Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

On April 25, 2003, a 62-year-old Japanese man had been admitted to a hospital because of heavy proteinuria and elevated serum creatinine level, and purpura on the lower extremities. On May 15, 2003, he was referred to our hospital for evaluation and treatment. Serum immunoglobulin and complements were within normal ranges. Immune serology was negative for antinuclear antibody, antiglomerular basement membrane antibody, and antineutrophil cytoplasmic antibodies. Histological examination of a percutaneous renal biopsy specimen revealed that all of the glomeruli had severe crescent formation without deposits of immunoreactants. A diagnosis of antineutrophil cytoplasmic antibody-negative pauci-immune crescentic glomerulonephritis was made. The patient was treated with one cycle of steroid pulse therapy (1000 mg methylprednisolone daily, given on 3 consecutive days), and subsequently with prednisolone (60 mg/day). Despite this treatment, renal failure progressed rapidly and hemodialysis was started 1 month after the acute presentation. On May 30, 2003, he suddenly developed massive hematochezia. A technetium-targeted red-blood-cell scan suggested bleeding in the small intestine. On June 11, he presented with massive melena. A bleeding ulcer was found in the third part of the duodenum, and was treated successfully with endoscopy, using a heater probe. On June 19, he presented with massive hematochezia again. Mesenteric angiography revealed active bleeding from the iliac branch of the superior mesenteric artery. He was treated with continuous intraarterial vasopressin infusion by a catheter seated in the branch artery. The majority of patients with pauci-immune crescentic glomerulonephritis, one of the most common causes of rapidly progressive glomerulonephritis, have glomerular disease as part of a systemic vasculitis. Massive gastrointestinal bleeding, although rare, should be considered one of the serious complications in these patients.
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PMID:ANCA-negative pauci-immune crescentic glomerulonephritis complicated with recurrent massive gastrointestinal hemorrhage. 1598 Sep 55

Hepatorenal syndrome (HRS) is a serious complication of advanced liver disease. Historically, the development of HRS was considered a pre-terminal event due to a lack of efficacious therapy. Although liver transplantation remains the optimum therapy for HRS, many patients may be unsuitable for liver grafting. In addition, organ shortage may necessitate the institution of alternative pharmacological therapies to bridge patients to transplantation or to maintain renal function. This article reviews the definitions of Types-1 and -2 HRS, and addresses strategies for the prevention of the syndrome. It will also discuss management approaches to the cirrhotic patient with renal failure, specifically, assessment of novel vasoconstrictor therapies, such as vasopressin analogues, alpha-adrenoreceptor agonists, and the use of transjugular intra-hepatic shunts either alone or in combination with other therapeutic agents.
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PMID:Current management of the hepatorenal syndrome. 1609 65

Splanchnic arterial relaxation is the most important pathology in systemic circulation of portal hypertensive patients. Progressive decline of splanchnic vascular resistance is responsible for development of circulatory dysfunction syndrome (CDS), associated with reduction of effective blood volume within central vascular compartment and compensatory stimulation of vasopressor and natrium retaining hormonal mechanisms. Advanced CDS is characterized by increased cardiac output, tachycardia and low arterial pressure. Complications of CDS have functional nature and comprise: renal failure (hepatorenal syndrome), respiratory failure in context of hepatopulmonary syndrome, cardiac insufficiency produced by portopulmonary hypertension or portal cardiomyopathy, hemorrhages from digestive tract caused by hypertensive portal gastropathy or derangements of brain perfusion. The management of CDS relies on adequate filling of vascular system (albumin), constriction of arterial splanchnic vessels (beta-blocker, analogs of vasopressin and somatostatin), reduction of cardiac output (beta-blocker) and giving support to local vasoprotective mechanisms (prostaglandins, nitric oxide, blockade of ET-A receptors).
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PMID:[Circulatory dysfunction syndrome associated with liver cirrhosis]. 1619 May 66

Hepatorenal syndrome (HRS) is defined as functional renal failure that develops in patients with advanced liver disease. HRS may be either slowly or rapidly progressive (type I and II HRS, respectively). Untreated HRS carries a high mortality. Liver transplantation is the best available treatment for HRS. However, all patients with HRS are not suitable candidates for transplantation. Moreover, an organ is often not available in a timely manner in those who are candidates for transplantation. Treatment with vasoconstrictors (terlipressin, octreotide, and midodrine) and plasma expansion with albumin is beneficial and serves as a bridge to transplantation in such cases. The vasopressin analog, terlipressin, produces a sustained reversal of HRS in about 57% to 78% of the patients. The benefits of terlipressin are seen mainly in those who are also receiving albumin simultaneously. In those who improve, recurrence of HRS is reported to be relatively uncommon in the short and intermediate term. In the United States, terlipressin is not available, and octreotide and midodrine are often used for the medical management of HRS. Unfortunately, there are only limited uncontrolled data to support the use of these drugs for HRS. In those who respond to octreotide and midodrine, the subsequent placement of a transjugular intrahepatic portasystemic shunt (TIPS) has been shown to produce a sustained improvement in renal function. TIPS alone also improves renal functions in selected patients with HRS. The exact role of TIPS in HRS needs further evaluation, as patients with HRS are particularly at risk for complications such as encephalopathy and liver failure. Molecular adsorbent recirculating system (MARS) is an albumin-based dialysis system that has a promising role in the treatment of HRS and liver failure. MARS is a very expensive form of treatment, and further clinical trials are needed to establish its utility. Development of HRS can be prevented by adding albumin to the antibiotic regimen to treat spontaneous bacterial peritonitis and through pentoxifylline administration to the patients with acute alcoholic hepatitis.
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PMID:Hepatorenal syndrome. 1631 61

The mechanism behind iodinated radiocontrast nephropathy remains elusive. Direct oxidative damage is the prevailing hypothesis, but the apparent protective effect of iodine against oxidation contradicts this view. We propose that autonomic dysfunction participates in the pathogenesis of radiocontrast nephropathy and may account for other contrast-associated reactions previously attributed to allergy. Iodine, through its effects on thyroid function and chemoreceptor response to metabolic acidosis, may induce hyperadrenergia and consequently diminish renovascular flow and urine output. The renal response to adrenergia likely served an adaptive function during prehistoric evolution when trauma was a dominant source of hypovolemia and adrenergia, but the response may behave maladaptively today as evolutionarily nai ve triggers for adrenergia have emerged. Autonomic dysfunction can further impair renal function by deranging renovascular autoregulation and inducing oxidative reperfusion injury as a secondary phenomenon. Many other causes of acute renal failure such as drug toxicity, surgery, hospitalization, and diabetes may operate through hyperadrenergia, impaired renovascular autoregulation, and oxidative reperfusion injury. Dialysis, a volume reduction therapy for renal failure, can counterintuitively worsen renal dysfunction by exacerbating adrenergia, which may explain its association with accelerated atherosclerosis, inflammation, and cancer. Other examples of vicious cycles that perpetuate renal dysfunction may include renal artery stenosis, carotid stenosis, and atherosclerosis as well as the cardio-renal, hepato-renal, and pulmonary-renal syndromes. The benefits of hydration and bicarbonate in protecting renal function may operate in part through baroreceptor- and chemoreceptor-mediated reduction of sympathovagal ratio, respectively. New treatment paradigms for renal failure including pharmacologic and electro-mechanical therapies are envisioned based on autonomic remodeling, reduced sympathovagal ratio, and neuromodulation of pathways typically associated with trauma such as renin, angiotensin, vasopressin, and aldosterone.
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PMID:Contrast nephropathy may be partly mediated by autonomic dysfunction: renal failure considered as a modern maladaptation of the prehistoric trauma response. 1633 Jan 57

In patients with cirrhosis and type 1 hepatorenal syndrome (HRS), systemic vasodilation, which is mainly attributable to splanchnic vasodilation, plays a critical role in the activation of endogenous vasoconstrictor systems, resulting in renal vasoconstriction and functional renal failure. It has been suggested that the use of splanchnic (and systemic) vasoconstrictors such as terlipressin (a vasopressin analog) or alpha-1-adrenoceptor agonists (midodrine or noradrenaline) may improve renal function in patients with type 1 HRS. Six studies (with only one randomized study in a small series of patients) have shown that terlipressin improves renal function in these patients. However, there is evidence that terlipressin alone may be less effective than terlipressin combined with intravenous albumin in improving renal function. Future randomized studies should confirm this difference and evaluate the impact of terlipressin therapy (with or without intravenous albumin) on survival. Interestingly, in nonrandomized studies, the use of alpha-1 agonists combined with other therapies (octreotide and albumin for midodrine; furosemide and albumin for noradrenaline) has been shown to improve renal function in patients with type 1 HRS. The efficacy and safety of combined therapies including alpha-1 agonists should be confirmed in randomized studies. Finally, preliminary evidence suggests that vasoconstrictor administration may be a novel therapeutic approach targeting vasodilation involved in the mechanism of: (1) renal failure in type 2 HRS; (2) paracentesis-induced circulatory dysfunction; and (3) arterial hypotension induced by byproducts of gram-negative bacteria. Further studies are needed in all these fields.
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PMID:The use of vasoconstrictors in patients with cirrhosis: type 1 HRS and beyond. 1649 52

An estimated 700,000 cases of sepsis occur each year in the United States alone, over half of which will develop renal failure. Of those that develop renal failure, 70% will die. This article will examine how the use of vasopressin in sepsis may improve some aspects of renal function. The effects of vasopressin on the renal system in vasodilatory shock.
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PMID:The effects of vasopressin on the renal system in vasodilatory shock. 1650 61

Hepatorenal syndrome (HRS), a feared complication of advanced cirrhosis, is characterized by functional renal failure, secondary to renal vasoconstriction in the absence of underlying kidney pathology. Extreme underfilling of the arterial circulation, caused by arterial vasodilation of the splanchnic circulation, activates vasoconstrictor systems, which lead to intense renal vasoconstriction and HRS. Factors predictive for the development of HRS include intense urinary sodium retention, dilutional hyponatremia, low blood pressure, decreased cardiac output, and increased activity of systemic vasoconstrictors. The prognosis for patients with HRS is extremely poor, especially for those with the acute, progressive (type 1) form. Liver transplantation is the best treatment for suitable candidates and should always be the management option considered first. Pharmacologic therapies are aimed at improving renal function to enable patients to survive until transplantation is possible. These therapies are based on plasma expansion with albumin, combined with the use of either vasopressin analogs or alpha-adrenergic agonists. Other nonpharmacologic therapies, such as transjugular intrahepatic portosystemic shunts and albumin dialysis show promise, but experience with these treatments is limited. For prevention of HRS, albumin infusion is recommended in patients with spontaneous bacterial peritonitis, and pentoxifylline treatment is recommended in patients with acute alcoholic hepatitis.
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PMID:Therapy insight: Management of hepatorenal syndrome. 1674 53

Hepatorenal syndrome (HRS) is a common complication of advanced cirrhosis, characterized by renal failure and major abnormalities in the systemic circulatory function. Renal failure is caused by intense vasoconstriction of the renal circulation. The syndrome is probably the final consequence of an extreme underfilling of the arterial circulation, secondary to vasodilatation in the splanchninc vascular bed and a decrease in cardiac output due to central hypovolemia. The diagnosis of HRS is based on the exclusion of other causes of renal failure. The survival of patients with HRS is very short, particularly when there is rapidly progressive renal failure (type-1 HRS). Liver transplantation is the best therapeutic option but its applicability is low. During the past few years effective treatment for HRS, such as vasoconstrictor drugs (vasopressin analogues, proportional variant-adrenergic agonists) associated with intravenous albumin infusion and transjugular intrahepatic portosystemic shunts (TIPS), have been introduced. They improve circulatory function, normalize serum creatinine, and may improve survival. Sequential treatment with vasoconstrictors plus albumin and TIPS is an attractive therapeutic possibility. Plasma volume expansion with albumin at infection diagnosis in patients with spontaneous bacterial peritonitis and the administration of pentoxiphilline in patients with severe alcoholic hepatitis significantly reduce the development of type-1 HRS.
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PMID:New treatments of hepatorenal syndrome. 1685 Mar 75

Hepatorenal syndrome is a particular form of functional renal failure which may develop in patients with liver cirrhosis. On a clinical standpoint, precise diagnostic criteria have been established to clearly define this entity, whereas recent advances in the understanding of the biology of vasoactive mediators and the physiology of microcirculation have allowed to better anticipate its pathophysiological mechanisms. During the course of cirrhosis, sinusoidal portal hypertension leads to splanchnic and systemic vasodilation, responsible for a reduction of effective arterial blood volume. As a result, a state of intense renal vasoconstriction develops, leading to renal failure in the absence of any organic renal disease. At this stage, liver transplantation is the only definitive therapy able to reverse renal dysfunction. In recent years, innovative therapies have shown promise to prolong survival in patients with hepatorenal syndrome, including the administration of analogs of vasopressin (mainly terlipressin), the insertion of transjugular intrahepatic portosystemic shunts and the use of novel techniques of dialysis. On a preventive viewpoint, several simple measures have been shown to reduce the risk of hepatorenal syndrome in cirrhotic patients, including the appropriate use of diuretics, the avoidance of nephrotoxic drugs, the prophylaxis of spontaneous bacterial peritonitis and optimal fluid management in patients undergoing large volume paracentesis.
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PMID:[Hepatorenal syndrome in patients with liver cirrhosis]. 1689 84


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