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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of transient renal ischemia on renal concentration and distribution of 99mTc-HEDP, 99mTc-DMSA, and 99mTc-DTPA was compared in rabbits with acute tubular necrosis. Scintigrams were obtained after injection in normal rabbits or ones with unilateral or bilateral ischemia. 99mTc-HEDP concentration in ischemic tissue was 8 to 18 times normal 1--4 hours after injection, and the resulting images delineated the morphological changes in the ischemic kidneys more accurately than those obtained with DMSA or DTPA. Calcium concentration in the ischemic kidneys increased sixfold. 99mTc-HEDP may be useful in evaluation of renal failure secondary to tubular injury.
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PMID:Renal hyperconcentration of 99mTc-HEDP in experimental acute tubular necrosis. 22 Jun 70

Ten patients received kidneys from living, related donors, the transplants having multiple renal arteries; a retrospective analysis of the postoperative Hippuran renograms is presented. All seven kidneys that had the large artery reopened before anastomosis of the smaller, developed scintigram findings suggestive of acute tubular necrosis (ATN) in the region with the more prolonged ischemia. Three similar kidneys with simultaneous recanalization of both renal arteries had normal Hippuran scintiphotos. Electron photomicrographs from upper- and lower-pole biopsies--in one case undergoing sequential revascularization--confirm the development of ischemic changes consistent with ATN in the half of the kidney developing scan findings of ATN.
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PMID:Segmental acute tubular necrosis in kidneys with multiple renal arteries transplanted from living related donors. 33 16

Renal allograft blood flow (RBF) was measured at operation by electromagnetic flow meter and probes in 45 patients (34 cadaver donors and 11 living related donors). Mean RBF in 26 patients without acute tubular necrosis (ATN), was 412 +/- 80 ml/min and in 19 patients with ATN, 270 +/- 100 ml/min (p less than .001). Only two of 24 transplants (8%) with RBF greater than 350 ml/min had ATN; whereas, 17 of 21 transplants (81 per cent) with RBF less than 350 ml/min had ATN (p less than .001). In cadaver donor transplants, RBF did not correlate with duration of ATN, warm ischemia time, total ischemia time, pulsatile perfusion time or renal vascular resistance during perfusion. Measurement of renal allograft blood flow can predict presence or absence of postoperative ATN in 87% of patients.
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PMID:Human renal allograft blood flow and early renal function. 33 86

Warm ischemia is a potential problem during the harvesting of cadaveric kidneys for transplantation purposes. This ischemia can cause impaired renal function following transplantation. The purpose of our study was to determine whether the beta-adrenergic blocking agent propranolol was effective in improving renal function after ischemia. Dog kidneys were subjected to 30 minutes of warm ischemia followed by hypothermic pulsatile preservation for 24 hours. The kidneys then were autotransplanted with immediate contralateral nephrectomy. In this model only 50% of the untreated control group survived. Three different protocols using propranolol were tested. Administration of propranolol to dogs before the ischemic period, or installation of propranolol into the renal artery at the start of the ischemia, or addition of propranolol to the preservation perfusate lessened the severity of acute tubular necrosis and resulted in 100% long-term survival. Although the mechanism was not investigated, it has been suggested that propranolol is acting through its blockade of beta-mediated renin release and/or through its so-called membrane-stabilizing effect.
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PMID:Protective effect of propranolol in the treatment of ischemically damaged canine kidneys prior to transplantation. 35 13

Autotransplantation of the kidney was performed in seven adult mongrel dogs. A model of acute tubular necrosis (ATN) was developed by subjecting the kidney to warm ischemia (37 degrees C) for 40 to 60 minutes. Serial ultrasound examinations were performed every 12 hours until the animal died or was killed. Sonographic findings were correlated with laboratory and histological data. Throughout the course of ATN, the characteristic normal echo pattern of the kidney remained unchanged in six of seven dogs. In one animal there were changes in the renal cortex, while the medullary pyramids showed no alteration from the base-line study. This contrasts with extensive abnormalities found during rejection.
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PMID:Evaluation of acute post-transplant renal failure by ultrasound. 38 18

Experimental examinations were performed in 22 dogs to find out the mechanism which leads to a permanent or a reversible damage of the renal parenchyma after normo- and hypothermic ischemia. For this reason the perfusion and the distribution were examined with 133Xe, the vascular changes by angiography, and the parenchymal function with 131I-Hippuran. After normothermic ischemia a short-term reactive hyperemia appeared, which however could not compensate the damage of the renal tubular cells and the resulting excretory insufficiency. After hypothermic ischemia the perfusion was reduced, probably as a consequence of a vasconstriction by cold, however, the function of the tubular cells remained intact, because of the protective mechanism of the hypothermia. The importance of these findings for the development of the so-called "shock-kidney" (acute tubular necrosis) and for the conservative renal surgery in hypothermia is discussed and the application of measures beneficial to perfusion, are suggested.
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PMID:[Changes in perfusion and blood flow distribution following normo- and hypothermic ischemia of the kidneys]. 98 Jul 93

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

Metabolic and morphologic changes occurred in the kidneys of rats within 3 hours after inciting acute tubular necrosis by completely clamping the renal blood supply, by intramuscular injections of glycerol, and by subcutaneous injections of HgC12. Although the initial trend was for p-aminohippurate and tetraethylammonium transport to decrease and for oxygen consumption, ammonia production, and gluconeogenesis to increase after glycerol, all of these parameters changed in opposite directions after renal pedicle clamping and after subcutaneous HgC12 (4.7 mg. per kg;). In addition, early morphologic changes in glycerol-injected rats differed from those seen with pedicle clamping and low dose HgC12. With high dose HgC12 (25 mg. per kg.), the metabolic and morphologic changes were somewhere in between those seen with the other insults. Coinciding with early metabolic and morphologic changes, cardiac output and renal blood flow decreased soon after the glycerol was given. On the basis of our findings, we cannot ascribe all of the early metabolic and morphologic changes in the glycerol model to ischemia, and we postulate that the circulating heme proteins may be nephrotoxic to ischemic renal tissue.
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PMID:Early events in various forms of experimental acute tubular necrosis in rats. 112 11

In unilateral nephrectomized beagle dogs the remaining kidney was subjected to 2 hrs of ischemia in situ. The ischemic organ was cooled to 22--23 degrees C by initial hypothermic perfusion over a 5-F catheter introduced into the renal artery via the carotid artery. It was then left in the open abdominal wound without any further attempts of cooling. Three perfusates were used: an isoosmolar Dextran solution (Eisenberger), a hyperosmolar, "intracellular" electrolyte solution (Sacks), and a hyperosmolar, "extracellular" electrolyte solution. There was a mean postoperative increase in serum creatinine levels of 0.6 mg-%. By the 3rd p.o. day at latest the serum creatinine was again within normal limits. The inulin and PAH clearances on the 7th and 14th p.o. day showed no significant differences to preoperative determinations. No definite advantage or disadvantage was noted among the three perfusates. All control dogs whose kidneys were made ischemic for 2 hrs without perfusion died due to acute tubular necrosis. Apparently the homogenous cooling and flushing by the initial perfusion is of more importance for good preservation in this situation than the composition of the perfusate.
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PMID:[Short time in-situ preservation of the ischemic kidney by a simple initial hypothermic perfusion with various cold solutions. An animal experimental study]. 115 70

Glucagon in small intravenous (i.v.) doses markedly increases glomerular filtration rate (GFR) in normal anesthetized dogs. In this study, the effects of glucagon 5 mug/min (i.v.) on renal hemodynamics was tested in four canine models of acute pre-renal failure (hemorrhage, barbiturate overdose; renal arterial clamping and renal arterial infusions of noradrenaline) and in a model of unilateral acute tubular necrosis at 4 h and 6-7 days following completion of the ischemic insult. Following hemorrhage and barbiturate excess, with arterial blood pressure maintained at 65-70 mm Hg, whole-kidney GFR and clearance rate of p-aminohippurate decreased by 50-70%. During this reduction of perfusion pressure, the subsequent infusion of glucagon increased GFR by 90-130%. In models where arterial pressure was normal during the period of ischemia (clamping and noradrenaline infusion), not only did glucagon significantly increase renal perfusion, but the ischemic kidney proved to be far more sensitive to the hemodynamic effects of glucagon (delta GFR - 120-160%) than the contralateral control (deltaGFR = 30-40%). In three dogs completely anuric following renal arterial clamping, glucagon was able to improve blood flow and restart urine formation. Glucagon, but not dopamine, was able to simulate the beneficial effects of hypertonic mannitol on renal function in dogs with hemorrhagic hypotension. Glucagon was without effect in established acute tubular necrosis. This study, therefore, indicates that, during renal ischemia, glucagon may be quite effective in preserving urine output and perfusion of the kidneys.
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PMID:The effect of glucagon on glomerular filtration rate in dogs during reduction of renal blood flow. 117 90


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