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Hepatorenal syndrome

Hepatorenal syndrome—type 1 (rapid, progressive decline in renal function)... [Pg.114]

Most patients with large ascites also retain sodium avidly and may become hyponatremic if there is a decrease in free water excretion. Untreated, this can lead to a decrease in renal function and the hepatorenal syndrome.4,13... [Pg.326]

Frequent monitoring for signs of hepatorenal syndrome, pulmonary insufficiency, and endocrine dysfunction is necessary. [Pg.256]

Hepatopulmo- diuretics, volume resuscitation, liver transplantation Paracentesis, 02 therapy Dyspnea, presence of ing other nephrotoxins Liver transplantation tor refractoiy hepatorenal syndrome Acute relief of dyspnea... [Pg.261]

Intrinsic Vascular damage Hypercalcemia Hepatorenal syndrome Vasculitis Polyarteritis nodosa Hemolytic uremic syndrom thrombotic thrombocytopenic purpura Emboli Atherosclerotic Thrombotic... [Pg.864]

Hepatic function impairment In patients with preexisting severe liver disease, hepatic encephalopathy (manifested by tremors, confusion, and coma, and increased jaundice) may occur. Because amiloride is not metabolized by the liver, drug accumulation is not anticipated in patients with hepatic dysfunction, but accumulation can occur if hepatorenal syndrome develops. [Pg.695]

Liver transplantation this is indicated for those with failing liver function, for instance with hepatorenal syndrome. Details are beyond this text. [Pg.631]

Gines P, Arroyo V, Rhodes J. Ascites, hepatorenal syndrome, and spontaneous bacterial peritonitis. In MacDonald JWD, Burroughs AK, Feagan BG, editors. Evidence-based gastroenterology and hepatology. 2nd ed. London Blackwells Publishing, BMJ Books 2004. p. 487-503. [Pg.634]

It is important to note that, even more than in heart failure, overly aggressive use of diuretics in this setting can be disastrous. Vigorous diuretic therapy can cause marked depletion of intravascular volume, hypokalemia, and metabolic alkalosis. Hepatorenal syndrome and hepatic encephalopathy are the unfortunate consequences of excessive diuretic use in the cirrhotic patient. [Pg.340]

Hepatic granulomas have been reported as a hypersensitivity reaction to chlorpropamide (101). Cholestatic jaundice from sulfonylureas is also probably of allergic origin it is rare and has been described with glibencla-mide (102), also in combination with hepatorenal syndrome (103), acetohexamide (104), chlorpropamide (105), gliclazide (106), and tolazamide (107). [Pg.447]

The use of vasopressin and terlipressin for the management of septic shock has been reviewed a maximum dose of 0.04 U/minute is recommended (5). Vasopressin 0.23 U/minute in patients with hepatorenal syndrome did not appear to be associated with the adverse effects that occur at the lower doses that are used to treat other critically ill patients (6). [Pg.521]

Of 10 patients with hepatorenal syndrome one had to be withdrawn 2 hours after receiving 12 units of ornipres-sin (6 IU/hour) because of a ventricular tachydysrhyth-mia, and an infusion of dopamine 2-3 micrograms/kg/ minute was started (8). [Pg.521]

One of 21 patients with hepatorenal syndrome developed finger ischemia on the fourth day of intermittent intravenous terlipressin and recovered after terlipressin was stopped (14). [Pg.521]

An elderly patient (over 70 years old) with cirrhosis and hepatorenal syndrome developed severe bronchospasm and died after intravenous terlipressin administration the mechanism was not determined (15). [Pg.521]

Kiser TH, Fish DN, Obritsch MD, Jung R, MacLaren R, Parikh CR. Vasopressin, not octreotide, may be beneficial in the treatment of hepatorenal syndrome a retrospective study. Nephrol Dial Transplant 2005 20 1813-20. [Pg.523]

Gulberg V, Bilzer M, Gerbes AL. Long-term therapy and retreatment of hepatorenal syndrome type 1 with ornipres-sin and dopamine. Hepatology 1999 30(4) 870-5. [Pg.523]

Ortega R, Gines P, Uriz J, Cardenas A, Calahorra B, De Las Heras D, Guevara M, Bataller R, Jimenez W, Arroyo V, Rodes J. Terlipressin therapy with and without albumin for patients with hepatorenal syndrome results of a prospective, nonrandomized study. Hepatology 2002 36(4 Pt l) 941-8. [Pg.523]

Glypressin) on hepatorenal syndrome in cirrhotic patients results of a multicentre pilot study. Eur J Gastroenterol Hepatol 2002 14(2) 153-8. [Pg.523]

The roles of leukotrienes and cytochrome P450 products in the human kidney are currently speculative. Recently, the 5,6-epoxide has been shown to be a powerful vasodilator in animal experiments. Another recent discovery is that free radicals attack arachidonic acid-containing phospholipids to yield an 8-ep/-PGF2[J that has powerful thromboxane-like properties. Synthesis is not blocked by COX inhibitors but can be blocked by antioxidants. This vasoconstrictor, which is present in humans, is thought to be another important mediator causing renal failure in the hepatorenal syndrome. [Pg.446]

Renal disease is seen in 17% of infants with oq-antitrypsin deficiency. It causes massive protein loss, hypoalbuminemia, and renal failure. The kidney disease is an immunological disorder occurring only in patients with liver disease, resulting in a membranoproliferative glomerulonephritis with immunoreactive antitrypsin antigen present, as well as complement and immunoglobulins. It should not be confused with the nonspecific spotty asymptomatic glomerulonephritis or hepatorenal syndrome, commonly seen in cirrhosis. [Pg.45]

The patient was developing hepatorenal syndrome with hypematraemia, a coagulopathy and was agitated. The lactate continued to rise to 8, urea 89, creatinine 158 and urine output fell to <30 mL/h. [Pg.345]

The next day the patient had decreased respiratory rate, became tired with falling blood sugar and acidosis. She had acute renal failure with urine output <30 mL/h and was in fluid overload. The doctors started her on terlipressin 2 mg q.d.s. and HAS (Human Albumin Solution) 20% to maintain central venous pressure 8-12 mmHg and prevent hepatorenal syndrome. Terlipressin is a prodrug for vasopressin. [Pg.345]

Why does sodium rise and potassium fall in liver failure. The reverse happens in hepatorenal syndrome, why ... [Pg.345]

Arroyo V, Terra C, Gines P (2007) Advances in the pathogenesis and treatment of type-1 and type-2 hepatorenal syndrome. / Hepatol 46 935-946. [Pg.143]

These need to be considered in light of the patient s current and potential problems, for example, a decompensated cirrhotic may not have any signs of renal impairment but the use of a renally toxic drug may increase the risk of developing hepatorenal syndrome. See Chapter 6 for more information on side effects. [Pg.165]

Other things to consider are the raised INR and low platelet count (avoid drugs that affect coagulation or cause bleeding), the risk of encephalopathy if the liver function decompensates (caution with any drugs causing sedation, constipation, fluid or electrolyte disturbances) and the risk of hepatorenal syndrome (avoid renally toxic drugs). [Pg.201]

Increased risk of renal dysfunction and hepatorenal syndrome... [Pg.201]

In hepatorenal syndrome (HRS), which is an acute episode, the clearance of renally excreted drugs and metabolites (pravastatin, simvastatin, rosu-vastatin, acipimox, fibrates) may be reduced. During an episode of HRS, anti-hyperlipidaemic medication should be withheld. [Pg.226]


See other pages where Hepatorenal syndrome is mentioned: [Pg.196]    [Pg.112]    [Pg.362]    [Pg.791]    [Pg.98]    [Pg.792]    [Pg.373]    [Pg.440]    [Pg.442]    [Pg.8]    [Pg.141]    [Pg.164]    [Pg.179]   
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