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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of Sacks solution for hypothermic preservation of dog kidneys was determined. Complete ischemia was produced in one kidney for thirty minutes by clamping the renal pedicle in situ, followed by excision and immediate washout with the cold preservation fluid. Kidneys were stored in Sacks solution at 2 degree C. for forty-eight hours, reimplanted in the donor, and the normal, contralateral kidney was removed. Complete reversal of renal impairment with long-term survival was observed in 2 of 9 animals. Of 7 animals with graft failure, 2 showed the beginning of a tendency to reverse a rising serum creatinine at the time of death or sacrifice. In the remaining 5, creatinine rose unrelentingly until death or sacrifice occurred. The observed 22 per cent survival rate was significantly (p less than 0.05) less than the 83 per cent survival reported by Sacks, Petritsch, and Kaufman. Evidence suggestive of intrarenal deposits of MgHPO4-3H2O was found in 2 of 4 dogs sacrificed for graft failure. This raises questions of the solution's safety as well as its efficacy. We are unable to confirm the success of the original investigators with this new preservation solution.
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PMID:Evaluation of Sacks solution for hypothermic preservation of kidneys. 110 20

Ischemic hepatitis is not an uncommon complication of reversible severe hypotension or cardiac failure. The prognosis usually is determined by the cause of the initial hypotension or cardiac failure, rather than the subsequent hepatic dysfunction. We report a retrospective analysis of nine patients with ischemic hepatitis in which previously unreported clinical and biochemical abnormalities are noted. The clinical and biochemical course of the patients were reviewed until recovery or death from ischemic hepatitis. All the patients had a rapid striking elevation of aspartate aminotransferase, and lactic dehydrogenase, with an equally rapid resolution of these parameters. Abnormal serum glucose levels occurred in six patients (none of whom had a prior carbohydrate intolerance). Insulin therapy was given to three patients for a limited period. Renal impairment was manifest in all nine patients, and it resolved spontaneously within 10 days. Altered mental status was detected in six patients; the changes reverted to normal within 7 days of their onset. A preexisting anemia (hemoglobin less than 11.0 g/dl) was noted on admission in four patients, and it did not appear to potentiate the manifestations of the hepatic ischemia. We conclude that ischemic hepatitis should be anticipated in all patients with a recent history of systemic hypotension. It should be considered in the differential diagnosis of patients with unexplained hepatitis; the early massive rise in lactic dehydrogenase, the rapid fall in transaminases, and the early mild/moderate renal failure strongly suggest ischemic hepatitis. Patients with ischemic hepatitis can manifest reversible renal failure, mental confusion, and hyperglycemia which may require insulin for its control.
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PMID:Ischemic hepatitis: widening horizons. 848 Jul 56

We examined the effects of dietary deficiency of vitamin E and selenium on the ischemia-reperfusion model of renal injury in the rat. Deficient diets imposed for six weeks on three-week-old weanling rats led to no significant differences in body weights, serum creatinine, GFR, RBF, TmPAH or urinary total protein excretory rates prior to ischemia. Twenty-four hours after one hour of ischemia, animals on the deficient diet demonstrated more markedly impaired GFR, RBF, TmPAH and urine to plasma creatinine concentrations and an increased renal failure index. Tubular damage was more severe injury in the deficient animals. Lipid peroxidation, 15 minutes after the release of the ischemic clamp, was increased in the deficient animals. We confirmed the effects of our dietary manipulation in impairing the oxidant scavenging system in the deficient animals since glutathione peroxidase activity was reduced to less than 5% in the basal state, and this striking reduction persisted following ischemia. Plasma vitamin E concentrations were also markedly depressed in the deficient diets. This dietary deficiency also worsened the course of acute renal injury and was accompanied by 50% mortality compared to 0% mortality in the control animals. Thus, dietary deficiency of vitamin E and selenium led to greater structural and functional renal impairment and increased lipid peroxidation following ischemia. These data provide support for the role of reactive oxygen species in mediating ischemia-reperfusion injury.
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PMID:Dietary deficiency of antioxidants exacerbates ischemic injury in the rat kidney. 207 54

In 10 patients undergoing aortic bypass grafting with peroperative aortic cross-clamping we measured the levels of myoglobin and creatine phosphokinase. The duration of peroperative lower limb arterial clamping ranged from 50 min to 95 min. No significant increase in either serum myoglobin or in serum creatine phosphokinase was found during lower limb arterial clamping or for the first two hours after release of ischemia. Both parameters reached a maximum value at 24 hours after release of ischemia, with a median serum myoglobin concentration of 565 micrograms/l (range: 132-2688 micrograms/l) and a median serum creatine phosphokinase activity of 457 U/l (range: 190-1602 U/l). The increase in serum myoglobin and creatine phosphokinase was not associated with the duration of lower limb arterial clamping. Renal impairment was not found in these patients, as evaluated by the serum concentration of beta 2-microglobulin.
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PMID:Myoglobin and creatine phosphokinase in serum during and after aortic bypass grafting. 243 46

To evaluate the combined effects of a brief ischemic insult and cyclosporine, four groups of male Munich Wistar rats were given: a) parenteral cyclosporine (60 mg/kg i.p.) for 4 days following 20 minutes of bilateral renal ischemia, b) the castor oil cyclosporine vehicle in a comparable volume and the same ischemic insult, c) saline in the same volume and ischemia, or d) saline and sham surgery. The cyclosporine animals ate and drank poorly, and therefore the other groups were pair-fed and watered with them. The cyclosporine-ischemia group developed significant renal failure. The other groups exhibited only a mild rise in blood urea nitrogen. Tubular vacuolization was a prominent feature in the cyclosporine and vehicle groups, but not in the saline groups. Vacuolization was correlated with severity of renal impairment. Lipid stains showed that many of the vacuoles contained lipid. Eosinophilic cytoplasmic inclusions were seen only in the cyclosporine or vehicle- (castor oil) treated animals. These findings emphasize the probable functional importance of tubular lesions in cyclosporine-induced acute renal failure, and suggest that the castor oil vehicle of parenteral cyclosporine may have renal effects of its own.
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PMID:Acute renal failure produced by combining cyclosporine and brief renal ischemia in the Munich Wistar rat. 370 29

A double-blind study comparing electrocardiographic (ECG) abnormalities induced by methyglucamine iodamide and methylglucamine/sodium diatrizoate was conducted in 189 patients. The media were each administered by both bolus and infusion. Iodamide caused fewer ECG changes both by injection and infusion. This contrast medium also resulted in fewer ECG changes in the patient groups with known prior ECG abnormalities, cardiovascular disease, arrhythmias, ischemia, or renal impairment and in those over 50 years of age. Digitalis did not increase the frequency of ECG abnormalities with either medium. With diatrizoate, the lower bolus dose produced as many major ECG changes in the presence of preexisting ECG abnormalities (arrhythmias, ischemia) or prior cardiovascular disease as the three-times-larger infusion dose more slowly administered; conversely, the opposite was found when renal insufficiency or older age existed. The conclusion is that iodamide media caused fewer ECG abnormalities and may be less hazardous.
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PMID:Contrast-medium-induced electrocardiographic abnormalities: comparison of bolus and infusion of methylglucamine iodamide and methylglucamine/sodium diatrizoate. 660 Mar 6

Among 61 patients with severe pregnancy induced hypertension, cerebral lesions were detected on CT scans in 23 cases (37.7%). The positive rates were 5/25 cases in preeclampsia and 18/36 cases in eclampsia. The incidence rate of cerebral lesions in eclampsia was significantly higher than that in preeclampsia (chi 2 test, P < 0.05). Furthermore, it showed that patients with renal impairment and retinal changes were more susceptible to cerebral lesions (P < 0.05), through comparative study of the relationships between either the function of liver and kidney or retinal changes and cerebral lesions. Main manifestations of cerebral lesions were ischemia, edema and infarction. The represented the different pathological stage of cerebral lesions. The cerebral lesions were mainly involved at cortical or subcortical area of bilateral parietal or occipital lobe (60%), secondly at the deep basal ganglia and the superior sagittal sinus. The pathological process of cerebral lesions and the management of pregnancy induced hypertension were analysed.
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PMID:[Cerebral lesions in the severe pregnancy induced hypertension: 61 cases of X-ray computed tomography of the brain]. 824 45

NSAIDs pose little threat of renal insult in normal, healthy persons at therapeutic dosages. However, NSAID administration to susceptible persons may cause decrements in renal plasma flow and glomerular filtration rate within hours. Such acute noxious renal effects are mediated by products of arachidonic acid metabolism. Precipitous decrements in glomerular filtration and renal ischemia, manifested by increased serum creatinine and urea nitrogen, are possible. However, these effects are usually fully reversible with prompt discontinuation of the offending NSAID. Risk factors for the development of these acute renal effects are known. Acute interstitial nephritis with or without nephrotic syndrome is a rare form of renal toxicity that typically occurs between 2-18 months of use. Renal impairment may be so severe as to require temporary hemodialysis; however, renal function usually returns to normal upon discontinuation of the NSAID. The mechanism of acute interstitial nephritis is presumed to be of allergic origin but could also be caused by a reactive metabolite. Fenoprofen use appears to be associated with a much higher risk for its development. In contrast to the acute effects of NSAIDs, irreversible, analgesic-associated nephropathy manifested by papillary necrosis and chronic interstitial nephritis may occur following months to years of high doses of analgesic mixtures. The mechanism by which combination analgesics produce this form of renal injury is unknown and could be either a result of medullary ischemia or a direct effect of a reactive metabolite. An important issue to be resolved is the relationship between the acute, reversible, prostaglandin-mediated renal effects of the NSAIDs and chronic, irreversible destruction, if such a relationship exists. Theoretically, continual or repeated decrements in renal function in patients with predisposing risk factors could cause or contribute to progressive deterioration in renal function. Elevations in blood pressure or interference with the effects of antihypertensive medications could theoretically also contribute to long-term renal deterioration. In addition to renal syndromes caused by NSAIDs that result in renal impairment, other transient effects on electrolyte and water metabolism may also occur. Reduced secretion of sodium may result in formation of edema, exacerbation of heart failure, or increased blood pressure. Hyporeninemic-hypoaldosteronism may produce hyperkalemia. Finally, reduced excretion of water has rarely caused hyponatremia. It has been suggested that NSAIDs may be renoprotective in patients with nephrotic syndrome. Others have suggested that sulindac is "renal-sparing" because of a unique metabolic pathway that supposedly limits the exposure of the kidney to the active sulfide metabolite.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renal toxicity of the nonsteroidal anti-inflammatory drugs. 849 47

Despite the high incidence of coronary artery disease in patients with renal impairment, its diagnosis and management remains difficult. The treatment of acute coronary syndrome in this particular group of patients is more complex than in patients with normal renal function. They have a high prevalence of asymptomatic cardiac ischemia. Abnormal baseline electrocardiogram (ECG) findings and nonspecific elevation of cardiac enzymes may be present. Studies are lacking regarding their management mainly because they have been excluded or were not studied as a subgroup in the clinical trials. Thrombolytics are underused during acute myocardial infarction. Heparin, mainly low-molecular weight heparin, for unstable angina and non-Q wave myocardial infarction, should be used with caution because the higher risk for bleeding. Other medications, such as aspirin, metoprolol, and nitroglycerin should be used as in the general population. The newer platelet glycoprotein IIb/IIIa inhibitors may need renal dose adjustment. Revascularization should be pursued if necessary by percutaneous coronary intervention or coronary artery bypass grafting. However, the prognosis and risk of revascularization versus medical therapy have not been determined yet.
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PMID:Medical and revascularization management in acute coronary syndrome in renal patients. 1117 56

Pathogenic mechanisms of renal injury by thrombotic microangiopathies present a challenge to the multidisciplinary team caring for a patient with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-HUS). First recognized 77 years ago as a rare disorder characterized by reversible platelet aggregation in the microcirculation causing ischemia in various organs, the prognosis was always fatal. In the past 20 years, due to effective treatment with plasma exchange therapy, there has been a decline in the mortality rate to 10-20%. The classic pentad of symptoms of TPP-HUS include thrombocytopenia, microangiopathic hemolytic anemia, neurologic abnormalities, fever, and renal impairment. Frequency of TTP-HUS appears to be increasing. Due to the urgent need for a diagnosis, sufficient diagnostic criteria for TTP-HUS are currently thrombocytopenia and microangiopathic hemolytic anemia in the absence of another apparent cause. It is imperative to have a solid understanding of the pathophysiology and current standards of practice of TTP-HUS in order to facilitate positive patient outcomes in this unique group of patients.
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PMID:Thrombotic thrombocytopenic purpura-hemolytic uremic syndrome: pathophysiology and management. 1199 52


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