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)

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

The acute onset of oliguria and azotemia in the postoperative setting may be caused by pre-renal causes or intrinsic renal damage. The first step in arriving at a diagnosis is to review the history as noted above for clues regarding fluid balance, treatment with nephrotoxins, etc. The typical patient with prerenal azotemia will present with evidence of the recent onset of worsening of pre-existing cardiac disease, renal or gastrointestinal fluid loss, or the accumulation of acites, edema, or retroperitoneal fluid. In the absence of very recent diuretic therapy, he will be excreting a scant amount of concentrated (greater than 400 mOsm per L) sodium free (less than 10 to 20 mEq per L) urine. The serumBUN/Cr ratio is often greater than 15 to 20:1, and their urinary sediment will be bland. In an occasional patient in whom these studies give equivocal results, additional help may be obtained with measurements of central venous pressure (CVP) or pulmonary wedge pressure (PWP) and by noting their response to intravenous fluid loading. A rising CVP or PWP in the face of salt loading is, of course, evidence against prerenal azotemia. Patients with obstructive uropathies may be oligoanuric or polyuric-occasionally a characteristic alternating polyuria and oliguria is found (due to displacement of a stone or relief of edema). When oliguric their urine typically contains substantial amounts of sodium (greater than 20 mEq per L), is isotonic, and their OsmU:OsmP is les s than or equal to 1.2. Their urinary sediment will reflect the cause of their obstruction as noted above. A renal scan, ultrasound study, or infusion IVP are mandatory to rule out the possibility of obstructive uropathy. If these nonivasive studies are equivocal, one must consider doing a unilateral retrograde. The development of ATN usually occurs in the setting of hypotension, sepsis, dehydration, and with exposure to nephrotoxins. Most patients with be excreting scant amounts of isotonic urine containing more than 20 to 30 mEq per L of sodium. Their CrU:CrP is less than or equal to 20:1 and their urinary sediment reveals many epithelial cells and casts. Those patients with nonoliguric ATN have urine outputs which may exceed 2 liters per day. Despite this output they demonstrate a stepwise increase in serum urea and creatinine. Urine sodium and osmolality are not very helpful in this setting. Many such patients do have low (less than 20 mEg per L) urine sodium concentration and excrete isotonic urine.
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PMID:Pre- and postoperative renal failure. 96 Mar 14

The case report of a 27-year-old woman who had been normotensive before her 1st pregnancy 6 years earlier is presented. At 2 months postdelivery she began taking estro-progesterone. She was given Enidrel R (norethynodrel 4.925 mg, mestranol .075 mg) for 18 months and then Ovariostat (lynestrenol 2.5 mg, mestranol .075 mg). Her blood pressure was not recorded until 2 years later when it was 180 mm Hg systolic. Contraceptive therapy was then stopped. A month later pregnancy occurred. At that time her blood pressure was 120 mm Hg. The delivery was normal. 4 months later she began taking Ovariostat again. Headaches soon developed and her blood pressure was found to be 270/150 mm Hg. On admission to the hospital 3 weeks later her blood pressure was 250/100 mm Hg. Renal failure was present. Creatinine clearance was 12 ml/minute. No cause for this hypertension was found. 1 month later hypertension was 210/160 mm Ha. Retinal hemorrhaging had lessened but azotemia persisted. Heart failure and oliguria followed. Dialysis was done weekly. A bilateral nephrectomy was done. Microscopic study of renal tissue showed malignant nephroangiosclerosis. After 10 days her blood pressure was 150/100 mm Hg. Her general condition improved. A salt-free diet was prescribed. Blood pressure subsided to 140/80 mm Hg before dialysis. A renal graft was done and 10 months later blood pressure was normal. These hypertensions are usually benign and subside when the contraceptive therapy is discontinued. When estrogen-progesterones are prescribed, blood pressures should be recorded frequently and therapy stopped if hypertension arises.
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PMID:Malignant hypertension with irreversible renal failure due to oral contraceptives. 119 51

Between January, 1986 and September, 1988, the Taiwan National Poison Center recorded 97 telephone consultations (49 male, 48 female) on cases of ingestion of glyphosate-surfactant herbicide concentrate containing the isopropylamine salt of glyphosate (N-phosphonomethyl glycine, CAS 1071-83-6) and a non-ionic tallow amine surfactant. Eleven of the cases resulted in fatalities, all among those attempting suicide. The average amount ingested by survivors was 120 +/- 112 mL and by nonsurvivors was 263 +/- 100 mL (p less than or equal to 0.0001). The average age of survivors was 35 +/- 15 years compared to 54 +/- 11 years for fatalities (p less than or equal to 0.0002). Irritation of the oral mucous membrane and gastrointestinal tract was the most frequently reported effect. Other effects recorded were pulmonary dysfunction, oliguria, metabolic acidosis, hypotension, leukocytosis and fever. Fourteen patients received either atropine or pralidoxime plus atropine despite the fact that glyphosate does not inhibit acetylcholinesterase. Thirteen percent of patients received a urine test for paraquat or treatment customarily used for paraquat ingestion, possibly reflecting similar initial presentations following ingestion of these two herbicides. Laboratory differentiation is essential if any doubt exists about which herbicide was ingested. Patients ingesting large volumes of concentrated glyphosate-surfactant herbicide formulations require close observation and supportive treatment.
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PMID:Taiwan National Poison Center survey of glyphosate--surfactant herbicide ingestions. 200 70

Brain serotonin depletion induced by peripheral parachlorophenylalanine (pCPA) is frequently used to evaluate the role of the central serotoninergic system in the regulation of a number of physiological functions, including the secretion of renin by the kidney. We found that due to the treatments applied in the protocol used for the investigation of pCPA effect on renin and vasopressin secretion in rats (300 mg/kg i.p. 64 and 40 h before sacrifice) renal injury was induced as well. Typical changes indicating acute renal failure were observed--an initial polyuria, natriuresis and body mass loss, succeeded by oliguria, decreased glomerular filtration rate, and salt and creatinine retention. Morphological changes in the glomeruli included a thickening of the basal membranes, a confluence and a reduced number of podocyte pedicles. A slight to moderate granular degeneration was observed in epithelial cells of the proximal convoluted tubule, combined with mitochondrial changes--an increase in number, matrix disorganization, and myelin degeneration. In conclusion, the renal function changes after i.p. pCPA may be due not to brain serotonin depletion-alone, but also to nephrotoxic effect.
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PMID:Nephrotoxic effect of the specific brain serotonin depletor para-chlorophenylalanine. 215 5

There are three phases of acute hemorrhagic shock after trauma. In phase I (from injury to operation for control of bleeding) the patient suffers from low cardiac output, tachycardia, reduced organ perfusion, oliguria and decreased capillary hydrostatic pressure, which in turn reduces extravascular fluid loss. Contraction of the interstitial space matrix replenishes plasma volume. Optimal therapy includes blood and crystalloid replacement to restore plasma volume, red cell mass and interstitial fluid. Three litres of crystalloid are usually required for each litre of blood lost. After operation, a period of obligatory extravascular fluid sequestration occurs as the intracellular and interstitial spaces expand (phase II). Optimal replacement therapy during this phase maintains plasma volume. Replacement is provided according to the patient's vital signs, because extravascular fluid expansion cannot be influenced by therapeutic manipulation. Phase III is a mobilization and diuretic phase. During this phase systolic hypertension may occur, and the patient must be treated with restriction of fluid, diuresis and careful monitoring of the heart and lungs. Attempts to alter these physiologic responses with supplemental albumin have proved detrimental. The albumin causes salt and water retention in the nephron, leading to weight gain, higher central filing pressures and worsening pulmonary function, and a greater need for diuretic and inotropic therapy. Albumin therapy also induces relocation of non-albumin proteins into the interstitial space, leading to impaired immunocompetence and coagulation. Successful resuscitation is facilitated by adaptation to these physiologic responses of hemorrhagic shock rather than manipulation of them.
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PMID:Update on trauma care in Canada. 4. Resuscitation through the three phases of hemorrhagic shock after trauma. 225 21

Although a wide variety of disease processes can result in a failure of renal excretory function, the vast majority of cases with "acute renal failure" (ARF) are due to the syndrome of acute tubular necrosis (ATN). The syndrome is usually initiated by an acute injury to the proximal renal tubular epithelial cells by ischemic or nephrotoxic events. This is followed by progressive and often rapid increases in the concentration of blood urea nitrogen (BUN) and serum creatinine. In the average case, the failure of renal excretory function persists for 1 to 3 weeks, to be followed by recovery. Oliguria (urine volume less than 400 ml) is present in about half of the patients. The pathogenesis of the retention of nitrogenous waste in human ATN is the subject of controversy, but the balance of data in most patients suggests that the predominant mechanism is a profound secondary vasoconstriction in response to tubular cell injury. This may represent a teleologically appropriate response to prevent catastrophic losses of fluid that would occur, if the normally high rates of glomerular filtration continued, in the face of reduced tubular reabsorptive capacity. The mechanisms by which the tubular cell injury is communicated to the vasculature, and the mediators of the hemodynamic changes, remain to be established. The differential diagnosis in a patient with ARF, usually involves exclusion of an obstruction to the urinary tract as an initial step. The next step is to differentiate the patients with ATN from those who have renal hypoperfusion in response to events in the systemic circulation, but who otherwise have functionally and structurally intact kidneys, i.e., prerenal ARF. The kidneys of patients with prerenal ARF exhibit the normal renal response to an acute reduction in renal blood flow and glomerular filtration rate (GFR). This consists of avid reabsorption of the filtered salt and H2O, so that a small amount of concentrated and NaCl-poor urine is elaborated. The tubular cell injury in ATN syndromes prevents this response from maximally occurring, so that the urine is isosmotic and relatively rich in NaCl.
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PMID:Acute renal failure. 264 37

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

A new case of oxytocin-induced water intoxication is reported in a 30 year old gravid woman. The severe symptoms of this uncommon complication are principally neurological; biological signs are a hyponatraemia with low plasma osmolality. Usually, biological and clinical signs are rapidly cleared up by treatment, but maternal death or neonatal water intoxication may occur. Such accidents must be prevented by clinical monitoring, watching out for alarm signals (oliguria is always found, resulting from the effect of oxytocin on the kidney), minimum fluid and proportional salt intakes, careful monitoring of oxytocin infusion rates, facilitated by the use of a constant flow-rate pump.
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PMID:[Acute water intoxication induced by oxytocin]. 407 15

This article will provide a pathophysiologic basis for the assessment of critically ill children who have developed disorders of urine volume. The anatomical and pathophysiologic causes of oliguria and polyuria are considered. The physiologic basis for the use of urinary sodium and osmolarity as a guide to the assessment of patients with disorders of urine volume are discussed in detail. In addition, guidelines for the management of children with acute renal failure, with particular emphasis on the consideration for nutritional support of these patients, is discussed as a part of the comprehensive approach to this problem. This article emphasizes an understanding of the pathophysiology of salt and water excretion by the kidney as a foundation to the diagnosis and management of patients with oliguria and polyuria.
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PMID:Disorders of urine volume in the critically ill child. 637 63


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