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

A prospective analysis of the value of urinary diagnostic indices in ascertaining the cause of acute renal failure was undertaken. Our results show that in the setting of acute oliguria a diagnosis of potentially reversible prerenal azotemia is likely with urine osmolality greater than 500 mosm/kg H2O, urine sodium concentration less than 20 meq/litre, urine/plasma urea nitrogen ratio greater than 8, and urine/plasma creatinine ratio greater than 40. Conversely, a urine osmolality less than 350 mosm/kg, urine sodium concentration greater than 40 meq/liter, urine/plasma urea nitrogen ratio less than 3, and urine/plasma creatinine ratio less than 20 suggest acute tubular necrosis. A significant number of oliguric patients will not have urinary indices that fall within these guidelines. In this setting, urine sodium concentration divided by the urine-to-plasma creatinine ratio (the renal failure index) and the fractional excretion of filtered sodium provide a reliable means of differentiating reversible prerenal azotemia from acute tubular necrosis.
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PMID:Urinary diagnostic indices in acute renal failure: a prospective study. 66 84

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

Warm ischemic (90 minutes) acute renal failure (ARF) was evaluated in the dog and found to cause polyuric ARF in the injured kidney if the opposite normal kidney was removed. In contrast, if the normal kidney were left intact, oliguric ARF was noted in the injured kidney. To further evaluate the mechanisms for oliguria and polyuria, chronic reinfusion of urine from a normal kidney into the inferior vena cava (ureterocaval anastomosis) resulted in polyuria in the opposite warm ischemic injured kidney; whereas chronic reinfusion of urine into the portal vein (ureteroportal anastomosis) resulted in profound oliguria in the opposite injured kidney. In separate additional experiments, urine acutely infused into the inferior vena cava at a rate of 0.38 ml/minute caused a significantly greater diuretic and renal hemodynamic response than seen with urine infused into the portal vein. Acute infusions of urea solution (0.38 ml/minute) with the same osmolality of urine were completely devoid of diuretic and renal hemodynamic effects. These studies reveal that urine contains a powerful hemodynamic and diuretic factor which appears to convert oliguric to polyuric ARF following warm ischemic renal injury in the dog. This factor is not urea and can be destroyed by the liver.
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PMID:Mechanisms for oliguria in acute renal failure. 87 51

Five patients aged between 40 and 70 days were admitted to our Clinic with an initial diagnosis of "renal failure", but the high levels of urea nitrogen, metabolic acidosis and oliguria were found to be related to a high renal solute load and to the very high protein and electrolyte content of the diet. By calculating urinary output (V/m'), clearance of osmotically-active substances (COsm), clearance of free water (CH2O), maximum tubular reabsorption of water (TcH2O) and the change in metabolic H+ production, it has been possible to demonstrate that dietary protein and electrolytes were both responsible for the high blood urea nitrogen levels and metabolic acidosis.
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PMID:Mechanism of diet-induced uraemia and acidosis in infants. 88 47

A heroin addict had rhabdomyolysis with cardiac involvement. The patient was admitted with edema of the right leg and oliguria. Admission diagnoses were right illofemoral thrombophlebitis, acute renal failure, and heroin addiction. Urinalysis was strongly positive for "blood" in the absence of hemolysis or marked hematocyturia, and a diagnosis of rhabdomyolysis was made. Peritoneal dialysis succeeded in lowering blood urea nitrogen and serum potassium levels, but the patient died on the fourth hospital day. Postmortem examination disclosed focal myocardial myolysis, diffuse rhabdomyolysis of the right soleus muscle, and acute renal tubular necrosis. Direct toxicity or hypersensitivity to heroin or an adulterant is considered in the pathogenesis of myolysis.
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PMID:Heroin-associated rhabdomyolysis with cardiac involvement. 90 Oct 98

The renal profile was studied in 61 patients having leptospirosis. Leptospira-induced acute renal failure conformed to one of two distinct clinical patterns, either oliguric on non-oliguric renal failure. The prognosis was excellent in the latter variety of renal failure and mortality was confined to patients with oliguric renal failure, where severe glomerular and widespread tubulo-interstitial lesions were invariably present. These patients had unfavourable prognostic features during life, such as prolonged oliguria and anuria, absence of a diruetic phase, persistent elevations in BUN and persistently low urea excretion. The prognostic significance of the age of the patients, hypotension and jaundice in relation to the occurrence and type of acute renal failure have been discussed. Retrospective observations indicate that both a vasculotoxic or haemorrhagic state and oliguric acute renal failure are important causes for mortality in human leptospiral infections.
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PMID:Patterns of acute renal failure in leptospirosis. 95 64

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 nutrient intake and urinary excretion characteristics of eight young university women were studied over a 4-day period at low altitude (140 m) and subsequently over a 7-day sojourn on Pikes Peak (4,300 m). High-altitude exposure was associated with a transient decrease in the consumption of protein, carbohydrate, fat, sodium, calcium, phosphorus, vitamin A, riboflavin, thiamin, and niacin and a more sustained decrease in the consumption of potassium and ascorbic acid. In most instances minimal values were observed during the first 3 days of exposure. The carbohydrate fraction of energy intake was increased at the expense of fat during this time period. Individual hypophagic responses appeared to be related to severity of acute mountain sickness. Altitude had no effect on water consumption but did lead to an average body weight loss of 1 kg. Urinary measurements revealed a marked oliguria during the entire sojourn. These measurements also showed the first 3 days to be associated with a net loss of body nitrogen and sodium. During this time period body potassium and phosphorus were conserved, and probably increased. The urea fraction of body potassium and phosphorus were conserved, and probably increased. The urea fraction of total urinary nitrogen was not affected by altitude exposure, nor was the daily excretion of uric acid and creatinine. Ammonia excretion, however, was reduced to 50% of the low-altitude value and remained at this level throughout the sojourn. With a few exceptions, the qualitative characteristics of altitude hypophagia in women were similar to those reported for men. Quantitatively, however, the responses were much more transient in women.
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PMID:Nutritional aspects of high-altitude exposure in women. 106 32

Under the proper experimental conditions, disseminated intravascular coagulation,"an intermediary mechanism of disease," results in the classic endotoxin-induced generalized Shwartzman reaction. Other substances, such as liquoid, a highly negatively charged anticoagulant, trigger a generalized Shwartzman reaction-like phenomenon in rabbits. We studied the effects of a single high intravenous dose of liquoid (12.5 mg.) upon the rat's coagulation and complement systems and their correlation with the kidney morphology by light, fluorescence, and electron microscopy. Thrombin time was prolonged; fibrinogen, plasminogen, and factors VIII and XII concentrations were markedly decreased, whereas fibrin degradation products were increased in the experimental animals when compared with the saline-injected controls (p greater than 0.001). Total hemolytic complement, hemolytic activity of terminal components (C3 to C9), and C3 protein concentration were significantly reduced (p greater than 0.001). The liquoid-injected rats developed cortical necrosis and manifested oliguria and anuria, with elevated blood urea nitrogen levels, when survival was longer than 3 hours. Histologically, thrombi of fibrin-like material filled the glomerular capillaries. Deposits of fibrin, and also of immunoglobulin G and C3, were readily identifiable by specific immunofluorescence, Linear or granular fluorescent deposits (or both) along the glomerular basement membranes and in the mesangium were observed. Electron microscopy demonstrated necrosis of glomeruli and abundant thrombi of fluffy, compact granular, or fibrillar electron-dense material. No typical fibrin periodicity was detected. These experiments support the concept of activation of the coagulation and the complement systems. We postulate that liquoid produced not only a consumptive coagulopathy in the rat but also a direct or perhaps anindirect activation of complement. Whether this latter has occurred through the classic or an alternate pathway remains to be elucidated.
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PMID:Disseminated intravascular coagulation induced by liquoid in the rat. I. Correlation of hematologic and complement abnormalities with renal lesions studied by light, fluorescence, and electron microscopy. 112 10

Previous evaluation of diagnostic tests for acute renal failure in children demonstrated that osmolality urine/plasms (U/P) ratio below 1.3, urea ratio below 4.8 and a negative mannitol test (absence of a diurteic response within one hour after intravenous administration of 60 ml/m2 of 12.5% mannitol solution) may be considered as valuable factors in this diagnosis. However, the validity of those ratios were in doubt in selected populations such as newborns and in severe malnourished children in whom an impairment in concentrating urine capacity can be anticipated. With the purpose to test the validity of these parameters, a group of 53 newborns and 68 children with severe malnutrition were studied. They were admitted to the hospital with dehydration secondary to acute diarrhea presenting oliguria and hyperpnea and before any treatment was given, urine and blood samples were taken to determine urea and osmolality U/P ratios besides routine chemistries. Mannitol test was performed when urine could not be obtained and in some cases in whom U/P results deserved confirmation with the biological test. Seven of the 53 newborn patients developed acute renal failure with negative mannitol test and further clinical course of persistent oliguria. Urea and osmolality U/P ratios were 3.0 +/- 1.5 and 1.07 +/- 0.01 respectively, whereas the remaining 46 newborns had afterwards an uneventful recovery presenting U/P ratios of 12.4 +/- 8.5 for urea and 1.32 +/- 0.57 for osmolality. The difference between the average values of urea U/P ratio of the patients with acute renal failure and those with functional oliguria, were statistically significant at the level of p less than 0.01, but there was no significant difference between osmolality ratio values.
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PMID:[Evaluation of the urinary and plasma urea ratio and osmolarity in newborn infants and malnourished children with pathological and normal renal function]. 127 67


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