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)

In cirrhosis of the liver, according to the peripheral arterial vasodilation hypothesis, relative underfilling of the arterial tree triggers a neurohumoral response (activation of renin-angiotensin-aldosterone system, sympathetic nervous system, nonosmotic release of vasopressin) aimed at restoring circulatory integrity by promoting renal sodium and water retention. Evidence has accumulated for a major role of increased vascular production of nitric oxide as the primary cause of arterial vasodilation in cirrhosis. Ascites is a common complication in cirrhosis. Treatment of ascites consists of a low salt diet with diuretics, and paracentesis together with plasma volume expanders in diuretic-resistant patients. Progression of cirrhosis may result in hepatorenal syndrome, a state of functional renal failure that carries an ominous prognosis. Orthotopic liver transplantation has remained the only curative treatment for patients with advanced liver disease; other modalities such as transjugular intrahepatic portosystemic shunt or vasopressin analogues may serve as a bridge to transplantation. Another complication of decompensated cirrhosis is spontaneous bacterial peritonitis, the incidence of which can be reduced by primary or secondary antibiotic prophylaxis by using orally active antibiotics.
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PMID:Update on peripheral arterial vasodilation, ascites and hepatorenal syndrome in cirrhosis. 1111 Jun 23

In diabetes mellitus (DM), the urine flow rate is increased, and the fluid turnover in the body is accelerated because of the glucose-induced osmotic diuresis. On the other hand, plasma vasopressin (VP) is elevated in both type 1 and type 2 DM. This elevation seems to be due to a resetting of the osmostat. A high VP level is beneficial in the short term because it limits to some extent the amount of water required for the excretion of a markedly enhanced load of osmoles (mainly glucose). However, in the long run, it may have adverse effects by favoring the development of diabetic nephropathy. VP has been shown in normal rats to induce kidney hypertrophy, glomerular hyperfiltration, and an increase in urinary albumin excretion (features also occurring in association in the period preceding diabetic nephropathy). Moreover, VP has been shown to participate in the progression of renal failure in rats with five-sixths reduction in renal mass. In recent studies, we have shown (1) that creatinine clearance, albuminuria and renal mass increased much less during experimental DM in Brattleboro rats unable to secrete VP than in their VP-replete Long-Evans controls, and (2) that albuminuria was prevented during experimental DM in Wistar rats when a VP nonpeptidic, highly selective V2 receptor antagonist was administered chronically for 9 weeks. Taken together, these results strongly suggest that VP plays a crucial role in the onset and aggravation of the renal complications of DM. The mechanisms by which VP exerts these adverse V2-dependent effects are not yet elucidated. They are most likely indirect and may involve several intermediate steps comprising VP-induced changes in the composition of the tubular fluid in the loop of Henle (due to solute recycling in the renal medulla associated with improved concentrating activity of the kidney), inhibition of the tubuloglomerular feedback control of glomerular function, and alterations in glomerular hemodynamics by the intrarenal renin-angiotensin system.
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PMID:Vasopressin and diabetes mellitus. 1117 21

Perioperative hyponatremia has been recognized as a serious in-hospital complication for many years. Because the kidney responds to changes in extracellular fluid tonicity by adjusting water excretion, a defect in any of several key elements of water excretion can lead to water retention and hyponatremia. Most cases of hyponatremia are caused by impaired renal water excretion in the presence of continued water intake. For the kidney to excrete excess free water and thereby protect the extracellular fluid against hyponatremia, there must be an adequate glomerular filtration rate (GFR), adequate delivery of glomerular filtrate to the diluting segments of the distal nephron, intact tubular diluting mechanisms, and appropriate inhibition of antidiuretic hormone (ADH) synthesis and release. Virtually all of the clinical disorders producing hyponatremia are based on abnormalities of these few mechanisms of water regulation. Finding the reason for impaired renal water excretion is the key to diagnosing the cause of hyponatremia. Impaired renal water excretion may be caused by impaired GFR (renal failure), impaired water delivery to the diluting segments of the distal nephron because of increased proximal reabsorption (decreased extracellular fluid volume and edematous states), impaired renal diluting mechanism (thiazide diuretics), the syndrome of inappropriate ADH (SIADH) due to a variety of causes including the perioperative state, and hypothyroidism or adrenal insufficiency. Any of the states that impair water excretion can produce hyponatremia in a patient with an initially normal serum sodium concentration if sufficient free water is supplied. Therefore, a patient who has one of the conditions listed above, including the perioperative state, may be considered "water intolerant" even if the serum sodium is normal. Such a patient is at risk for developing severe hyponatremia if given hypotonic IV fluids or a large oral water load. An understanding of the basic mechanisms leading to impaired water excretion and "water intolerance" is therefore an important key to avoiding perioperative hyponatremia.
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PMID:University of Miami Division of Clinical Pharmacology Therapeutic Rounds: the water-intolerant patient and perioperative hyponatremia. 1131 70

Central diabetes insipidus is clinically masked in dialysis patients. We report a 12-year-old girl receiving a living-related donor graft for renal failure from Alport syndrome, in whom a craniopharyngioma had been resected 6 months before transplantation. Pretransplant evaluation had documented central hypothyroidism, growth hormone deficiency, and presumptive hypogonadotropic hypogonadism. The corticotropin-releasing factor test had been normal. Four hours after transplantation, urine output exceeded 1,000 ml/h without diuretic therapy. Serum sodium concentration was 155 mmol/l, serum osmolality 333 mmol/kg, and plasma antidiuretic hormone 4.9 ng/l, while urine osmolality was 233 mmol/kg. Desmopressin acetate was started by continuous intravenous infusion at 1 microgram/day. Serum electrolytes rapidly normalized, urine output stabilized at 2 l/day. The patient was discharged 4 weeks after transplantation with good allograft function, receiving intranasal desmopressin acetate 10 micrograms twice daily. Pre-existing central diabetes insipidus is unmasked after successful kidney transplantation, leading to rapid dehydration and hypernatremia, which can be prevented by prompt institution of desmopressin therapy.
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PMID:Perioperative management of central diabetes insipidus in kidney transplantation. 1135 73

The hepatorenal syndrome is a form of renal failure occurring in patients with advanced liver disease. The diagnosis is based both on the demonstration of low GFR and exclusion of other common causes of renal failure that may occur in patients with cirrhosis. Orthotopic liver transplantation remains the only curative treatment for this poor outcome disease; other modalities such as vasopressin analogues, transjugular intrahepatic portosystemic shunt or renal replacement therapies may serve as a bridge to transplantation. This article reviews the pathophysiology, diagnosis and current treatment of hepatorenal syndrome.
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PMID:[Update on hepatorenal syndrome]. 1188 72

Type 1 hepatorenal syndrome (HRS) is a severe complication of end-stage cirrhosis. Type 1 HRS is an acute functional renal failure (i.e. glomerular hypofiltration) with no other explanation than the presence of the circulatory and neurohumoral alterations associated with severe chronic liver disease. Plasma volume expansion does not improve renal function. In contrast, administration of the vasopressin analog terlipressin, a splanchnic and systemic vasoconstrictor, may improve renal function and be used while awaiting liver transplantation.
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PMID:Hepatorenal syndrome in patients with cirrhosis. 1212 2

Milrinone is a phosphodiesterase type III inhibitor with positive inotropic and vasodilatory effects. A common side effect of milrinone is hypotension from the peripheral vasodilation. Although mild elevations in serum creatinine have been described previously in the setting of milrinone-induced hypotension, acute oligoanuric renal failure requiring renal replacement therapy has not yet been described. This case report is the first to document such a result and to report the successful use of peritoneal dialysis in this setting. Previous case reports documented vasopressin as an effective alternative to catecholamines in the treatment of milrinone-induced hypotension. This report documents the use of four vasopressor agents (including vasopressin) in this patient, with only vasopressin resulting in improvement in systemic vascular resistance and blood pressure. Vasopressin may be the most effective vasopressor agent in the treatment of milrinone-induced hypotension.
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PMID:Acute renal failure secondary to milrinone in a patient with cardiac amyloidosis. 1214 28

The Authors report 3 cases with clinical renal manifestations where the indication to perform a renal biopsy was defined as borderline. The uncertain indication was related to the clinical presentation, with a pattern of urinary abnormalities, such as isolated microscopic hematuria, microscopic hematuria associated with mild proteinuria, and isolated proteinuria. In addition, similar questions on biopsy are raised for chronic renal failure and elderly patients. In the literature, microscopic hematuria without significant proteinuria shows that 25% of adult patients have no histological abnormalities. A higher percentage is found among children. The other cases exhibit a pattern of IgA nephropathy, Alport's syndrome, thin BM nephropathy and arteriolar C3 deposition. The percentage of an abnormal histological picture increases if the patients have a family history of hematuria, and if there are concomitant episodes of macroscopic hematuria, because of an increase in IgA nephropathy and Alport's syndrome, respectively. In the last cases, therefore the indication to perform a renal biopsy increases. For those patients without these characteristics, a renal biopsy can be delayed whereas in cases of microscopic hematuria with proteinuria or isolated proteinuria the indication for a renal biopsy is stronger, because the spectrum of glomerulopathies is wider, and the possible evolution to renal failure after 10 years is higher (10-14% of cases). In patients with chronic renal failure the biopsy is contraindicated for cases where the thickness of the cortical section of the kidney is lower than 8-10 mm, because of possible technical difficulties, lower diagnostic information due to sclerosis and higher risk of complications. The prolonged bleeding time and the consequent risk of bleeding can be avoided by i.v. infusion of vasopressin 2 hours prior to biopsy. The higher indications are for those patients who may be susceptible to a medical treatment, capable to slowing down the progression of nephropathy. Finally, in elderly patients the biopsy is indicated in almost all cases because of the recently confirmed high incidence of glomerulopathies. In the aged there is a higher frequency of membranous GN, crescentic-ANCA associated GN, amyloidosis and, according to some Authors, post-infectious GN. In all cases a precise histological diagnosis can correct an erroneous diagnosis made according to clinical data alone. In the elderly the indication for biopsy aims at making an exact diagnosis of nephropathy, especially for acute renal failure: for this purpose age itself should not become an obstacle.
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PMID:[Borderline indications for renal biopsy]. 1219 3

In conscious, chronically instrumented rats we examined 1) renal tubular functional changes involved in lipopolysaccharide (LPS)-induced acute renal failure; 2) the effects of LPS on the expression of selected renal tubular water and sodium transporters; and 3) effects of milrinone, a phosphodiesterase type 3 (PDE3) inhibitor, and Ro-20-1724, a PDE4 inhibitor, on LPS-induced changes in renal function. Intravenous infusion of LPS (4 mg/kg b.wt. over 1 h) caused an immediate decrease in glomerular filtration rate (GFR) and proximal tubular outflow without changes in mean arterial pressure (MAP). LPS-induced fall in GFR and proximal tubular outflow were sustained on day 2. Furthermore, LPS-treated rats showed a marked increase in fractional distal water excretion, despite significantly elevated levels of plasma vasopressin (AVP). Semiquantitative immunoblotting showed that LPS increased the expression of the Na(+),K(+),2Cl(-)-cotransporter (BSC1) in the thick ascending limb, whereas the expression of the AVP-regulated water channel aquaporin-2 in the collecting duct (CD) was unchanged. Pretreatment with milrinone or Ro-20-1724 enhanced LPS-induced increases in plasma tumor necrosis factor-alpha and lactate, inhibited the LPS-induced tachycardia, and exacerbated the acute LPS-induced fall in GFR. Furthermore, Ro-20-1724-treated rats were unable to maintain MAP. We conclude 1) PDE3 or PDE4 inhibition exacerbates LPS-induced renal failure in conscious rats; and 2) LPS treated rats develop an escape from AVP in the CDs, which could be aimed to protect against water intoxication in septic conditions associated with decreased GFR and high levels of AVP.
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PMID:Lipopolysaccharide-induced acute renal failure in conscious rats: effects of specific phosphodiesterase type 3 and 4 inhibition. 1223 72

The hepatorenal syndrome (HRS) is a unique form of acute renal failure with entirely normal renal histology in advanced liver disease. Its diagnosis is made by exclusion of all causes of renal failure and by all the five major criteria as set by the International Ascites Club. The presence of hepatomegaly, poor nutritional status, and oesophageal varices at endoscopy are associated with a high risk of HRS. The liver tests, the Child-Pugh score, are of no value in prediction of its occurrence. Contraction of the effective blood volume, which may lead to renal hypoperfusion with preferential renal cortical ischaemia, is proposed pathogenesis of the condition. Because understanding of the pathogenesis of HRS is incomplete, therapy is supportive only. Optimal fluid management is vital as there is almost invariably a reduction in effective arterial blood volume. Dopamine, frusemide and haemofiltration may be helpful in management of fluid overload but do not affect renal function. TIPS has been used successfully in small series of patients. The vasopressin analog also has been used with early excellent response. The treatment of HRS has been discouraging and the only proven cure for HRS is liver transplantation at this point of time.
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PMID:Hepatorenal syndrome: pathophysiology and treatment. 1224 Aug 52


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