PubMed HealthSearch

SEARCH · PubMed Health

Results for “Oliguria”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

Oliguria and its sequelae.

Fifty-nine patients were seen with oliguria in 1975. Forty had acute renal failure (ARF) and 19 rapidly reversible oliguria (RR). The causes of the oliguria were medical (64%), surgical (27%) and obstetrical (9%). The following were valuable in the assessment of patients with oliguria: urine sodium concentration (UNa) and osmolality, coagulation studies and high dose intravenous urography. Patients presenting with a high UNa or a coagulation abnormality were more likely to have ARF. Central venous pressure monitoring was helpful in the initial management but the administration of diuretics was not. Twenty patients with ARF were treated conservatively and the remainder by dialysis. Infection was both the commonest complication of ARF and the most frequent cause of death. Seventy percent of those with ARF died. Death was more common in the elderly or patients with a medical aetiology. The mortality of ARF remains high in spite of advances in the management of its metabolic and infective complications because of the acceptance of more high risk patients. An improved awareness of the preventable causes of oliguria is apparent.

Acute Kidney Injury

[Aspects of the treatment of postoperative oliguria].

The importance and differential diagnosis of postoperative oliguria are discussed. A plea is made for the recognition of undesired postoperative antidiuretic hormone (ADH) secretion as a separate entity in the aetiology of postoperative oliguria. Five patients are described who suffered from postoperative oliguria and in whom the diagnosis of undesired ADH secretion was made. The successful treatment of this condition with diphenylhydantoin is emphasized.

Adult

[Mechanism of oliguria in experimental hypoparathyroidism].

Diuresis was found to diminish considerably in dogs with removed (by enucleation or burning out) parathyroid glands chiefly on account of intensified tubular reabsorption. In the mechanism of oliguria in hypoparathyroidism a definite role is played by hypocalciemia. An acute reduction of blood calcium in intact dogs also suppressed diuresis. Dogs with hypoparathyroidism displayed a marked elevation of blood plasma antidiuretic activity and a high level of reabsorption of osmotically free water. Intravenous injection of adrenoblocker dihydroergotamine eliminated the suppression of diuresis in the parathyroprived dogs. Apparently, a definite role in the origin of oliguria belonged to substances of adrenergic nature.

Absorption

Mechanisms for oliguria in acute renal failure.

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.

Acute Kidney Injury

Oliguria in the incubating neonate. Emergency aortography and urography in neonates using mobile X-ray equipment.

Neonates in incubators underwent umbilical aortography, excretory urography and suprapubic cysto-urethrography using a mobile X-ray machine in the Premature Baby Unit to define the cause of their oliguria. The techniques were easy to perform without endangering the infants by moving them. The radiological findings in the four neonates investigated contributed significantly to the management of their illnesses.

Anuria

Renal decapsulation in the prevention of post-ischemic oliguria.

The delayed onset of anuria/oliguria in acute tubular necrosis has been theorized to represent a complicating compartment syndrome, i.e., parenchymal swelling within an unyielding capsule. To test this proposition, 12 monkeys had suprarenal aortic cross-clamping, followed by unilateral renal decapsulation to create an experimental as well as a control kidney unit in the same animal. Histologic examination uniformly confirmed tubular necrosis at death or sacrifice. Subsequent split renal function studies (creatinine, urea, and free water clearances) indicated significantly greater maintenance of renal function by the decapsulated kidney than by its paired control. Clinical evaluation in 21 hemorrhagic shock patients, with the capsule of one kidney stripped, revealed on follow-up that 15 developed a renal failure consistent with acute tubular necrosis. Although three patients with polyuric failure died before split studies could be run and two others have been too recent for computer analysis to have been completed, nine of the remaining ten had significantly greater renal plasma flows (194 versus 121 ml/min M(2), p < .01) and significantly greater urine flows (.99 versus .18 ml/min M(2), p < .01) on the decapsulated side than on the control, as determined by differential renal scans. No significant difference in these same lateralized renal functions was noted in the tenth patient with renal failure and in the six survivors without renal failure. Renal decapsulation as prophylaxis reduced the anticipated incidence of oliguria/anuria from an expected 75% to 7% (p < .01) in these 21 shock patients. Such data suggest that delayed renal ischemia, possibly based on a compartment syndrome, may be the cause for a progression of acute tubular necrosis from polyuria to oliguria and then to anuria.

Adolescent

Acute oliguria.

Explore the source record for details and available documents.

Acute Disease

Dopamine and saralasin antagonism of renal vasoconstriction and oliguria caused by amphotericin B in dogs.

Amphotericin B (2.5 mg/kg, administered intravenously) increased vascular resistance (renal more than pulmonary more than systemic) and decreased glomerular filtration and urine flow 94% in 16 anesthetized female mongrel dogs. Dopamine decreased renal vascular resistance 31% in 14 dogs; when amphotericin B was given with dopamine, there was partial antagonism of amphotericin B-induced renal vasoconstriction. Saralasin partially antagonized amphotericin B-induced renal vasoconstriction in seven dogs. When amphotericin B was given during combined infusion of dopamine and saralasin in eight dogs, renal blood flow remained at initial control levels, urine flow increased above initial levels, and glomerular filtration decreased only 21% from initial values. Amphotericin B increased renal vascular resistance 296% when given alone but only 41% in dogs during injection of both dopamine and saralasin (P = 0.002). The antagonism of amphotericin B-induced renal effects by the combination of dopamine and saralasin was significant and specific for the renal vascular bed.

Amphotericin B

Reversal of oliguria and renal cortical ischemia of hemorrhagic shock in the dog with tris (hydroxymethyl) amino methane (THAM). Hemodynamic studies.

We investigated the functional and hemodynamic effects on the kidney of tris (hydroxymethyl) amino methane (THAM) infusion during sustained hemorrhagic hypotension in dogs. The large osmotic load introduced into the vascular compartment during hemorrhagic hypotension resulted in a marked reduction in systemic vascular resistance and a return of cardiac output, total renal blood flow, and the renal arteriographic pattern to normal range. The observed diuresis is probably due to an osmotic effect, because the glomerular filtration rate remains significantly depressed. Anatomical assignment of the mathematical components of the xenon washout curve led to an assessment of intrarenal blood flow distribution that was at variance with the arteriographic pattern and the intrarenal distribution of tagged microspheres.

Animals