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)

Three cases of Hantaan virus infection (Korean haemorrhagic fever) leading to acute renal failure are described. All three had mild haemorrhagic fever with a renal syndrome. It had started with acute fever followed by oliguria, proteinuria and microhaematuria (in two patients) in the further course of the disease, as well as urea and creatinine retention. One patient needed to be dialysed twice. Hantaan virus-specific IgG antibodies were demonstrated in all three patients; one also had IgM antibodies.
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PMID:[Hantaan virus infections as a cause of acute kidney failure. 3 cases in West Germany]. 289

A middle aged man (48 years) with short duration of illness (7 days) was admitted in the state of acute renal failure with erythema nodosum leprosum. He had repeated episodes of erythema nodosum leprosum in the past. His blood pressure was normal (150/80 mmHg). During his hospital stay he was in the state of progressive anaemia (Hb = 8.8 g/dl to 7.2 g/dl), oliguria (urine out-put = 250-350 ml/day), azotaemia (blood urea = 198 mg/dl to 218 mg/dl) and impaired renal function tests with fatal outcome. Kidneys were smooth, congested and weighing 150 g each with histological features of rapidly progressive (crescentric) glomerulonephritis, a result of immune complex deposition from recurrent erythema nodosum leprosum episodes.
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PMID:Rapidly progressive (crescentric) glomerulonephritis in erythema nodosum leprosum: case report. 326 17

Growing male rats were fed dietary Pirimiphos-methyl at 0, 500, 1000 and 1500 ppm for 28 days and selected blood and urine constituents were measured at weekly intervals. Dietary intake of Pirimiphos-methyl induced an initial, transient hypoglycemia and a marked elevation in blood urea at all dosages. Though it did not produce any significant change in the urine output initially, marked oliguria was observed after 12 days of feeding. The alterations observed in urine constituents were: increased urea, proteinuria, transient increase in creatinine and significant increase in the excretion of glucuronic acid and ethereal sulfate at all intervals. However, since no pathological alterations were evident in the kidney, the anomalous urinary excretion of various body constituents might be due to the anticholinesterase action of the insecticide at the central nervous system.
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PMID:Toxicity of pirimiphos-methyl: II. Effect of dietary feeding on blood and urine constituents in albino rats. 338 34

TI-31 (TEI-3096; 6-p-chlorobenzyl-5H-2,3,6,7-tetrahydro-5,7-dioxothiazolo[3,2-a]pyr imidine) is a novel immunomodulator. Various nephritic changes observed in female NZB/NZW F1 (B/W) mice with aging were suppressed by TI-31 when administered orally 5 times per week for 16 weeks at doses of 2, 10, or 50 mg/kg. It suppressed proteinuria, oliguria, the decrease of erythrocyte count, and increase of serum urea nitrogen, immune complex and anti-double-stranded DNA antibody levels. The anti-nephritic effect of TI-31 was confirmed by histopathological evaluation. TI-31 (10 mg/kg) could improve both the elevated polyclonal B cell activation and the depressed antibody response to sheep red blood cells in B/W mice, in comparison with age- and sex-matched BALB/c mice, without any effect on the antibody response in these normal mice. These findings indicate that TI-31 may inhibit B/W nephritis by regulating the antibody production through a mechanism different from that of anti-inflammatory drugs or immunosuppressants.
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PMID:Inhibitory effect of TI-31 on autoimmune nephritis in NZB/NZW F1 mice through regulation of the immune response. 349 22

Acute oliguria in the critically ill postoperative patient, or in the trauma victim after resuscitation, is a substantial clinical problem. The mortality associated with ARF in these settings remains unacceptably high. Evaluation of the oliguric patient must include thorough monitoring for, and correction of, prerenal and postrenal causes of oliguria. In this sense, diagnosis of ARF is one of exclusion. Differential diagnosis is facilitated by microscopic examination of urine and by biochemical analyses of blood and urine for calculating indices of tubular function (urinary-to-plasma ratios of blood urea nitrogen and creatinine, sodium excretion, and clearances of sodium, creatinine, solute, and water). The early detection of an intrarenal defect, as accomplished by using serial measurements of free water clearance, may allow interruption of the process and prevention of ARF. Preventive measures include optimization of hemodynamic status and the use of osmotic diuretic agents (mannitol) and loop diuretics (furosemide, ethacrynic acid, and bumetanide). Dopamine is useful for increasing both renal blood flow and urine flow and may be useful for preventing ARF, but this is not firmly established. Experimentally, other approaches such as modulating the renin-angiotensin system, prostaglandin system, and cellular calcium fluxes have been attempted, but the clinical applicability of these measures is not established. The best approach to ARF is preventing it by knowing which patients are at high risk, by studiously preventing renal insults, and by aggressively treating early indications of renal malfunction using established therapies.
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PMID:Acute renal failure following traumatic injury or major operation. 355 12

In exploratory studies aimed at elucidating CNS effects due to heavy metal toxicity, signs of compromised renal function were seen in rats. The studies reported here describe the sequential steps of the development of nephrotoxicity by trimethyltin chloride (TMT) in rats. Single doses of 12.25 mg/kg TMT administered orally to 150- to 175-g Long-Evans rats elicited overt signs of toxicity including behavioral abnormalities and marked weight loss. Concurrent with the development of these signs, nephrotoxicity was manifested as functional kidney compromise and associated histopathologic evidence of tubular damage. Pathological changes in the kidneys from treated rats were hyaline droplet inclusions, attenuated brush border, basolateral vacuolization, and eosinophilic granular casts in the proximal tubule cells. These lesions were detected as early as 2 days post-treatment and progressed with time in an orderly and sequential fashion. Renal lesions between 5 and 8 days were mild to severe cortical tubular dilatation, hydropic degeneration, and diffuse hyaline droplet deposition in the lower nephron tubules. Medullary edema and exfoliation of degenerated tubular epithelial cells with cast formation followed from 8 to 11 days. The morphological changes were accompanied by marked elevation of blood urea nitrogen, parallel with polyuria at Day 2 and oliguria by Day 14. Behavioral abnormalities as well as weight loss correlated well with the time course and severity of renal dysfunction and progression of morphological changes. A second experiment compared the effects of TMT in rats of different weights. Heavier rats were more sensitive than lighter rats to the nephrotoxic effects of TMT. These effects were independent of recognizable neurotoxic effects of TMT in the hippocampus.
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PMID:The pathogenesis of trimethyltin chloride-induced nephrotoxicity. 355 27

We have developed a rabbit model of toxic shock syndrome that uses a subcutaneous infusion pump to administer toxic shock syndrome toxin 1 (TSST-1). A dose of 150 micrograms, infused at a constant rate over a period of 7 days, resulted in a characteristic illness highlighted by fever, conjunctival hyperemia, cachexia, and lethargy. The illness was uniformly fatal, with a mean interval until death of 3.2 +/- 0.4 days. Serial determinations of serum chemistries confirmed the multisystem nature of this illness. Rabbits developed profound hypocalcemia, with levels falling from 15.5 +/- 0.2 to 7.6 +/- 0.4 mg/dl under the influence of TSST-1. Blood urea nitrogen and creatinine rose dramatically, in the setting of oliguria or anuria. Serum glutamicpyruvic transaminase was the most reliable indicator of hepatic dysfunction, with the mean rising from 48 U/liter before administration of TSST-1 to 546 U/liter among rabbits surviving 2 days of the infusion. Creatine phosphokinase also rose dramatically in 10 of 16 rabbits. Rabbits demonstrated relative neutrophilia and lymphopenia as well as an increase in the partial thromboplastin time. Histopathologic examination demonstrated disease of multiple organs, particularly the liver, spleen, and lymph nodes, all of which demonstrated inflammation, thrombosis, hemorrhage, and erythrophagocytosis. The concurrent administration of prednisolone with TSST-1 prevented death in four of four rabbits and greatly lessened the morbidity. Rabbits were not protected from morbidity or mortality by the concurrent administration of polymyxin B. We believe that a constant, subcutaneous infusion of TSST-1 in rabbits provides a reproducible model for studying the pathogenesis of TSS.
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PMID:A rabbit model of toxic shock syndrome that uses a constant, subcutaneous infusion of toxic shock syndrome toxin 1. 357 Apr 55

Urinary ascites may be the most common cause of ascites in the neonate, and should be suspected in an infant with abdominal distention, oliguria, hyponatremia, and hyperkalemia. The diagnosis is confirmed when analysis of the peritoneal fluid shows creatinine, urea, and potassium concentrations higher than corresponding serum concentrations. The establishment of adequate urinary drainage by catheterization of the bladder or nephrostomy rapidly corrects electrolyte abnormalities.
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PMID:Analysis of peritoneal fluid in urinary ascites. 370 26

The effects of treatment with either cysteine (2 X 150 mg/kg) or diethylmaleate (0.7 ml/kg) on renal function and response to the nephrotoxicant hexachloro-1,3-butadiene (HCBD) were examined. Cysteine caused oliguria, blocked the polyuric and glucosuric effects of HCBD and attenuated the reduction of urine osmolality. Diethylmaleate (DEM) decreased urine osmolality; further decreases of urine osmolality were not seen after HCBD. DEM pretreatment increased HCBD-induced proteinuria. HCBD-induced elevation of plasma creatinine concentration was not affected by either of the pretreatments whereas the plasma urea nitrogen concentration was greater in the DEM-pretreated group. The latter may represent an effect of DEM on non-filtration handling of urea. The results suggest that cysteine and diethylmaleate each have effects on kidney function which alter the response of the nephron tubule to a subsequently administered toxic agent.
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PMID:Effects of cysteine and diethylmaleate pretreatments on renal function and response to a nephrotoxicant. 374 Nov 49

The role of blood volume regulatory mechanisms located in the low pressure system in the control of urinary excretion was studied using hypobaric pressure breathing in normal and diabetes insipidus (Brattleboro strain with a congenital lack of vasopressin) rats. Rats were placed in an altitude simulator chamber for 4 h. A pump maintained pressure reduced to 701, 577 and 472 mbar simulating respectively altitude of 3,000, 4,500 and 6,000 m. In normal rats, hypobaric breathing induced an increase in urine flow, urinary urea and K+ excretion and urinary pH but did not significantly modify creatinine and Na+ excretion. In diabetes insipidus rats, hypobaric breathing produced oliguria and an decrease in urea, creatinine, Na+, K+, Cl- urinary excretions. Since acute hypobaric pressure breathing induced opposed effects in normal and Brattleboro rats, it is suggested that this kind of experimental procedure which increases intrathoracic blood volume elicits a diuretic response through an inhibition of vasopressin release. These experiments confirm the main role of vasopressin in the control of central blood volume.
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PMID:Renal effect of acute hypobaric pressure breathing in normal and diabetes insipidus rats. 376 Dec 5


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