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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regular drug treatment in mild hypertension (diastolic blood pressure 90-104 mm Hg) reduces death from stroke, and other non-coronary vascular events. The optimum strategy remains sequential monotherapy with the lowest effective dose, with drug combinations as an option. A beta-adrenoceptor blocker or low-dose thiazide is good value treatment for many patients. beta-Blockers are good for young (under 50 years), anxious non-smoking men, men after myocardial infarction, and renal failure patients. Older persons over about 65 years, women, smokers, stroke victims, and liver disease patients should generally take a thiazide or calcium ion-channel blocker. Pregnant women and untreated gouty patients should avoid diuretics. Calcium blockers and angiotensin-converting enzyme inhibitors are preferable in severe or insulin-dependent diabetes and renal failure, and angiotensin manipulators or thiazides in heart failure or peripheral vessel disease. Hyperlipidaemia should not generally exclude thiazides or beta-blockers. Some hypertensive stroke patients without encephalopathy may not need antihypertensive drug treatment for the first 24-48 hours. Drug treatment should be tailored to individuals according to their general condition, physiological age, and any concurrent disease or medication. Unwanted drug reactions should not deter patients from fulfilling social and economic goals. The desired treatment end-point is a diastolic pressure of 85-89 mm Hg, but a compromise is usual in poorly motivated young men, and the elderly.
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PMID:Optimising drug management of individuals with cryptogenic hypertension. 202 55

The study was undertaken to evaluate the occurrence of renal failure following perinatal asphyxia in the newborns. Thirty newborns with severe birth asphyxia were included in the study along with 30 normal newborns who comprised the control group. Any neonate presenting with oliguria or blood urea more than 40 mg/dl or creatinine more than 1 mg/dl was subjected to a fluid and diuretic challenge. If oliguria or renal dysfunction persisted then the child was labelled as renal failure and these subjects were further investigated. It was observed that 43% of asphyxiated babies developed acute renal failure (ARF); 69.2% babies had oliguric renal failure. While no significant correlation could be seen between Apgar scores at 5 and 10 min and development of ARF, a significant relationship was seen between hypoxic-ischemic encephalopathy and ARF. Patients with oliguric ARF carried a poorer prognosis as compared to non-oliguric ARF.
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PMID:Acute renal failure in asphyxiated newborns. 205 7

We studied fifty seven episodes of cirrhotic spontaneous bacterial peritonitis in order to know its microbiological, clinical and evolutive characteristics. One third of the patients had presented some previous peritonitis episodes. Ninety three percent of the patients referred some symptoms at time of diagnosis. Ascitic fluid Gram stain showed the presence of bacteria in 72% of the samples. Culture of ascitic fluid was positive for a single microorganism in 50 cases (88%). Seventy seven percent of microorganisms were Gram negative being Escherichia Coli in 63% of cases. Hemoculture was positive in 68% of cases with an almost complete correspondence with germs found in ascites. Seventy four percent of patients presented some complication throughout their hospital stay being the most frequent renal failure (49%) and encephalopathy (46%). Sixty three percent of patients died being the mortality rate higher amongst the older patients and amongst those who did not present neither high temperature or peritonism, or those who developed some complication.
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PMID:[A microbiological and clinical study of 57 cases of spontaneous bacterial peritonitis in liver cirrhosis patients]. 209 Nov 10

Behavioral and electrophysiological evidence implicating the GABA-benzodiazepine receptor complex in the pathogenesis of hepatic encephalopathy was obtained using an improved rat model of hepatic encephalopathy caused by thioacetamide-induced fulminant hepatic failure. After the administration of thioacetamide together with supportive therapy, acute hepatocellular failure developed in rats as a result of massive hepatocellular necrosis without evidence of renal failure or hypoglycemia. The evolution of hepatic encephalopathy in this model was sufficiently slow to readily permit the staging of the syndrome. Prominent features of the encephalopathy include a marked reduction in open field activity and an abnormal visual evoked response. Both the deficits in spontaneous motor function and visual evoked response abnormalities of rats in stages III to IV hepatic encephalopathy were significantly improved after the administration of the benzodiazepine receptor ligands flumazenil or Ro 15-4513. Doses of flumazenil or Ro 15-4513 that produced these effects in rats with hepatic encephalopathy had no detectable action on either the behavior or the visual evoked responses of normal rats. The ability of benzodiazepine receptor ligands to ameliorate both the behavioral depression and the visual evoked response abnormalities associated with hepatic encephalopathy in the thioacetamide-induced rat model suggest an involvement of the GABA/benzodiazepine receptor complex in the pathogenesis of hepatic encephalopathy. In addition, the similarity of these observations to those in rabbits with hepatic encephalopathy caused by galactosamine-induced fulminant hepatic failure is compatible with the hypothesis that the mechanisms of hepatic encephalopathy in these two distinct models share a common final pathway, the allosteric enhancement of GABAergic tone through the benzodiazepine receptor.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reversal of the behavioral and electrophysiological abnormalities of an animal model of hepatic encephalopathy by benzodiazepine receptor ligands. 215 65

An encephalopathy and cardiomyopathy developed in a seventeen-year-old girl with chemotherapy-induced renal failure while receiving an intravesical aluminum infusion for hemorrhagic cystitis. Premortem serum and postmortem tissue aluminum levels were markedly elevated. It is likely that her inability to excrete absorbed aluminum contributed to her death. Aluminum infusions should be used with caution in patients with renal failure.
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PMID:Acute aluminum toxicity after continuous intravesical alum irrigation for hemorrhagic cystitis. 221 19

Children presenting with advanced leukaemia and non-Hodgkin's lymphoma may develop life-threatening complications in the early stages of management. Major metabolic disturbances with encephalopathy, septicaemic shock, pneumonitis, massive haemorrhage, or the physical effects of tumour masses may on occasion warrant intensive therapy. Close liaison between paediatric oncologists, oncological surgeons, and anesthesiologists is essential in establishing admission criteria for such cases and in defining therapeutic end points in the event of multisystem failure. This paper discusses the principles of intensive care management of patients with haematological malignancies by considering two cases who developed the tumour lysis syndrome with respiratory and renal failure. A case associated with metabolic encephalopathy is also described.
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PMID:Tumour lysis syndrome and the anaesthesiologist: intensive care aspects of paediatric oncology. 234 46

A previously healthy 35-year-old woman was seen at 37 weeks' gestation with a 10-day history of fever, vomiting, diarrhea and malaise. Serum laboratory findings included elevation of serum bilirubin and AST, prolongation of serum prothrombin time and a positive monospot. A tentative diagnosis of acute fatty liver of pregnancy was made, and a healthy male infant was delivered by emergency cesarean section because of fetal distress. Over the subsequent 3 days, acute progressive oliguric renal failure, disseminated intravascular coagulation, hypoglycemia requiring intravenous dextrose infusion and pancreatitis developed; her mental status progressed to stage III encephalopathy. Quantitative computed tomography estimated the liver volume to be 770 cm3. The decision to proceed with orthotopic liver transplantation was made on the basis of progressive clinical deterioration despite aggressive support and because of her small liver size. After transplant, the patient's multisystem failure rapidly reversed. Histopathological examination of the native liver demonstrated predominantly zone 3 microvesicular steatosis with characteristic ultrastructural changes consistent with acute fatty liver of pregnancy. Southern blot analysis for Epstein-Barr virus DNA was negative. We conclude that orthotopic liver transplantation should be considered for the small group of patients with fulminant hepatic failure associated with acute fatty liver of pregnancy who manifest signs of irreversible liver failure despite delivery of the fetus and aggresive supportive care.
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PMID:Fulminant hepatic failure caused by acute fatty liver of pregnancy treated by orthotopic liver transplantation. 240 63

We examined autopsied brain from 10 patients with end-stage renal failure who had undergone repeated hemodialysis. Eight had classic symptoms, and two had suggestive symptoms of dialysis encephalopathy. Findings were compared with those in autopsied brain from control adults who had never been hemodialyzed. Mean gamma-aminobutyric acid (GABA) contents were significantly reduced in frontal and occipital cortex, cerebellar cortex, dentate nucleus, caudate nucleus, and medial-dorsal thalamus of the hemodialyzed patients, the reduction being greater than 40% in cerebral cortex and thalamus. Choline acetyltransferase activity was reduced by 25-35% in three cortical regions in the hemodialyzed patients. These two abnormalities were observed in the brain of each hemodialyzed patient, regardless of whether or not the patient died with unequivocal dialysis encephalopathy. Pyridoxal phosphate contents were substantially reduced in brains of the hemodialyzed patients, but metabolites of noradrenaline, 3,4-dihydroxyphenylethylamine (dopamine), and 5-hydroxytryptamine (serotonin) were present in normal amounts. Aluminum levels were abnormally high in frontal cortical gray matter in the hemodialyzed patients. Although this study does not clarify the role played by aluminum toxicity in the pathogenesis of dialysis encephalopathy, the abnormalities we found suggest the need for further neurochemical investigations in this disorder.
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PMID:Neurochemical abnormalities in brains of renal failure patients treated by repeated hemodialysis. 241 64

Relatively little is known concerning Al toxicity in man or animals. Current literature associates encephalopathy, osteodystrophy, and anemia with excessive Al accumulation. The normal gastrointestinal tract is probably an efficient barrier to absorption and the normal kidney appears to eliminate Al efficiently. When administered parenterally, the g.i. barrier is by-passed. In the presence of renal failure, accumulation may occur. "Toxic" levels of Al have not been clearly established to guide clinicians, nor have "safe" levels in parenterals been defined. The extent of intoxication as a clinical problem is unknown, but may be more common in selected patient groups than is recognized. In the absence of reliable data, specific regulatory action has not been taken. In the interest of public health, the FDA is attempting to accumulate information for guidance of parenteral drug manufacturers and clinical practitioners.
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PMID:Aluminum in parenteral products: LVP and SVP, FDA medical perspective. 249 68

The surgical results are not satisfactory yet in Japan and only 46% of the patients are free of jaundice 3 years ago. However, we found many presentations which reported jaundice disappearance rate with more than 80% in the last several years. The main cause of death in jaundiced patients with the failed hepatic portoenterostomy was hepatic failure. Other causes of deaths in these patients, including those died within one month after operation, were peritonitis, cardiac and/or renal failure, hemorrhagic tendency and lung edema. The main cause of death in jaundice-free patients was rupture of the esophageal varices. We examined 48 long-term survivors ranging in age from 10 to 33 years. There were 41 cases without and 7 with jaundice. Thirty-seven (77%) of 48 cases were leading their normal lives. Among them, 6 cases were enjoying their lives after overcoming the sequelae, such as portal hypertension. The morbidities of the remaining 11 (23%) long-term survivors were jaundice in 7, portal hypertension in 5, encephalopathy after splenorenal shunt in 1 and so on. The cured states of most cases without jaundice are satisfactory and eventually these former patients can achieve a favorable quality of life.
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PMID:[The present status and problems in the treatment of biliary atresia with special reference to surgical and long-term results]. 258 16


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