the ability to concentrate urine during water deprivation, and the presence of protein, glucose, or hemoglobin in urine. Animals were then killed and their kidneys weighed. A dose of 20 mg/kg was needed to induce mortality in pups treated at 1 day of age, and 15 mg/kg was needed in pups treated at 8 days of age. In contrast, the 6.25-mg/kg dose given to 15-day-old pups produced some mortality, and all rats given higher doses at 15 days of age died within 2 days. There was marked oliguria or anuria in the rats that died. Kidney weight was increased in a dose-related fashion at all ages. In those animals not rendered oliguric by the treatment, urine volume increased and the ability to secrete a more concentrated urine during water deprivation decreased. Urinary pH was decreased in a dose-related manner. Urinary chloride excretion was temporarily decreased after HgCl2 treatment on Day 1 , but was increased thereafter. Proteinuria, glucosuria, and hematuria were detected in the treated rats, again increasing in frequency and severity with age and dose.
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PMID:Toxicity of mercuric chloride to the developing rat kidney. II. Effect of increased dosages on renal function in suckling pups. 623 55

Intraperitoneal injection of oligomycin into the rat (0.5 mg per kg, corresponding to the LD33 dose) reduces the oxygen consumption by about 50%, whereas the arterial pO2 remains normal. The large extent of this decrease points to an involvement of liver and muscle tissue. Triiodothyronine pretreatment (3 doses of 0.075 mg/100 g body weight) is not able to prevent this effect. From the blood metabolites measured glucose, pyruvate and the parameters of lipid metabolism remain unchanged; only lactate is significantly increased, causing compensated metabolic acidosis. Heart rate, systolic blood pressure and electrocardiogram are essentially unchanged. Oliguria, reduced renal excretion of urea and increase of plasma urea also indicate a nephrotoxic action. The results are discussed in comparison with some effects of experimental uremia.
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PMID:Oligomycin toxicity in intact rats. 653 86

Patulin, a secondary metabolite produced by species of the genera Penicillium and Aspergillus, was administered to male Sprague-Dawley rats, weighing 50-60 g, by the oral, sc and ip routes. The 72-hr LD50 values (in mg/kg weight) were: oral, 55.0; sc, 11.0; ip, 10.0. Mortality was greatest 0-24 hr after administration by the oral and sc routes and 49-72 hr after ip dosing. Gross alterations consisted of gastric and intestinal hyperaemia and distention. Histopathological alterations consisted principally of ulceration and inflammation of the stomach. Patulin was administered orally to rats daily or every other day for 2 wk at doses of 50 or 75% of the oral LD50. Mortality in the treated groups was greater than in controls but was similar for all treated groups. No evidence of cumulative toxicity was found and the gross and histopathological alterations were similar to those found in the LD50 studies. Clinicopathological alterations included metabolic alkalosis with respiratory compensation, oliguria, decreased serum sodium, elevated blood glucose, reduced plasma protein and an elevated total leucocyte count which differential leucocyte counts indicated to be due to neutrophilia. The inflammatory alterations observed in the gastro-intestinal tract may be due to the irritant properties of patulin or to an alteration in the gastro-intestinal flora by the antibiotic activity of patulin.
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PMID:Patulin mycotoxicosis in the rat: toxicology, pathology and clinical pathology. 720 55

In a retrospective study we analyzed the clinical and blood chemical data of 12 patients with severe tropical malaria in the intensive care units of the University Hospital Zurich and the Stadtspital Triemli, Zurich, between 1991 and 1994. None of the 12 patients had been exposed to malaria before or had taken drugs for chemoprophylaxis. 7 patients survived, 5 died from complications of malaria. According to the criteria of severe tropical malaria defined by the WHO, the following pathological clinical and blood chemical parameters were noted on admission: cerebral coma (2/12); blood hemoglobin < 5 g/dl (0/12), < 8 g/dl (2/12); serum creatinine > 265 mumol/l (3/12); blood glucose < 2.2 mmol/l (0.12); circulatory collapse/shock (0/12); bleeding/signs of disseminated intravascular coagulation in laboratory tests (4/12); acidosis with pH < 7.25 (1/12). Further signs of severe tropical malaria were: hyperparasitemia > 5% (9/12); qualitative and quantitative disturbances of consciousness (6/12); thrombocytopenia < 30 x 10(9)/l (9/12); hyponatremia 125-135 mmol/l (9/12), < 125 mmol/l (2/12); rhabdomyolysis with creatine kinase > 1000 U/l (4/12). The basic treatment consisted of parenteral quinine hydrochloride in all patients; doxycycline was added in 8 cases, clindamycin in 3. Adjuvant therapy with desferrioxamin was given in 3 cases. 6 patients had exchange transfusions. Parasitemia cleared in all patients within 5 to 6 days. Later in the course, 5 patients developed acute respiratory distress syndrome, 6 required hemofiltration due to oliguria, and one became comatose.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Intensive care aspects in severe tropical malaria: clinical aspects, therapy and prognostic factors]. 777 Jul 59

The effect of intravenous (i.v.) essential amino acids (EAA) in the treatment of acute renal failure was evaluated in 50 patients. Thirty patients (Group A) received daily 13.4 g of i.v. EAA solution [Nephramine (Don Baxter, McGraw) 250 ml/d]+dopamine i.v. 2 micrograms/kg/min + 20% hypertonic glucose solution 500 ml/d as compared with twenty patients (Group B) who received dopamine i.v. 2 micrograms/kg/min + 20% hypertonic glucose solution 500 ml/d. In Group A patients showed lower daily increase in blood urea nitrogen (BUN) (p < 0.05), higher serum total protein and albumin levels on the 15th day of the posttherapy period (p < 0.001), lower complication rate (p < 0.005), lower mortality rate (p < 0.005) and a reverse relation between serum total protein concentration, duration of oliguria and age (p < 0.01, r2 = 0.26; p < 0.001, r2 = 0.32). These data suggest that treatment of such patients with i.v. EAA solutions significantly improves survival.
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PMID:Effect of essential amino acid supplementation in acute renal failure. 858 27

Dilation of the pulmonary arteries and increased pulmonary blood volume are recorded in sudden infant death syndrome and in infants living at low barometric pressures (high altitude). Low barometric pressure leads to chronic alveolar hypoxia (1,2). There is diversion and loss of body-fluid under conditions of microgravity (near-weightlessness) encountered in human space-travel and prolonged bedrest (3). The condition mimics shock and oligemia (4,5). The human neonate has underdeveloped postural mechanisms and low muscle-power. A transformation begins at about two months of age, which enables the human infant to adapt to the extrauterine environment (6). The neonate resembles the space traveller who, in a near-weightlessness antigravity environment, develops baroreceptor incompetence, visceral and venous congestion and oliguria. The low birthweight infant displays many of the disorders of the space traveller, viz. poor circulation, high blood-glucose, insulin resistance, weak muscles, slow gut absorption and bone demineralization (7-10). These conditions are virtually identical with the internal adjustments the body makes on lying down (negative gravity or near-weightlessness). We discuss the similarities of sudden infant death syndrome to low barometric pressure environment, orthostatic intolerance, the Pickwickian syndrome and X disease.
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PMID:Sudden infant death syndrome: near-weightlessness and delayed neural transformation. 873 69

We report a patient with rhabdomyolysis secondary to hyperosmolar nonketotic diabetic coma (HNKC), who progressed to acute renal failure. A 43-year-old male with diabetes mellitus for three years was admitted to our hospital because of loss of consciousness. The laboratory findings at admission were as follows: serum glucose 1792 mg/dl, serum Na 129 mEq/1, BUN 71 mg/d1, serum creatinine 3.3 mg/d1, CPK 715 IU/1, plasma osmolality 370 mOsm/1, and negative urine ketone bodies. A diagnosis of HNKC was made. On the 2nd day, he had oliguria and the serum creatinine increased despite adequate treatment of HNKC by the administration of intravenous fluid and insulin. On the 4th day, CPK reached 47,300 IU/1, and serum myoglobin was also increased, indicating rhabdomyolysis. His renal function improved gradually and was almost normalized on the 20th day. Renal biopsy on the 23rd day showed myoglobin at the distal renal tubules, which appeared to be involved in the pathogenesis of renal failure by rhabdomyolysis. However, we found little abnormality association with diabetic nephropathy in the renal tissue. Since HNKC is known to induce acute renal failure rarely without diabetic nephropathy, these findings suggested that the acute renal failure was caused mainly by the rhabdomyolysis. Acute renal failure induced by rhabdomyolysis in patients with HNKC is rare, but fatal. The present study showed that the measurement of serum CPK and urine myoglobin was helpful for early diagnosis. Only 12 cases have been reported to have developed renal failure due to rhabdomyolysis among patients with HNKC. To our knowledge, we demonstrated for the first time that myoglobin at the distal renal tubules after renal function was normalized.
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PMID:[Rhabdomyolysis related-acute renal failure in a patient with hyperosmolar nonketotic diabetic coma (HNKC): demonstration of myoglobin casts after normalization of renal function]. 882 59

To determine whether ginsenoside-Rd ameliorates the renal injury induced by cephaloridine, the effect of cephaloridine was investigated in rats given ginsenoside-Rd preceding cephaloridine administration and in control rats given no ginsenoside-Rd. In control rats, blood, renal and urinary parameters and the activities of antioxidative enzymes in renal tissue deviated from the normal range, indicating dysfunction of the kidneys. In contrast, when ginsenoside-Rd was given orally for 30 consecutive days prior to cephaloridine injection, the activities of the antioxidation enzymes superoxide dismutase and catalase were higher, while malondialdehyde levels in serum and renal tissue were lower in the treated rats than in the controls. The urea nitrogen and creatinine levels in serum were decreased in rats given ginsenoside-Rd. Decreased urine volume, increased urinary osmotic pressure, and decreased urinary levels of glucose, protein, sodium and potassium demonstrated a protective action against the renal dysfunction caused by cephaloridine. In addition, it was demonstrated that ginsenoside-Rd affected cultured proximal tubule cells exposed to cephaloridine.
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PMID:Effect of ginsenoside-Rd in cephaloridine-induced renal disorder. 993 56


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