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

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.
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PMID:Renal decapsulation in the prevention of post-ischemic oliguria. 40 54

Renal ischemia of 90 min duration provokes initial oliguria and hyperazotemia; however, in rats with high diuresis, with or without renal renin depletion, protection against acute renal failure is observed in this model. The protection is directly proportional to the diuresis.
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PMID:[Protection against acute renal insufficiency by means of forced diuresis in an ischemic rat model]. 92 53

Oliguria has been considered a cardinal feature of acute renal failure. Most studies indicate that non oliguric forms of acute renal failure are associated with less morbidity and mortality than oliguric forms. Mannitol, loop diuretics and dopamine have been used to prevent and treat renal ischemia. Although the final fate of patients with oliguric acute renal failure is more influenced by the primary disease than by anuria per se the possibility of reversing anuria seems to represent a better prognostic factor in the outcome of these patients.
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PMID:Acute renal failure: prevention and treatment. 211 13

Twenty-four patients with septic shock (cardiac index [CI] greater than or equal to 4 L.min-1.m-2, systemic vascular resistance index [SVRI] less than or equal to 350 dyne.sec.cm-5.m-2, systolic BP less than or equal to 90 mm Hg, oliguria less than 30 ml/h) were treated with norepinephrine (NE) infused either alone or in combination with dopamine and/or dobutamine. In all patients, NE resulted in either an increase in BP, no change, or an increase in CI and restored SVRI to the normal range. In 20 patients, normalization of systemic hemodynamics was followed by re-establishment of urine flow, decrease in serum creatinine, and increase in creatinine clearance. None of these 20 patients received low dose dopamine or furosemide. Four patients remained oliguric. Two of these four patients died and two developed acute renal failure. These findings suggest that NE infusion does not worsen renal ischemia related to hemodynamic disturbances in septic shock patients, and may have beneficial effects on renal function.
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PMID:Renal effects of norepinephrine used to treat septic shock patients. 230 53

Renal ischemia is a multifactorial insult consisting of both hypoxia and stagnation of blood flow. This study compared the renal response with hypoxia alone versus ischemia (hypoxia and stagnation of flow). Isolated rat kidneys were perfused at 90 to 110 mm Hg and 37 degrees C with an asanguinous modified Krebs' buffer. Perfusate flow rate, vascular resistance, urine flow rate, glomerular filtration rate (GFR), percent sodium reabsorption, and oxygen consumption were measured. Five groups were examined: 10-minute hypoxia (HYP10), 30-minute hypoxia (HYP30), 10-minute ischemia (ISC10), 30-minute ischemia (ISC30), and time-matched controls. HYP10 resulted in isolated tubular dysfunction, as evidenced by an increase in urine flow rate and a decrease in percent sodium reabsorption. ISC10 caused decreased GFR, oliguria, and more severe tubular dysfunction. The pattern of glomerular and tubular dysfunction after HYP30 was similar to that after ISC30. Glomerular dysfunction was associated with a decrease in perfusate flow rate and an increase in vascular resistance only after ISC30. This suggests that the decrease in GFR seen with postischemic renal dysfunction is not a primary result of decreased flow. Furthermore, hypoxia does not account for the entire reduction in renal function after ischemia of similar duration. The more severe dysfunction after ischemia may be a consequence of the stagnation of renal flow (anaerobic waste product accumulation and inadequate nutrient supply).
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PMID:The contribution of hypoxia to postischemic renal dysfunction. 340 59

One hour occlusion of total renal blood flow results in oliguric acute renal failure as defined by an abrupt and severe diminution in glomerular filtration rate. In rats, after 1-2 h of such ischemia, the acute renal failure which follows is characterized by decreased renal blood flow and by intratubular obstruction with necrotic cellular debris. The present study has examined the possible role of the complement system in the development of this model of acute renal failure. Immunoreactive C3 was extensively localized within necrotic tubular epithelial cells and the walls of small muscular arteries in reperfused kidneys after 1 h of total renal ischemia. Depletion of complement by the administration of cobra venom factor 18 h prior to the induction of ischemia abrogated C3 localization and significantly attenuated the subsequent fall in renal blood flow following reperfusion but did not alter the oliguria or marked fall in glomerular filtration.
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PMID:The role of complement in the pathogenesis of postischemic acute renal failure. 403 2

In the present study 1 h of total occlusion of the left renal artery in conscious rats was chosen as experimental model of ischemic acute renal failure (ARF), while the contralateral kidney was left intact. Chronic high dietary sodium intake, acute isotonic saline infusion, or administration of saralasin did not protect from ARF. Furosemide, mannitol, and verapamil converted oliguric into non-oliguric ARF in 100%, 75%, and 60% of the animals, resp. Protection from oliguria and preservation of GFR inversely correlated with the depression of cortical ATP-concentration (control: 1.32 +/- 0.07 mumoles/g wet weight) 6 h after ischemia by 16%, 41%, and 58% in mannitol- and verapamil- treated rats and in untreated rats, resp. At this time, Na-K-ATPase enzyme activities in renal cortex and papilla were unaffected, while enzyme activity in outer medulla was suppressed from 15.4 +/- 1.4 to 9.4 +/- 1.0 mumoles Pi/mg protein h in all groups of animals. The results suggest that in this model of ARF renal ischemia not only affects cellular energy supply in renal cortex but also causes severe structural and functional impairment in the outer medulla, probably leading to tubular obstruction and depression of glomerular function. Pharmacological protection from ischemic oliguric ARF cannot be achieved by prior induction of high urine flow rates alone but depends on the degree of metabolic and functional reserve of the injured tubular epithelium.
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PMID:Renal functional and metabolic studies on the role of preventive measures in experimental acute ischemic renal failure. 641

Acute renal failure is most commonly associated with renal ischemia, although nephrotoxins such as antibiotics, radiographic contrast media and anesthetic agents have become important causes. Although the pathophysiology has not been completely explained, renal vasoconstriction appears to be an important factor. Oliguria, isosthenuria and a urinary sodium concentration over 25 mEq per L are characteristic features. Control of volume and avoidance of metabolic disequilibrium can be accomplished by careful management and dialysis. The major causes of death are infection and the primary disease itself.
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PMID:Acute renal failure. 705 95

Although acute renal failure, caused either by renal ischemia or nephrotoxic agents, is usually characterized by oliguria, a severe fall in glomerular filtration rate, and a fall in renal blood flow, some patients and experimental models display a non-oliguric pattern of renal injury. The present study was designed to evaluate the mechanism of preservation of high urinary flow rate under this condition. Following the administration of the aminoglycoside gentamicin to rats for five days, a decrease in concentrating ability was demonstrated, caused by impaired vasopressin-mediated water transport. Further treatment resulted in a fall in Cin to 15 percent of control, although RBF was reduced to only 67 percent of control, and urine flow rate rose above control levels. Induction of acute and renal failure with dichromate was associated with variable high or low urinary flow rates according to pre-injury intake of sodium. Urine volume correlated directly with cortical blood flow. These data suggest that the non-oliguric pattern of acute renal injury is caused by preservation of cortical perfusion in the setting of severe tubular injury.
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PMID:Studies on the mechanism of non-oliguric experimental acute renal failure. 732 6

Acute renal failure (ARF) is defined as a renal insufficiency of sudden onset (increase of creatinine and urea in the serum) combined with or without oliguria (less than 500 ml of urine per day). Nephrotoxins (drugs, contrast medium) or renal ischemia (hypovolemia, hypotension, shock, septicemia, treatment with CEI) may affect the renal tubulus through several pathways, all of which may result in ARF. Ultrasound allows to distinguish hydronephrosis from ARF which is characterized by increased width of the parenchyma and low echodensity of the medulla. ARF is usually reversible. If conservative therapy fails, dialysis treatment is necessary.
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PMID:[What should the general practitioner know about diagnosis and treatment of acute kidney failure?]. 778 97


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