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)

Twenty-six pregnant women complicated with acute renal failure (ARF) were admitted to Beijing Friendship Hospital during Jan. 1972 to Dec. 1990, the incidence rate was 0.045%. Among them, 4 cases of ARF were due to non-specific factors to pregnancy (15.4%) and 22 cases (84.6%) were due to factors correlated with pregnancy. Severe pregnancy induced hypertension (PIH) was the main cause of ARF in late pregnancy accounting for 86.4% (19 cases). In this series, 7 cases with eclampsia and 12 cases with preeclampsia, the incidence rate of ARF in preeclampsia and eclampsia was 0.91% and 11.3% respectively. The average age was 28.3 yr. 9 out of 19 cases were parous women. During pregnancy and labour, patients had more than one complications. 4 cases each were complicated with abruptio placentae, postpartum hemorrhage, intracranial hemorrhage and serious puerperal infection respectively. 3 cases were complicated with HELLP syndrome and one each with acute fatty liver, hypertension or gentamycin nephrotoxicity. 10 cases had deliveries preceded admission. The cesarean rate was 52.6% (10 cases). ARF onset before labour in 9 cases and postpartum in 10 cases. Developed only in 1 case of postpartum ARF in our department, this patient had a twin gestation, also complicated with severe PIH and acute fatty liver. Auria and oliguria ARF were found in 18 cases, nonauria in only 1 case. In this study, the highest serum BUN was 7.5-39.3 mmol/L (21-110 mg/dl). Medical management and rectal dialysis or peritoneal dialysis were performed in 10 cases who were in early stage, mild ARF or those ARF occurred before admission.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Acute renal failure in severe pregnancy induced hypertension: a report of 19 cases]. 824 47

Acute mountain sickness (AMS) affects, to varying degrees, all travelers to high altitudes (elevations greater than 5280 feet). In a small percentage of patients, AMS can lead to high-altitude pulmonary edema (HAPE) or high-altitude cerebral edema (HACE). Symptoms of AMS range from a combination of headache, insomnia, anorexia, nausea, and dizziness, to more serious manifestations, such as vomiting, dyspnea, muscle weakness, oliguria, peripheral edema, and retinal hemorrhage. Although the primary cause of these symptoms is related to the reduced oxygen content and humidity of the ambient air at high altitudes, the physiologic pathway relating hypoxemia to AMS and its sequelae remains unclear. Tips on self-diagnosis and symptom recognition are critical elements to be included in educating patients who are contemplating a trip to high altitudes. Preventive strategies include allowing 2 days of acclimatization before engaging in strenuous exercise at high altitudes, avoiding alcohol, and increasing fluid intake. Conditioning exercise for patients older than 35 years is also recommended before departure. A high-carbohydrate, low-fat, low-salt diet can also aid in preventing the onset of AMS. Acetazolamide (125 mg two or three times daily, or once at bedtime) has also been shown to reduce susceptibility to AMS and the incidence of HAPE and HACE. Although effective in treating cerebral symptoms of AMS, dexamethasone is not routinely recommended as a prophylactic agent for AMS.
J Am Osteopath Assoc 1995 Dec
PMID:A trek to the top: a review of acute mountain sickness. 855 56

A prospective one year study was conducted on children between the ages of 1 month to 5 years hospitalised in the pediatric ward of Christian Medical College, Ludhiana, with the aim of determining the predictive utility of certain clinical and stool parameters in diagnosing bacterial diarrhoea. Among the 204 children enrolled in the study, fever was observed in 40% in both the culture positive and negative groups. Clinical features such as abdominal distension, vomiting and oliguria although had low positive predictive values, their negative predictive values were high. Among the stool parameters, watery consistency and pus cells > 5 HPF were significantly more often observed in culture positive cases. The presence of mucus and pus cells > 5 HPF had good sensitivity (70-80%) but poor specificity (27-40%), while the reverse was true of blood (sensitivity 23%, specificity 89%). Again the positive predictive values were uniformly low while the negative ones were high. In conclusion the clinical and stool parameters were found to be more useful by their absence than by their presence in excluding a positive stool culture.
Indian J Med Sci 1995 Dec
PMID:Predictive utility of clinical and stool parameters in bacterial diarrhoea in children. 877 34

Oliguria in patients following spinal cord injury was first mentioned in 1649, but has since been referred to only occasionally. The work detailed here was completed 30 years ago but is reported because of the lack of any comparable study and because suitable patients are not now readily available. A total of 27 water load tests were carried out on 20 patients. The test included measurement of serum osmolality to confirm absorption of ingested water. Impaired response to the water load was obtained in 17 tests: 12/13 between 1 and 5 days after onset of the cord lesion and 5/14 more than 2 weeks after injury. The possibilities that oliguria was due to dehydration, failure to absorb ingested water, hypotension or renal failure are discounted. In the first few days after injury, oliguria may be due to release of antidiuretic hormone as part of the metabolic response to trauma. The impaired response seen later is discussed in relation to possible neural and hormonal mechanisms. There is a need for further study of factors influencing water excretion in tetraplegic and paraplegic patients.
Paraplegia 1995 Dec
PMID:The reduced urinary output after spinal cord injury: a review. 892 12

Previous experimental and human data suggests a detrimental effect on the course of acute renal failure related to exposure of blood to artificial dialysis membranes of poor biocompatibility. We performed a 2.5-year prospective randomized trial to compare the clinical course of acute renal failure (post-operative ischemic acute tubular necrosis, ATN) in patients receiving a cadaveric renal transplant requiring supportive hemodialysis in the immediate post-transplant setting. Patients were randomized to either a cuprophane or polymethylmethacrylate (PMMA) conventional hollow fiber dialyzer. All patients received a standard immunosuppressive regimen which included induction therapy with either horse anti-thymocyte gamma globulin (ATGAM) or the murine anti-CD3 monoclonal antibody (OKT3). Of 53 patients randomized, 17 were excluded (2 for intervening biopsy-proven rejection prior to recovery from ATN, 10 for primary graft nonfunction and 5 for other reasons), leaving 36 evaluable cases of uncomplicated ATN, 18 in each group. There was no difference by age, race, gender, cause of ESRD, immunosuppressive regimen, cold or warm ischemia time, use of pre-transplant dialysis, percent oliguria or the incidence of intra-dialytic hypotension between the 2 groups. There was no difference in the mean time to recovery from ATN posttransplant (8.9 days in the cuprophane group vs 9.5 days in the PMMA group, p = NS) or in the average number of hemodialysis treatments required (3.6 in both groups, p = NS). There was also no difference in long term allograft outcome in terms of the nadir serum creatinine, the number of episodes of subsequent acute rejection or in the development of chronic rejection. An intent-to-treat analysis of all 53 originally randomized patients similarly yielded no significant differences. A subsequent, non-randomized study using a membrane of intermediate biocompatibility (Hemophan) also showed no difference in recovery time from ATN. Bioincompatible membranes do not seem to have a significant clinical impact on the course of recovery of this form of acute renal failure. The striking benefits of biocompatibility in the course of ARF seen in other human trials may relate more to the non-renal systemic toxic effects of bioincompatibility.
Clin Nephrol 1996 Dec
PMID:Biocompatible dialysis membranes and acute renal failure: a study in post-operative acute tubular necrosis in cadaveric renal transplant recipients. 898 57

Adequate amniotic fluid (AF) volume is maintained by a balance of fetal fluid production (lung liquid and urine) and resorption (swallowing and intramembranous flow). Because fetal urine is the principle source of AF, alterations in urine flow and composition directly impact AF dynamics. Intra-amniotic 1-desamino-8-D-arginine vasopressin (DDAVP) is rapidly absorbed into fetal plasma and induces a marked fetal urinary antidiuresis. To examine the effect of intra-amniotic- DDAVP-induced fetal urinary responses on AF volume and composition, six chronically prepared ewes with singleton fetuses (gestation 128 +/- 2 days) were studied for 72 h after a single intra-amniotic DDAVP (50-microgram) injection. After DDAVP, fetal urine osmolality significantly increased at 2 h (157 +/- 13 to 253 +/- 21 mosmol/kg) and remained elevated at 72 h (400 +/- 13 mosmol/kg). Urinary sodium (33.0 +/- 4.5 to 117.2 +/- 9.7 meq/l) and chloride (26.0 +/- 2.8 to 92.4 +/- 8.1 meq/l) concentrations similarly increased. AF osmolality increased (285 +/- 3 to 299 +/- 4 mosmol/kg H2O), although there was no change in fetal plasma osmolality (294 +/- 2 mosmol/kg). Despite a 50% reduction in fetal urine flow (0.12 +/- 0.03 to 0.05 +/- 0.02 ml.kg-1.min-1 at 2 h and 0.06 +/- 0.01 ml.kg-1.min-1 after 72 h), AF volume did not change (693 +/- 226 to 679 +/- 214 ml). There were no changes in fetal arterial blood pressures, pH, PCO2, or PO2 after DDAVP. We conclude the following. 1) Intra-amniotic DDAVP injection induces a prolonged decrease in fetal urine flow and increases in urine and AF osmolalities. 2) Despite decreased urine flow, AF volume does not change. We speculate that, in response to DDAVP-induced fetal oliguria, reversed intramembranous flow (from isotonic fetal plasma to hypertonic AF) preserves AF volume.
J Appl Physiol (1985) 1996 Dec
PMID:Ovine fetal adaptations to chronically reduced urine flow: preservation of amniotic fluid volume. 901 10

Acute renal failure is a serious problem following heart transplantation. In first uncontrolled clinical trials, Urodilatin revealed beneficial effects in the prophylaxis and therapy of acute renal failure following heart and liver transplantation. Here, we present the first randomized, placebo-controlled, double-blind study on 24 patients following heart transplantation to investigate whether prophylactic i.v. Urodilatin infusion can prevent acute renal failure requiring renal replacement therapy. Postoperative drug management was characterized by intravenous application of high furosemide, cyclosporine, and vancomycin doses. Urodilatin infusion was started postoperatively with a dose of 40 ng / kg bw / min for 6 days. 6 of the 12 patients in the Urodilatin group and 6 of the 12 patients in the placebo group had a stable diuresis (3 - 4 l / day) during the study period of 6 days. In contrast, the remaining 6 patients of each group developed oliguria / anuria and required subsequent hemofiltration / hemodialysis. Cumulative duration of hemofiltration (88 +/- 7.39 hours in the placebo treated patients versus 44 +/- 5.35 hours in the Urodilatin treated patients, p < 0. 05) as well as frequency of hemodialysis (3.0 +/- 0.49 times in the placebo group vs 1.2 +/- 0.29 times in the Urodilatin group, p < 0. 05) were significantly reduced using Urodilatin. Mean arterial blood pressure was stable during the Urodilatin infusion period and was not different to that observed in placebo patients. We conclude that Urodilatin does not reduce the incidence of acute renal failure and the subsequent requirement for hemofiltration / hemodialysis in our patient population, but seems to reduce the duration of hemofiltration and frequency of hemodialysis compared to the placebo group.
Eur J Med Res 1995 Dec 18
PMID:Significance of prophylactic urodilatin (INN: ularitide) infusion for the prevention of acute renal failure in patients after heart transplantation. 938 75

Ascites is a clinical manifestation of severe ovarian hyperstimulation syndrome (OHSS) which may complicate the induction of ovulation using exogenous gonadotrophins. In severe OHSS severe ascites may occur and can lead to dyspnoea, abdominal discomfort and oliguria. To relieve ascites paracentesis is performed two to three times weekly as needed. We report three cases where an indwelling peritoneal catheter was used to decrease the need for repeated paracentesis. Under ultrasound guidance a closed system Dawson-Mueller catheter with 'simp-loc' locking design was inserted to allow continuous drainage of the ascitic fluid. A total of 23 l of the ascitic fluid were drained from the first, 20 l from the second and 28 l from the third patient with significant decrease in abdominal discomfort and improvement in the urine output. No complications or adverse reactions were noted. Continuous drainage of the ascitic fluid is efficient. It quickly decreases the abdominal discomfort, improves the urine output and prevents the need for multiple abdominal paracenteses which some patients may require.
Hum Reprod 1997 Dec
PMID:A novel approach to the treatment of ascites associated with ovarian hyperstimulation syndrome. 945 23

Prophylactic hemodialysis has been employed in the treatment of 15 patients with acute renal failure due to acute tubular necrosis (12), bilateral renal cortical necrosis (two), and poststreptococcal glomerulonephritis (one). Dialyses, usually lasting six hours each, were begun before clinical evidence of uremia developed in each patient and/or before the nonprotein nitrogen reached 200 mg.%, and were repeated daily or often enough to maintain the nonprotein nitrogen below 150 mg.%. The hypothesis underlying this technic postulates (1) that wasting, sepsis and impaired wound healing in these patients may reflect tissue injury by the same dialyzable toxic agents which produce the uremic symptoms that are readily reversible by dialysis, and (2) that repeated dialyses should therefore prevent both clinical uremia and the later, often lethal sequelae. The results contrast dramatically with our own past experience in treating patients with acute renal failure with a carefully executed medical regimen together with hemodialysis on conventional indications. Except in one instance of crush injury with progressive intracerebral damage, and one brief occasion in another individual, these patients experienced a stable, convalescent clinical course, remained free of uremic symptoms or chemical imbalances, ate at least three meals daily which were unrestricted in amount and composition, and were ambulatory between dialyses unless confined to bed by associated disease. Wounds healed well. Infection either did not occur, or subsided after appropriate therapy. Fluid restriction was liberalized by means of ultrafiltration with dialysis. Regional heparinization of only the extracorporeal circuit eliminated actual or impending bleeding as a contraindication to dialysis. Chronic vessel cannulation made the frequent dialyses possible, but may have provided the route for repeated, transient bacterial contamination of the blood stream in the first hour of many dialyses. Marked anemia, despite reticulocytosis, moderate to mild weight loss and some mental deficit persisted in spite of the general clinical improvement and well-being. Three patients with tubular necrosis died after seven, 11 and 26 days of oliguria; both patients with bilateral renal cortical necrosis also succumbed, on the seventy-third and ninety-second days of renal failure, and after 29 and 40 dialyses, respectively. At autopsy, evidence of sepsis was conspicuously absent. The remaining 10 patients survived. Thus some, but not all, clinical manifestations of acute renal failure appear to be favorably influenced by prophylactic dialysis treatment. Our initial experience in this group of 15 patients does not of course prove that freedom from complications and a significantly better outlook for survival can be assured to patients with acute renal failure by these methods. However, it seems to offer a reasonable hope of this possibility which we cannot attach to management by medical measures alone, or by dialysis on conventional indications. If this hope is realized in greatly extended, subsequent series, then it seems inevitable that some form of prophylactic dialysis, or some equally effective alternative, should be adopted in treating the majority of patients with acute renal failure.
J Am Soc Nephrol 1998 Dec
PMID:Prophylactic hemodialysis in the treatment of acute renal failure. Annals of Internal Medicine, 53:992-1016, 1960. 984 96

Immunosuppressant-induced nephrotoxicity, in particular chronic progressive tubulointerstitial fibrosis/arteriopathy induced by the calcineurin inhibitors cyclosporin and tacrolimus, has become the 'Achilles heel' of immunosuppressive agents. The use of calcineurin inhibitors as primary immunosuppressants in hepatic and cardiac transplantation has led to end-stage renal disease and dialysis. Calcineurin inhibitor-induced acute renal failure may occur as early as a few weeks or months after initiation of cyclosporin therapy. The clinical manifestations of acute renal dysfunction are caused by vasoconstriction of renal arterioles, and include reduction in glomerular filtration rate, hypertension, hyperkalaemia, tubular acidosis, increased reabsorption of sodium and oliguria. The acute adverse effects of calcineurin inhibitors on renal haemodynamics are thought to be directly related to the cyclosporin or tacrolimus dosage and blood concentration. However, new clinical data indicate that calcineurin inhibitor-induced chronic nephropathy can occur independently of acute renal dysfunction, cyclosporin dosage or blood concentration. Several strategies have been evaluated to attenuate cyclosporin-induced nephropathy, but their efficacy remains unknown. Cytokine release syndrome associated with the use of muronomab-CD3 (OKT-3) can also contribute to the pathogenesis of transient acute tubular necrosis and renal dysfunction following renal transplantation. Continued research and clinical experience should provide information regarding the aetiology of cyclosporin-induced chronic progressive tubulointerstitial fibrosis/arteriopathy and its potential treatment.
Drug Saf 1999 Dec
PMID:Immunosuppressant-induced nephropathy: pathophysiology, incidence and management. 1061 71


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