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Query: UMLS:C0920646 (renal ischemia)
 2,515 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

In attempt to avoid a detrimental synergism between CsA and renal ischemia in the immediate postoperative period, ALG (425 lymphocytotoxic units/kg) with small doses of CsA (6-8 mg/kg) and P were applied as the initial immunosuppressive therapy in 14 recipients of cadaveric kidneys. ALG was administered for 5 to 14 days and 2 days before withdrawing ALG, Aza (2 mg/kg) was introduced. Results of this protocol were compared with those of 19 pts treated with CsA (12 mg/kg) and P. All the pts were followed for at least 12 months. The duration of posttransplant anuria was significantly reduced in the ALG/CsA/P group (p < 0.02). The sCr concentration after 12 months of observation was significantly lower (p < 0.05), no alterations in urinalysis were detected, the number of hypertensive pts was decreased. The acute rejection rates were equivalent in both groups, however 3 of 4 rejections in ALG/CsA/P group were resistant to steroids and occurred in pts with shortened period of ALG administration. The one year patient and graft survival in the ALG/CsA/P and control groups were respectively: 78.5%, 71.4% and 89.4%, 78.9%. Severe infectious complications in the group treated with ALG/CsA/P occurred in pts who were subsequently treated with OKT3.
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PMID:Antilymphocyte globulin with a small dose of cyclosporine A and prednisone as the induction of immunosuppression in renal allograft recipients. 129 76

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

Evidence has been presented in the past that muzolimine might act at a localization differently to sulfamoyl-type diuretics and/or with a different or additional mechanism. This is further supported by the fact that at the maximum of the dose-response curves for muzolimine and furosemide in rats, a combination of maximal oral doses still results in significantly higher sodium excretion. To further substantiate that this aspect of muzolimine is of relevance, e. g. for the therapy of acute renal failure, muzolimine treatment by food or implanted osmotic minipumps was employed in an obstructive model of severe renal ischemia in rats. Acute renal ischemia was induced in Wistar rats by clamping the left renal pedicle for 60 minutes with a microsurgery clamp. The right kidney had been removed four days before ischemia. Clearance data were obtained on the first, third and on the ninth to fourteenth days after ischemia in the surviving animals. Renal ischemia resulted in anuria, increased mortality and impaired renal function with histopathologically apparent tubular obstruction in the untreated controls. Treatment with muzolimine by food (in a concentration of 800 ppm for four days) and additional oral gavage one hour prior to ischemia prevented the sequelae of ischemia to a great extent. Similar beneficial effects could be obtained by therapeutic implantation of osmotic minipumps ensuring administration of 0.44 micrograms muzolimine/h per animal. These results in rats further support the suggestion that muzolimine might act differently to sulfamoyl-diuretics. Furthermore, they strongly implicate muzolimine as the diuretic of choice in acute renal failure.
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PMID:Beneficial effect of muzolimine in postischemic acute renal failure in rats. 400 95

A patient developed an occlusion of both renal arteries by extension of a thrombosis of the infra-renal aorta to the superior mesenteric artery. He presented with classical features of acute renal ischemia: lumbar pain, nausea, vomiting, anuria. Since surgery and intra-arterial thrombolytic therapy were not feasible, we performed two peripheral intravenous (i.v.) perfusions of 50 mg Recombinant Tissue-Type Plasminogen Activator (r-tPA) given at 24 hours interval. During the next month serum creatinine decreased from 8.8 mg/dl to 2 mg/dl and the creatinine clearance rose from 0 to 20 ml/minute. The patient never required any dialysis. Seven months later his renal function remains stable.
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PMID:A case of acute renal failure caused by thrombosis of both renal arteries. 794 28

Renal tubular dysgenesis (RTD), with hypoplasia especially of renal proximal convoluted tubules and clinical neonatal anuria or oliguria, has been reported as a congenital familial (autosomal recessive) disease, variably with features of oligohydramnios, Potter syndrome, or pulmonary hypoplasia. A similar tubular lesion due to antenatal tubular atrophy has been reported for conjoined twins with twin-twin transfusion syndrome or acardia and in infants of mothers given antihypertensive agents, including angiotensin-converting enzyme (ACE) inhibitors, during pregnancy, and it has been seen as a unilateral lesion in young infants with renal artery stenosis due to arteritis or medial arterial calcinosis. The renal tubular changes in RTD are very like those of the "endocrine kidney" in experimental animals and resemble those of the renal tubular atrophy of end-stage kidney diseases such as glomerulonephritis, tubulointerstitial kidney disease, obstructive uropathy/pyelonephritis, graft rejection of transplanted kidneys, or the renal parenchymal changes seen with protracted dialysis therapy. Labeled lectins that differentially mark proximal convoluted, distal convoluted and connecting, and collecting tubules showed no distinctive differences in staining patterns of the hypoplastic renal tubules of infants and children with RTD, postnatal renal artery obstruction, or the various types of end-stage renal disease with the lectins used (PNA, GSLI, UEA, and LTA). The findings suggest that the renal tubular changes in some if not all the conditions studied are the result of renal ischemia. The reported familial RTD with hypernephronic nephromegaly may be a specific disorder, but other forms could reflect renal ischemia acquired in utero or in early or later postnatal life.
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PMID:Labeled lectin studies of renal tubular dysgenesis and renal tubular atrophy of postnatal renal ischemia and end-stage kidney disease. 815 24

In the presence of a single functioning kidney, renal artery obstruction produces anuria, which can require hemodialysis. If the problem is diagnosed immediately and surgical intervention is not delayed, revascularization of the ischemic kidney is usually successful. Few authors, however, have reported the return of function to a small solitary kidney after occlusion lasting longer than 2 hours. We describe a case that involved thrombosis of the renal artery to an 8-cm solitary kidney; a successful endarterectomy was performed 29 hours after the onset of anuria. This case shows that the reversibility of renal ischemia is not necessarily determined by either the duration of occlusion or the size of the affected kidney.
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PMID:Thrombosis of the renal artery of a small, solitary kidney: successful return of renal function after prolonged anuria. 1522 64

The acute Page kidney phenomenon occurs as a consequence of external compression of the renal parenchyma leading to renal ischemia and hypertension. Between January 2000 and September 2007, 550 kidney transplants and 518 ultrasound-guided kidney biopsies were performed. During that time, four recipients developed acute oligo-anuria following ultrasound-guided allograft biopsy. Emergent doppler-ultrasounds were performed demonstrating absence of diastolic flow as well as a sub-capsular hematoma of the kidney. Prompt surgical exploration with allograft capsulotomy was performed in all cases. Immediately after capsulotomy, intraoperative Doppler study demonstrated robust return of diastolic flow. Three patients maintained good graft function, and one kidney was lost due to acute antibody-mediated rejection. We conclude that postbiopsy anuria associated with a subcapsular hematoma and acute absence of diastolic flow on doppler ultrasound should be considered pathognomonic of APK. All renal transplant specialists should be able to recognize this complication, because immediate surgical decompression can salvage the allograft.
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PMID:Acute Page kidney following renal allograft biopsy: a complication requiring early recognition and treatment. 1844 36

Acute aortic dissection (AAD) is a life-threatening condition with high morbidity and mortality, that involves renal arteries in at least 5-10% so leading to renal ischemia and insufficiency. AAD presenting with anuria and the necessity of renal replacement therapy occurs rarely. Here we describe a case of a hypertensive and obese patient presenting with anuria and acute kidney injury, who underwent to hemodialysis and later was diagnosed with aortic dissection. Through this case, we underline the importance of considering AAD as an important differential in patients with a long history of uncontrolled hypertension presenting with anuria.
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PMID:[An unusual case of acute kidney insufficiency]. 2503 14

Purpose. To describe the treatment of renal artery thrombosis with ultrasound-accelerated thrombolysis and discuss the management of prolonged renal ischemia. Case. A 76-year-old patient with a single functional kidney, mild chronic renal impairment, and a recent history of endovascular repair of a thoracoabdominal aneurysm with an aortic branch graft presented with acute flank pain, anuria, and renal failure. The side branch from the aortic stent graft to his single, right, functional kidney appeared to be completely thrombosed. Symptoms had started after cessation of oral anticoagulants because of a planned mastectomy for breast cancer. After identification of the occlusion, ultrasound-accelerated thrombolysis was started 19 hours after the onset of anuria. Angiography, 4 hours after beginning of therapy, already showed partial dissolution of the thrombus and angiographic control after 18 hours showed complete patency of the renal artery side branch. Despite a long period of ischemia, renal function was completely recovered. Conclusion. In patients with acute renal ischemia due to thrombosis of the renal artery, complete recovery of function can be achieved with ultrasound-accelerated thrombolysis, even after prolonged periods of ischemia.
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PMID:Successful reversal of acute kidney failure by ultrasound-accelerated thrombolysis of an occluded renal artery. 2527 40


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