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Query: UMLS:C0035078 (renal failure)
 31,970 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

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 a series of 114 consecutive patients with acute renal failure, the over-all mortality rate was 60 per cent; 62 per cent of the patients had a documented episode of hypotension just prior to the development of acute renal failure. In 11 patients, a second episode of renal failure developed following recovery from the initial episode of acute renal failure; all of these patients died. The urine output rate during the course of acute renal failure was inversely related to the mortality rate in the series as a whole. The mean duration of acute renal failure in survivors of the present series was 11.0 plus or minus 1.4 days. Complications of renal failure in the order of their frequency included hemorrhagic hypotension, sepsis, sepsis with hypotension and consumption coagulopathies; only 12 per cent had no complications. Only six of 51 patients whose clinical course was complicated by sepsis with or without an episode of hypotension survived. By contrast, 30 of 53 patients who had hemorrhagic hypotension without sepsis survived. The date suggest that although acute renal failure has a high mortality rate, it is a benign disease that is potentially reversible. Regardless of age and sex, renal functional recovery will take place if the patient is maintained in good physiologic condition long enough without a continued stress, such as sepsis, hypotension or hypovolemia, all of which prolong renal ischemia. During the course of renal failure, extreme care is essential to maintain adequate circulating volume without extracellular fluid overload; a second hemodynamic insult may result in serious damage to the regenerating renal tubules. We conclude that early recognition of acute renal failure, aggressive management of sepsis, careful titration of fluid and electrolyte therapy, meticulous monitoring, maintenance of the circulation and judicious utilization of dialysis will aid in reduction of mortality in these critically ill patients.
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PMID:Clinical determinants of survival from postoperative renal failure. 114 2

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

Out of 85 rabbits 2j received a purified 6% hemoglobin solution free of ghosts (1,8 gHb/Kg) and were compared to 14 animals receiving the same dose of a crude hemoglobin solution containing ghosts. 11 rabbits had 5 infusions with a daily dose of 1,2 g Hb/Kg of the stromafree solution. Controls were partly untreated partly infused with saline. Creatinin, urea, electrolytes, and haptoglobin were determined in the serum oxygen consumption was measured separately in cortex and medulla by Warburg technique, and all kidneys examined histologically. In both groups 20% of the animals died spontaneously. Both groups exhibited the typical morphological and functional signs of acute renal failure. There was an increase in creatinin, urea, and potassium in the serum and a gain in kidney weights. In cortex and medulla we found a 20% drop in O2 consumption in both groups. Thus there was no evidence that ghosts play any role in the pathogenesis of renal failure in hemolysis or in the course of Hb-infusions. even after 5 infusions with lower dose renal damage was demonstrable. The drop in haptoglobin levels indicates, that renal ischemia may be induced by a disturbance in hemoglobin breakdown. The pathogenesis of renal damage has to be elucidated before Hb-solutions come into therapeutical use.
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PMID:[Acute renal failure after the infusion of hemoglobin solutions with or without red cell ghosts in rabbits (author's transl)]. 123 60

The spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN) reduced the ischemia-reperfusion induced acute renal failure in the rat. Renal ischemia was produced in unilateral nephrectomized rats by complete occlusion of the left renal artery for 60 min. Perfusion of the kidney was then reestablished, and the rats were sacrificed 48 h later. PBN (100 mg/kg i.p.) administered 30 min prior to renal artery occlusion significantly reduced the increase in serum creatinine and urea and renal failure index, as well as the decrease in urine/plasma creatinine ratio and creatinine clearance compared to saline-injected ischemic rats. PBN injected to control rats had no effect on these parameters. These data support the hypothesis of an involvement of reactive free radicals in the pathogenesis of ischemia-reperfusion induced acute renal failure in the rat and suggest that PBN may be a useful agent for the prevention of renal ischemia-reperfusion damage.
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PMID:Ischemia-reperfusion induced acute renal failure in the rat is ameliorated by the spin-trapping agent alpha-phenyl-N-tert-butyl nitrone (PBN). 146 97

In several models of acute renal failure (ARF) in animals, acidosis has been found to worsen the renal failure, whereas alkalosis may ameliorate it. Most evidence points to a reduction in the degree of tubular obstruction by casts as the explanation for the beneficial effects of bicarbonate administration. However, alkalinization of the urine is effective only in some experimental conditions but not in others. The reason for these differences is not known but may relate to the nature of the obstructing casts. Alkalinization of the urine could decrease cast formation in Bence-Jones protein and hemoglobinuric ARF by increasing the negative charge on these molecules, thereby diminishing precipitation with anionic Tamm-Horsfall protein. In contrast, release of tubular cell contents into the urine, as occurs in renal ischemia, could lead to complex casts not responsive to alterations in urine pH. In aminoglycoside ARF, the beneficial effects of urine alkalinization may be due primarily to reduced uptake of the antibiotic by tubular epithelium, resulting in less cellular damage. Because tubular obstruction reduces net filtration pressure, new approaches to therapy which include efforts to raise net glomerular filtration pressure may improve the therapeutic efficacy of alkali administration.
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PMID:Acid-base balance and acute renal failure. 175 20

Post-ischemic renal failure is associated with a zone of vascular hyperaemia in the outer medulla of the kidney. The effect of this lesion on regional renal perfusion is, however, unclear. Acute unilateral renal ischemia was applied to four groups of ten adult male Wistar rats for a period of 60 min, followed by revascularisation for 0, 15, 30 or 60 min. The aorta was then clamped and Microfil was injected at a standard pressure to fill the renal vasculature. Gross and histological examinations of the renal parenchyma and vasculature were then performed. Regional renal Microfil perfusion was quantified by examination of unstained histological sections, giving rise to a vascular perfusion index (VPI) for each vascular region of the kidney. The VPIs were similar in control and ischemic kidneys that were not subjected to reflow (group 1). In contrast, the VPI was markedly decreased in the inner stripe and inner medulla in animals in which revascularisation had occurred (groups 2-4), and the vasculature in these regions was histologically shown to be packed with red blood cells. Post-ischemic renal failure is associated with hyperperfusion of the medulla resulting from blockage of the vasculature that occurs during revascularisation.
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PMID:Changes in regional renal perfusion following ischemia/reperfusion injury to the rat kidney. 192 62

In this study the interaction of endotoxemia and ischemic organ injury was investigated in a rat model. Animals received lipopolysaccharide to induce endotoxemia and were simultaneously subjected to renal ischemia. If only renal ischemia was induced, moderate azotemia occurred and all animals survived. Lipopolysaccharide treatment caused neither renal failure nor death. However, rats with both endotoxemia and renal ischemia showed severe azotemia, and 50% of the animals died within 48 hours. The observed mortality rate is unlikely related to renal failure since animals subjected to bilateral nephrectomy did not die within 48 hours after treatment with lipopolysaccharide. To further exclude the role of renal failure in the enhanced effect of endotoxemia, experiments were performed in which ischemic kidneys were excised from littermates and were placed in the abdomens of lipopolysaccharide-treated animals. A similar effect was observed: 50% of the animals died within 48 hours. Azotemia did not occur. Since tumor necrosis factor (TNF) is an important cytokine involved in endotoxemia-induced morbidity and death, we studied the role of TNF in our model. Plasma levels of TNF were increased during endotoxemia. Concomitant renal ischemic injury did not influence the concentration of TNF. When animals were treated with recombinant TNF and were subsequently subjected to renal ischemic injury, again a 50% mortality was observed, a rate similar to that in lipopolysaccharide-treated animals. We conclude that the sensitivity to endotoxemia is enhanced by tissue necrosis and may lead to death in the experimental model used in this study.
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PMID:Increased sensitivity to endotoxemia by tissue necrosis. 199 49

The objectives of this study were first to develop a reproducible and reversible model of acute renal failure following contrast medium infusion in the rat; second to use that method to compare the nephrotoxicity of low- and high-osmolar contrast agents. Contrast media or saline were perfused in the aorta while a clamp was applied on the aorta just above the renal artery. Three minutes of renal ischemia with or without infusion of isotonic saline induced no change in serum creatinine and a slight and transient decrease in creatinine clearance at 24 h. Urinary N-acetyl glucosaminidase (NAG) excretion was not modified in this control group. All 17 kidneys which were examined were normal. 2,100 mosm/kg hypertonic saline induced a significant increase in serum creatinine and a significant decrease in creatinine clearance (from 1.8 +/- 0.1 to 0.8 +/- 0.1 and 1.0 +/- 0.2 ml/min at 24 and 48 h, respectively). Urinary NAG excretion increased from 23 +/- 18 to 48 +/- 20 and 8 +/- 4 mumol h-1/mmol creatinine at 24 and 48 h, respectively (p less than 0.05). Histologic analysis of 5 kidneys revealed acute tubular necrosis (n = 3) and no histologic abnormalities (n = 2). Diatrizoate induced an acute and reversible renal failure. Creatinine clearance decreased from 1.6 +/- 0.1 to 0.4 +/- 0.1 and 0.8 +/- 0.1 ml/min at 24 and 48 h, respectively (p less than 0.01). Urinary NAG excretion increased also significantly from 43 +/- 9 to 352 +/- 79 and 64 +/- 23 mumol h-1/mmol creatinine at 24 and 48 h, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Renal effects of radiocontrast agents in rats: a new model of acute renal failure. 207 9


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