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Query: UMLS:C0036690 (sepsis)
59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In almost all cases of acute renal failure associated with cholestatic jaundice, the occurrence of renal failure is preceded by episodes of shock, hypotension, sepsis, or surgical intervention. The pathologic finding is usually that of acute tubular necrosis. A patient with obstructive jaundice developed renal failure; the clinical and pathologic features were consistent with those found in the hepatorenal syndrome. No episodes of shock or sepsis preceded the onset of that renal failure. At autopsy, the findings were normal.
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PMID:Hepatorenal syndrome associated with obstructive jaundice. 406 31

A survey has been made of 150 cases of acute renal failure (A.R.F.) seen between 1962 and 1981. The overall mortality was 43.3%. The patients ranged from 7 to 75 years old. The mean age of all the patients was 47.2 years old. The mean age of the patients seen between 1970 and 1981 was 58.1 years old, 20 years older than those seen between 1962 and 1969. Despite increasing expertise in management of the complications of surgical, medical, and obstetric disorders, and considerable technical advances in dialysis, there was no decrease in mortality over the 20-year period of survey. Many factors have been identified as having an adverse influence on prognosis, such as age of patient, surgical origin, and complications. Mortality rate was high in the patients over 71 years old, postsurgical group (55.6%), and hepatorenal syndrome group (92.3%). Five major complications had an adverse influence: septicemia (57.1%), respiratory infection (61.1%), cardiovascular disorder (46.3%), hemorrhage (59.6%), unconsciousness (62.2%), and hepatic dysfunction (56.8%). Between 1970 and 1981 the mortality in the patients dialyzed up to 3 times was 81.3%, compared with 26.5% in those dialyzed from 4 to 19 times (p less than 0.01). In the former group severity of the underlying disorder had an adverse influence on prognosis. Although the A.R.F. may be controlled in the earlier stages of illness, many of these patients die of overwhelming infection or other complications.
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PMID:[Clinical studies on the prognosis of 150 cases of acute renal failure]. 661 Feb 96

Fourteen thermally injured patients with severe inhalation injury were sequentially studied with the thermal-green dye double indicator dilution technique of extravascular lung water (EVLW) measurement. Eight females and six males (average age, 49 years, and average thermal burn, 37% body surface) were studied for 2-31 days postinjury. All were burned in a closed space, had facial burns, soot in their sputum, and a mean carboxyhemoglobin level of 30%. Nine patients died, six of sepsis, one each of acute renal failure, hepatorenal syndrome, and anoxic brain damage. Mean EVLW on admission was 7.0 +/- 2.9 ml/kg and remained normal in the five survivors and in the patients dying of acute renal failure and anoxic brain damage. Six patients had increases in EVLW, caused by altered pulmonary capillary permeability in five and by elevation of hydrostatic pressures in one patient (hepatorenal death). Of the five patients with permeability edema, one appeared to result from a direct early effect of inhalation injury resulting in an EVLW of 13.3 ml/kg on admission. The other four patients had EVLW increases after the onset of sepsis, resulting in a mean EVLW of 23.2 +/0- 7.2 ml/kg at death (p less than 0.01). Seventy-one per cent of all patients developed pneumonia, which appears to have caused an EVLW increase in one patient; the other EVLW increases were caused by systemic sepsis. In our present study of 14 patients with definite severe inhalation injury only one had an early increase in EVLW directly related to the inhalation injury, an early effect on capillary permeability presumably caused by direct chemical toxicity of inhaled gases. The remaining four cases of permeability edema occurred 4-24 days postinjury and resulted from burn wound or pulmonary sepsis. We thus conclude that increases in EVLW after thermal and inhalational injury are primarily caused by systemic or pulmonary sepsis, and have a delayed onset. Early increases in EVLW may be a result of the chemical toxicity of inhaled gases but are very uncommon, moderate in degree, and are seen only with the severest cases of inhalation injury.
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PMID:Effect of inhalation injury on lung water accumulation. 687 13

This report describes light and transmission electron microscopy (LM and EM, respectively) studies of kidneys from five cases of hepatorenal syndrome. The kidneys were removed and fixed for LM and EM between 30 and 120 min after death. All patients had progressive renal failure after admission to the hospital. All cases were jaundiced, had ascites, and exhibited features of hepatic encephalopathy. LM study revealed severe acute tubular lesions (ATL) or, more conventionally, acute tubular necrosis (ATN). EM study demonstrated necrosis of the proximal tubules characterized by swelling, disorganization of the cristae and appearance of dark bodies in the mitochondria, coalescence, fragmentation or displacement of the microvilli, loss of plasma membranes, rupture of the basement membranes, and separation of the cells from the basement membranes. Rupture of tubular basement membranes (tubulorrhexis) and mitochondrial dark bodies suggest an ATN due to ischemia or induced by vasoconstrictor substance(s). Glomerular lesions were infrequent (one in five) and therefore, do not seem to have contributed to renal failure. All cases terminally had extremely low urinary sodium (11 mEq/liter), high urinary potassium (50 mEq/liter), a remarkably low urinary sodium/potassium ratio (0.26, normal = 4.27), and a low urinary osmolality (less than 400 mOsm/kg). From this study we conclude that an ATN of variable severity may be associated with the hepatorenal syndrome. Since this ATN developed without preceding shock, sepsis, or hypotension it is possible that this ATN like that in ischemic acute renal failure may be due to reduced renal blood flow and intense cortical vasoconstriction which has been reported in hepatorenal syndrome. Finally, our data imply that low urinary sodium is consistent with this pathologic lesion in this clinical setting.
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PMID:Acute tubular necrosis in hepatorenal syndrome: an electron microscopy study. 714 28

Renal dysfunction often complicates the course of liver transplant recipients. Preoperative renal dysfunction, including hepatorenal syndrome (HRS) may be present. Assessment of renal function in the pretransplant patient with end-stage liver disease is fraught with pitfalls. Direct measurement of GFR by a method other than creatinine clearance is recommended wherever possible. Preoperative renal biopsy should also be considered in those patients with renal dysfunction in whom the diagnosis of HRS is not definite. With the routine use of veno venous bypass, renal perfusion is maintained and intraoperative events generally do not play a significant role in the development of postoperative dysfunction. Postoperatively immunosuppressive medications such as CsA or FK506 account for most of the renal dysfunction that is observed. Other factors such as graft dysfunction, sepsis, and nephrotoxic drugs may also participate in renal impairment. The exact mechanism of cyclosporine or FK506 nephrotoxicity remains unknown. In liver transplant recipients, no convincing therapeutic strategies exist to combat nephrotoxicity other than dose reduction of immunosuppressive therapy. Patients with HRS can be successfully treated by liver transplantation with recovery of renal function and with patient survival rates comparable to recipients without HRS, despite increased morbidity.
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PMID:The kidney in liver transplantation. 769 Dec 5

Twenty-five patients with liver cirrhosis and portal hypertension were admitted for creation of a transjugular intrahepatic portosystemic shunt (TIPS). The procedure was successful in 22 patients (technical success 88%). The mean portal pressure gradient was lowered from 24.5 mmHg before to 11.4 mmHg after TIPS. Two early and three late occlusions were observed (primary patency rate 78%). The rate of secondary interventions was 41%. Five times a hepatic vein stenosis was dilated and stented, two times an occluded shunt was recanalized, two times a new shunt was created parallel to an occluded (secondary patency rate within a maximum of 16 months 95%). In two patients sepsis occurred which was effectively treated with antibiotics, two patients died shortly after TIPS due to hepatorenal syndrome and hepatic failure, respectively. There was no recurrent bleeding. Two patients developed hepatic encephalopathy; both improved after protein restriction. The authors conclude that TIPS is an alternative procedure to shunt surgery, especially for patients who cannot benefit from sclerotherapy.
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PMID:[Clinical experiences with the transjugular intrahepatic portocaval shunt (TIPS)]. 837 9

Analysis of the factors influencing the prognosis of acute renal failure was carried out in cases experienced during the past 10 years. The factors presumed directly affecting the renal function (acute insults) and coexistent predisposing factors (risk factors) were analysed. The followings were considered to be acute insults: surgery/trauma/burn, drug intoxication, sepsis, hypotension, dehydration, rhabdomyolysis, hepatorenal syndrome, and hypercalcemia/hyperuricemia. Suspected risk factors included age, urine volume, underlying disorders/complications. Risk factors rather than acute insults were related to the outcome of acute renal failure. The mortality rate increased as the associated risk factors increase in number. In non-oliguric cases, maximum serum creatinine level was lower than the anuric cases, however there was no difference in the duration of the impaired renal function between 2 groups. In survival cases, the factors affecting the time for the recovery of renal function were also studied, but no definite factors could be determined.
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PMID:[Clinical analysis of the factors affecting the prognosis of acute renal failure]. 850 61

Sepsis, cellulitis, and necrotizing fasciitis rarely have been described as causes of compartment syndrome. We report a case in which forearm compartment syndrome presented as the initial symptom of systemic infection. Vibrio vulnificus, the etiologic pathogen of the compartment syndrome, was isolated from wound and blood cultures. The patient was treated with systemic antibiotic treatment and multiple forearm fasciotomies. The infectious process progressed rapidly, however and due to underlying liver insufficiency, the patient died of hepatorenal syndrome. This case illustrates the nature of V. vulnificus infections, which are characterized by shellfish transmission, predilection for soft tissue seeding, and a fulminant course in the compromised host.
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PMID:Compartment syndrome of the forearm as the initial symptom of systemic Vibrio vulnificus infection. 1044 62

Acute renal failure (ARF) associated with liver disease is a commonly encountered clinical problem of varied etiology and high mortality. We have prospectively analyzed patients with liver disease and ARF to determine the etiology, clinical spectrum, prognosis and factors affecting the outcome. Other than hepatorenal syndrome patients, out of 221 cases, 66 developed ARF secondary to various liver disease like cirrhosis (n = 29, mortality 8, risk factors-older age p < 0.01, grade III/IV encephalopathy p < 0.05), fulminant hepatic failure (n = 25, mortality 15, risk factor-prolonged prothrombin time p < 0.01), and obstructive jaundice (n = 12, mortality 7, risk factor-sepsis p < 0.01). In these three groups the factors leading to ARF were volume depletion (24), gastrointestinal bleed (28), sepsis (34), drugs (27) [aminoglycosides (9) and NSAID (18)] along with hyperbilirubinemia. Various types of ARF with contemporaneous liver injury were malaria (n = 37, mortality 15, risk factors-higher bilirubin p < 0.001, higher creatinine p < 0.05, anuria p < 0.05 and dialysis dependency p < 0.05), sepsis (n = 36, mortality 22, risk factors-age p < 0.001, higher bilirubin p < 0.01, oliguria p < 0.05), hypovolemia with ischemic hepatic injury (n = 14, mortality 5, risk factors-higher creatinine p < 0.05 and SGPT p < 0.01), acute pancreatitis (n = 12, mortality 4, risk factors-higher bilirubin p < 0.001, higher SGPT p < 0.01, dialysis dependency p < 0.05), rifampicin toxicity (n = 10, no mortality), paroxysmal nocturnal hemoglobinuria (n = 3, no mortality), CuSO4 poisoning (n = 3 mortality 2), post abortal (n = 11, mortality 6, risk factors higher creatinine p < 0.05 and SGPT p < 0.01), ARF following delivery including HELLP syndrome (n = 12, mortality 4, risk factors-higher bilirubin p < 0.01 and SGPT p < 0.01), and of uncertain etiology (n= 14 mortality 4). 133 patients (60.2%), required hemodialysis hemodialfiltration or peritoneal dialysis. ARF associated with liver disease is having high mortality (42.5%). Avoidance of dehydration, hypotension, nephrotoxic drugs and sepsis, with promote dialytic support are necessary to reduce mortality and morbidity.
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PMID:Acute renal failure associated with liver disease in India: etiology and outcome. 1104 Dec 94

Misoprostol, a prostaglandin E1 analog, is a racemate of four stereoisomers. On administration it rapidly de-esterifies to its active form, misoprostolic acid. Misoprostolic acid is 85% albumin bound and has a half-life of approximately 30 minutes. It is excreted in urine as inactive metabolites. No significant drug interactions have been reported. Besides its gastrointestinal protective and uterotonic activities, misoprostol regulates various immunologic cascades. It inhibits platelet-activating factor and leukocyte adherence, and modulates adhesion molecule expression. It protects against gut irradiation injury, experimental gastric cancer, enteropathy, and constipation. It improves nutrient absorption in cystic fibrosis. Misoprostol has utility in acetaminophen and ethanol hepatotoxicity, hepatitis, and fibrosis. It is effective in asthmatics and aspirin-sensitive asthmatic and allergic patients. It lowers cholesterol and severity of peripheral vascular diseases, prolongs survival of cardiac and kidney transplantation, synergizes cyclosporine, and protects against cyclosporine-induced renal damage. It works against drug-induced renal damage, interstitial cystitis, lupus nephritis, and hepatorenal syndrome. It is useful in periodontal disease and dental repair. Misoprostol enhances glycosoaminoglycan synthesis in cartilage after injury. It prevents ultraviolet-induced cataracts and reduces intraocular pressure in glaucoma and ocular hypertension. It synergizes antiinflammatory and analgesic effects of diclofenac or colchicine and has been administered to treat trigeminal neuralgic pain. It reduces chemotherapy-induced hair loss and recovery time from burn injury, and is effective in treating sepsis, multiple sclerosis, and pancreatitis.
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PMID:Misoprostol therapeutics revisited. 1119 38


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