Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Extracorporeal blood detoxification by sorbent therapy long has been applied in treatment of hepatic failure and encephalopathy, starting with hemoperfusion columns and more recently with the currently marketed Liver Dialysis Unit. Liver Dialysis employs hemodiabsorption (dialysis of blood against powdered sorbents including charcoal and cation exchanger) to remove selectively numerous small-molecular-weight toxins of hepatic failure. Liver Dialysis is used in treatment of acute hepatic encephalopathy (AHE) because of decompensation of chronic liver disease (A-on-C) or fulminant hepatic failure (FHF). Controlled, prospective and randomized studies of daily 6-hour Liver Dialysis have shown physiologic and neurologic improvement of patients with AHE, regardless of etiology. Liver dialysis significantly improved the incidence of positive outcomes (recovery of hepatic function or improvement for transplant) of A-on-C patients versus controls (71.5% treated, and 35.7% control, P =.036), but had an insignificant improvement in outcome of patients with FHF as compared with the control group. Other extracorporeal sorbent devices are now in clinical testing phase. The molecular adsorbent regenerating system (MARS) device employs a polysulfone high-permeability dialyzer with albumin on the dialysate side to aid transfer of protein-bound toxins such as bilirubin and bile acids across the membranes. Sorbent columns of charcoal and an anion exchanger remove hepatic toxins from the albumin dialysate, and a second dialyzer removes water-soluble toxins, such as ammonium. Clinical results of daily MARS treatments of patients with hepatic failure are similar to that of Liver Dialysis, with neurologic and physical improvement occurs in most patients with AHE, and improved outcome for patients with A-on-C. The system extends the life of patients with hepatorenal syndrome. PF-Liver Dialysis is an experimental device combining hemodiabsorption with push-pull sorbent-based pheresis with powdered sorbent surrounding plasmafilters. PF-Liver Dialysis (Hemocleanse, Inc, W. Lafayette, IN) has been tested in a few patients with hepatic failure, grade 3-4 encephalopathy, and respiratory and kidney insufficiency. Treatments appeared to be safe and resulted in marked decreases in plasma levels of bilirubin, aromatic amino acids, ammonium, creatinine, and interleukin-1beta (IL-1beta). The PF add-on module adds the capability to Liver Dialysis to remove bilirubin, bile acids, and other strongly protein-bound toxins from treated patients and may be of clinical benefit in management of patients with the most severe hepatic failure and encephalopathy, including patients with FHF or concomitant sepsis.
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PMID:Extracorporeal blood detoxification by sorbents in treatment of hepatic encephalopathy. 1192 2

296 patients with first clinical symptoms of alcoholic liver disease were hospitalized in Probationary-Infectious Diseases Department in Kielce, between 1994-2000. In 52 (17.6%) of them, acute hepatic failure was diagnosed by detection of hepatic encephalopathy. Initial laboratory data of those patients who died (6.1%), and those who survived (11.5%) was compared. No statistically significant differences in analyzed parameters were found, except for significantly higher bilirubin concentration in the group of deceased. In both groups of patients, the frequency of hepatic failure complications, present at the admission to the hospital or those developed in the course of the disease, was also analyzed. The following complications were observed significantly more often in deceased: ascites, hepatorenal syndrome (HRS), spontaneous bacterial peritonitis (SBP), and gastrointestinal haemorrhage (GIH), while sepsis was similarly frequent in both groups.
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PMID:Acute hepatic failure in alcoholic liver disease. 1221 30

In patients with cirrhosis, acute renal failure is mainly due to prerenal failure (caused by renal hypoperfusion) and tubular necrosis. The main causes of prerenal failure are "true hypovolemia" (induced by hemorrhage or gastrointestinal or renal fluid losses), sepsis, or type 1 hepatorenal syndrome (HRS). The frequency of prerenal failure due to the administration of nonsteroidal anti-inflammatory drugs or intravascular radiocontrast agents is unknown. Prerenal failure is rapidly reversible after restoration of renal blood flow. Treatment is directed to the cause of hypoperfusion, and fluid replacement is used to treat most cases of "non-HRS" prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy (with terlipressin, noradrenaline, or midodrine [combined with octreotide]) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for molecular adsorbent recirculating system) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. The most common condition leading to ischemic acute tubular necrosis is severe and sustained prerenal failure. Little is known about the natural course and treatment (i.e., renal replacement therapy) of cirrhosis-associated acute tubular necrosis.
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PMID:Acute renal failure in patients with cirrhosis: perspectives in the age of MELD. 1254 Jul 70

Kinins are peptide hormones that exert pathophysiological as well as pronounced beneficial physiological effects, mainly by stimulation of bradykinin (BK) B(2) receptors. Owing to the strong proinflammatory properties of kinins resulting from vasodilation, plasma extravasation, activation of mast cells, fibroblasts and macrophages, stimulation of sensory neurons, and the release of nitric oxide, prostaglandins, leukotrienes and cytokines, kinins are believed to play an important role in a variety of inflammatory diseases and pain. Beneficial effects of BK B(2) receptor antagonists in perennial rhinitis, asthma and brain edema have already been shown in clinical trials. Recently, the potential therapeutic utility of BK B(2) receptor antagonists has been extended by the discovery of orally active, nonpeptide BK B(2) receptor antagonists and the identification of novel indications for their use. On the other hand, kinins also have been identified as potent antihypertensive and organ-protective peptides. They have been shown to have vasodilatory, antihypertrophic, antiaggregatory and fibrinolytic effects due to the BK B(2) receptor-mediated release of the autacoids nitric oxide, prostacyclin and tissue plasminogen activator. A recent finding is that kinins are also involved in ischemic preconditioning. Orally active, nonpeptide BK B(2) receptor agonists as potential novel therapeutic agents in cardiovascular medicine have also been identified. In conclusion, interaction with the BK B(2) receptor by either its blockade or its stimulation offers promising therapeutic approaches. BK B(2) receptor antagonists may prove to be useful in the treatment of asthma, rhinitis, arthritis, colitis, pancreatitis, sepsis, edema, tissue injury, pain and possibly infections, hepatorenal syndrome, Alzheimer's disease and lung cancer. BK B(2) receptor agonists have potential in the treatment of cardiovascular diseases like hypertension, cardiac hypertrophy, restenosis and myocardial infarction and diabetic disorders.
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PMID:Bradykinin B2 receptor as a potential therapeutic target. 1293 26

Hepatorenal syndrome (HRS) is a severe complication of cirrhosis that develops in the final phase of the disease. Two types of HRS exist. Type 1 is defined by a rapid reduction of renal function and in type 2 HRS the reduction of renal function is slowly progressive. Type 1 HRS is diagnosed when the serum creatinine level increases by more than 50% of the baseline value to above 133 micromol/L. According to the International Ascites Club, HRS is defined by the presence of five criteria: (1) severe cirrhosis; (2) glomerular hypofiltration; (3) no other functional or organic causes; (4) failure of plasma volume expansion; (5) no proteinuria. Additional diagnostic criteria may be present. The diagnosis of HRS may be difficult in patients with severe cirrhosis. Other types of acute renal failure may occur. For example, ischaemic or toxic tubular necrosis or sepsis may cause renal failure in these patients. Furthermore, uncontrolled HRS may lead to ischaemic tubular necrosis; thus, these patients must be managed as soon as possible in an intensive care unit.
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PMID:Review article: hepatorenal syndrome--definitions and diagnosis. 1533 96

The use of folk remedies is widespread throughout Africa. Acute renal failure (ARF) is one of the most severe, but under-recognized, complications of folk remedy use. This report aims to describe the clinical presentation, outcomes, and nature of renal injury in patients with folk-remedy-associated ARF. Clinical data were evaluated retrospectively in 78 patients with ARF associated with recent folk remedy use. ARF was defined as elevated serum urea and creatinine above the age-appropriate normal ranges, persistent oligoanuria, worsening renal function with time, or need for dialysis. Overall mortality in patients with ARF was 41%. Mortality was higher in adults (45.5%) than in infants (36.6%), in patients with both renal and liver dysfunction (62.5%) than in those with renal dysfunction alone (22.6%), and in HIV-positive (44.4%) versus HIV-negative (34.6%) patients. Vomiting (51.3%) and diarrhea (43.6%) were the most frequent presenting symptoms. Metabolic acidosis (80.8%) and volume depletion (62.8%) were the most frequent clinical findings. The definable causes of ARF were pre-renal (26.9%), acute tubular necrosis (ATN; 26.9%), hepatorenal syndrome (6.4%), urinary tract infection/sepsis (7.7%), and primary renal disorders (7.7%). Twenty-seven patients had concomitant medical conditions unlikely primarily related to folk remedy ingestion. In conclusion, ARF occurring after use of folk remedies in South Africa is associated with significant morbidity and mortality. The most common contributors to ARF in this setting are volume depletion and ATN. Significantly, although a proportion of patients have underlying systemic or renal conditions that may contribute to renal dysfunction, in the majority of patients, folk remedy use appears to be the most likely proximate cause. In view of the large numbers of Africans living abroad, more widespread awareness of this important clinical problem needs to be raised.
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PMID:Acute renal failure associated with the use of traditional folk remedies in South Africa. 1571 33

Relative adrenal insufficiency is frequent in patients with severe sepsis and is associated with hemodynamic instability, renal failure, and increased mortality. This study prospectively evaluated the effects of steroids on shock resolution and hospital survival in a series of 25 consecutive patients with cirrhosis and septic shock (group 1). Adrenal function was evaluated by the short corticotropin test within the first 24 hours of admission. Patients with adrenal insufficiency were treated with stress doses of intravenous hydrocortisone (50 mg/6 h). Data were compared to those obtained from the last 50 consecutive patients with cirrhosis and septic shock admitted to the same intensive care unit in whom adrenal function was not investigated and who did not receive treatment with steroids (group 2). Incidence of adrenal insufficiency in group 1 was 68% (17 patients). Adrenal dysfunction was frequent in patients with advanced cirrhosis (Child C: 76% vs. Child B: 25%, P = .08). Resolution of septic shock (96% vs. 58%, P = .001), survival in the intensive care unit (68% vs. 38%, P = .03), and hospital survival (64% vs. 32%, P = .003) were significantly higher in group 1. The main causes of death in group 1 were hepatorenal syndrome or liver failure (7 of 9 patients). In contrast, refractory shock caused most of the deaths in group 2 (20 of 34 patients). In conclusion, relative adrenal insufficiency is very frequent in patients with advanced cirrhosis and septic shock. Hydrocortisone administration in these patients is associated with a high frequency of shock resolution and high survival rate.
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PMID:Adrenal insufficiency in patients with cirrhosis and septic shock: Effect of treatment with hydrocortisone on survival. 1798 20

In patients with cirrhosis, acute renal failure is due to prerenal failure (a result of decreased renal perfusion) and tubular necrosis. There are 3 main causes of prerenal failure: 'true hypovolemia' (which complicates hemorrhage, gastrointestinal or renal fluid losses), sepsis, and type 1 hepatorenal syndrome (HRS). Prerenal failure may also be due to the administration of non-steroidal antiinflammatory drugs, or intravascular radiocontrast agents. Prerenal failure is reversible after restoration of renal blood flow. Treatments target the cause of hypoperfusion, and fluid replacement is used to treat 'non-HRS' prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy with terlipressin (combined with intravenous human albumin), noradrenaline (combined with albumin and furosemide) or midodrine (combined with octreotide and albumin) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for Molecular Adsorbent Recirculating System) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. Studies are needed on the natural course and treatment (e.g., renal-replacement therapy) of acute tubular necrosis in patients with cirrhosis.
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PMID:Diagnosis and treatment of acute renal failure in patients with cirrhosis. 1722

The aim of this study was to determine the frequency, etiology, and outcomes of acute renal failure. We retrospectively collected data on all patients (n=1653) who received renal replacement therapy for acute renal failure at the Kaunas University of Medicine Hospital during 1995-2006. The number of patients with acute renal failure increased nine times during the 11-year period. The mean age of patients was 59.76+/-17.52 years and increased from 44.97+/-17.1 years in 1995 to 62.84+/-16.49 years in 2006. The most common causes of acute renal failure were renal (n=646, 39%), prerenal (n=380, 23%), and obstructive (n=145, 9%). The renal replacement therapy was discontinued because of recovery of renal function in 49.9% of cases. The overall hospital mortality rate was 45.1%. Renal function did not recover in 6.7% of patients. The mortality rate over the 11-year period varied from 37.8 to 57.5%. The highest mortality rate was in the neurosurgical (62.3%) and cardiac surgical (61.8%) intensive care units. High mortality rate (more than 50%) was in the groups of patients with acute renal failure that was caused by hepatorenal syndrome, shock, sepsis, and reduced cardiac output.
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PMID:[Frequency, etiology, and outcomes of acute renal failure (data of Kaunas University of Medicine Hospital in 1995-2006)]. 1755 Dec 73

Acute renal failure (ARF) and chronic kidney disease (CKD) are common complications after liver transplantation (LTx). The incidence of ARF post-LTx varies between 48% and 94%; 8% to 17% of patients require renal replacement therapy (RRT). The most common cause of ARF early after LTx is ischemic acute tubular necrosis, followed later by cyclosporine toxicity and sepsis. Preoperative serum creatinine >1.5 mg/dL and early hepatic allograft dysfunction are risk factors for the occurrence of postoperative ARF. Of patients with ARF due to the hepatorenal syndrome, approximately two-thirds will recover, although recovery may be delayed 3 months or longer after LTx. Mortality after LTx is affected modestly by the presence of ARF pretransplant (<2-fold increase), but increases markedly (up to 8-fold) in the face of ARF posttransplant. Mortality does not appear to be influenced by the mode of RRT used. The risk of CKD after LTx is approximately 18% at 5 years and increases to approximately 25% by 10 years after transplantation. Calcineurin inhibitor toxicity is the most common cause. Specific prognosticators for predicting CKD after LTx are presently lacking. The occurrence of CKD after LTx markedly impairs long-term survival.
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PMID:Acute renal failure and chronic kidney disease following liver transplantation. 1789 11


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