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)

An active approach to severe renal lithiasis is advocated, though operative procedures often require interruption of the blood supply. Te evaluate the effect of ischemia on the kidney the literature has been searched and we have reached the following conclusions. A warm ischemic time of more than 20 minutes causes a brief and transitory reduction in renal function. If ischemia exceeds 30-40 minutes many kidneys will not regain their previous function. If the kidney's temperature is lowered to about 15 degrees C, ischemia can be tolerated for up to 12 hours. A priori these time limits applicable to normal kidneys are to broad for use in diseased kidneys. Cooling of the kidney can be achieved by either perfusion-cooling or by external parenchymatous cooling. We describe a method using the latter system for stone removal in 14 patients with staghorn calculi or multiple stones. Preoperatively 9 patients (64%) had persistent urinary tract infection, whereas infection persisted in only 2 patients following the operation (14%). Complete stone removal was achieved in 13 patients (93%). Renal function evaluated by creatinine clearance and renography generally improved following operation. There were no deaths, but in 9 patients severe complications were seen (transient oliguria and septicemia). At follow-up investigation 1.5 years after operation renewed stone formation was found in 1 patient, while the incidence of urinary tract infection had increased to 3 patients (21%). It is concluded that extensive surgery for stone removal with the use of external parenchymatous cooling is worthwhile and promising in patients with staghorn calculi or multiple stones in the kidneys.
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PMID:Regional hypothermia in renal surgery for severe lithiasis. 84 6

Total ureteropelvic necrosis of the transplanted kidney occurred more than one month after transplantation in 5 of 575 consecutive renal transplants performed at the University of Minnesota Hospital since 1963. Necrosis became evident long after normal renal function had been established. Histologic signs of rejection were minimal, but perinephric or periureteral hematomas were found in 3 of 5 patients: post-transplant acute tubular necorsis requiring hemodialysis occurred in all. The pathogenesis of this complication probably involves (1) a primary deficit of blood supply from the renal vessels to the pelvis and ureter, (2) a failure to develop a new ureteral blood supply because of surrounding hematoma, (3) early swelling of the ischemic ureter resulting in oliguria interpreted as acute tubular necrosis, (4) resolution of edema resulting in diuresis, and (5) late patchy ureteral necrosis and fistula formation due to ureteral ischemia.
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PMID:Late ureteropelvic necrosis after transplantation. 109 Oct 63

In this study, we characterized the sequence of several intrarenal events and evaluated their relative importance in the pathogenesis of unilateral oliguric acute renal failure induced experimentally in rats by complete occlusion of a renal artery for 1 hour. Kidneys were studied prior to occlusion and 1-3 hours and 22-26 hours after release of the temporary occlusion. Renal blood flow measured by an electromagnetic flow transducer was reduced to 40-50% of control during both postocclusion periods. Flow of tubular fluid was markedly reduced, and the damaged kidneys were oliguric. Proximal and distal convolutions were filled with fluid and dilated 1-3 hours after occlusion; their pressures were greatly heterogeneous and were elevated, on the average, to 31 and 16 mm Hg, respectively. Glomerular capillary pressure at this time was normal or slightly increased. Histological sections showed extensive tubular obstruction. We conclude that initially the oliguria is primarily due to intraluminal obstruction in the absence of predominant increases in preglomerular vascular resistance. Observations at 22-26 hours after occlusion indicated acute tubular necrosis. Moreover, the combined involvement of preglomerular vasoconstriction, presisting tubular obstruction, and passive backflow of tubular fluid appeared to be important in the maintenance of the oliguria. Glomerular capillary, proximal intratubular, and peritubular capillary hydrostatic pressures were reduced below control values. After acute volume expansion, the reduced pressures and renal blood flow were reversed, yet the experimental kidneys remained oliguric. Thus, it is clear that tubular obstruction is a significant factor responsible for both the genesis and the maintenance of oliguria in this experimental model of ischemia-induced acute renal failure.
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PMID:Pathogenesis of acute renal failure following temporary renal ischemia in the rat. 119 55

A randomized, prospective comparison of OKT3 vs. ALG (University of Minnesota) was performed in patients who had acute renal failure after a cadaver renal transplantation. Criteria for admission to the study were oliguria or increasing serum creatinine in the first 12 hr after renal transplantation. ALG or OKT3 was administered after randomization beginning 12-36 hours posttransplantation. There were no significant differences in age, sex, original disease, ischemia time, or HLA matching between groups. Graft survivals at 1 and 6 months were 84% and 84%, respectively for the ALG group. One- and 6-month graft survival for the OKT3 group was 88% and 84%, respectively. These differences were not statistically significant. The number of rejection episodes and the number of patients with rejection episodes were greater, and the time to first rejection was shorter in the OKT3 group compared with the ALG group, although none of these differences reached statistical significance. There were significantly less side effects in the ALG group compared with the OKT3 group (P less than .05). The greatest reductions in side effects were in fever and hypotension. Patients were monitored with flow cytometry analysis measuring the number of CD2 (T11) and CD3 (T3) cells to adjust the dose of both OKT3 and ALG. Starting doses were 10 mg/kg/day of ALG and 5 mg/day of OKT3. There were no significant differences in the incidence of infections (viral or bacterial) between the two groups. There were no rejection episodes during the prophylactic therapy with either ALG or OKT3. In summary, both ALG and OKT3 provided effective prophylaxis for patients with acute renal failure after renal transplantation. OKT3 was associated with a statistically significant increase in incidence of symptomatic side effects.
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PMID:Comparison of OKT3 with ALG for prophylaxis for patients with acute renal failure after cadaveric renal transplantation. 167 2

Liver transplant is the first therapeutic choice in most of the advanced liver diseases. Nevertheless, its performance originates a number of complications derived from: a) conservation techniques of the organ (in our study a prolonged time of hot ischemia was significantly associated with); b) surgery (all patients who required massive blood transfusions developed metabolic alkalosis); c) the graft itself (all the F 1. degrees were significantly infected), and d) extrahepatic causes (cyclosporin was responsible for high blood pressure and nephrotoxicity which appeared as oliguria with good response to furosemide, as well as hyperglycemia). Some other relevant results in our series were: right pleural effusion and thrombopenia which appeared with a high incidence. Infections were usually originated the staphylococcus which grows in half of the cultures. We also want to highlight the short mean stay and the low mortality incidence in the ICU.
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PMID:[Complications of liver transplant in intensive care. Experience in 130 cases]. 176 10

The results of five 'en bloc' kidney transplants from 5 anencephalic newborns are reported. The receptors were 8-50 years old. The graft survival 12 months after transplantation was 60%. The average plasma creatinine level the 1st month after transplantation was 4.0 +/- 0.8 mg/dl, after 6 months 1.5 +/- 0.8, and is currently 1.2 +/- 0.6 mg/dl. The follow-up time ranged from 17 to 55 months (mean 30.3 +/- 17.5 months). Two grafts were lost during the early posttransplantation period (due to arterial thrombosis and vascular rejection, respectively); the other grafts are still functioning. Two grafts showed initial oliguria. All of the patients required hemodialysis or peritoneal dialysis for 5-60 days (mean 22.5 +/- 21.4 days). The time of cold ischemia ranged from 15 to 35 h (mean 25.6 +/- 7.7 h). The literature published on the subject is reviewed, and it is concluded that anencephalic donors are an acceptable option for transplantation.
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PMID:Kidney transplantation from anencephalic donors. Report of 5 cases and a review of the literature. 228 20

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

The outcome of patients with acute renal failure following cadaveric renal transplant has been evaluated in a prospective, controlled trial, comparing treatment with cyclosporine (CSA) to prednisone, azathioprine, and antilymphocyte globulin (AZA). There was a high incidence of acute post-transplant renal failure in both groups: 37 of 51 CSA and 31 of 45 AZA patients, due to the long exposure of kidneys to warm and cold ischemia. Onset of adequate renal function was delayed for three or more weeks in 27 (53%) CSA and only nine (20%) AZA patients, and the only predisposing factor found was donor hypotension. All nine AZA and 18 of the 27 CSA patients with prolonged oliguria subsequently had a spontaneous diuresis. Nine of the CSA patients were changed to azathioprine and prednisone because of suspected CSA toxicity, and eight of these kidneys began functioning within days, even though they had been oliguric for 21 to 83 days. Of these nine patients, five had adequate long-term function on AZA, three developed CMV infections that were fatal to two individuals, and two rejected their grafts. Plasma CSA levels fluctuated widely in all patients, but were not higher in any group, including those with prolonged oliguria. During the oliguric period, biopsy specimens proved rejection was more common in the nine patients who had their CSA stopped than in the other CSA patients, and seven of these nine developed a diffuse interstitial fibrosis that was thought to be a manifestation of CSA toxicity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Post-transplant acute renal failure in cadaver renal recipients treated with cyclosporine. 391 72

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


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