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      Acute Kidney Injury: New Concepts


      Nephron Physiology

      S. Karger AG

      Vasoconstrictors, Cirrhosis, Ascites, Portal hypertension, Hepatorenal syndrome

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          Type 1 hepatorenal syndrome (HRS) is prerenal failure specific to decompensated cirrhosis. In patients with HRS, there is marked splanchnic/systemic vasodilation resulting in arterial hypotension, arterial baroreceptor unloading, overstimulation of the sympathetic nervous and renin-angiotensin systems. This reflex neurohumoral hyperactivity via endogenous vasoconstrictors/vasopressors such as angiotensin II and noradrenaline induces arterial vasoconstriction in different extrasplanchnic vascular beds (including preglomerular arteries in the kidneys). Decreased arterial pressure (i.e. low renal perfusion pressure) and preglomerular vasoconstriction are thought to play a major role in the decline of the glomerular filtration rate (GFR). Nonrandomized studies in patients with HRS have shown that the administration of a splanchnic vasoconstrictor (vasopressin analogue or α<sub>1</sub>-adrenoceptor agonist), usually combined with intravenous albumin, causes increases in arterial pressure, arterial baroreceptor uploading, decreased neurohumoral activity, decreased renal vascular resistance, and increased GFR. Randomized clinical trials have shown that treatment with a combination of the vasopressin analogue terlipressin and intravenous albumin improves renal function in patients with type 1 HRS. Vasopressor therapy with terlipressin plus intravenous albumin is the medical treatment of choice for type 1 HRS.

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          Most cited references 25

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          Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club.

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            Reversal of type 1 hepatorenal syndrome with the administration of midodrine and octreotide.

            The aim of the study was to verify the effects of the administration of an inhibitor of the release of endogenous vasodilators together with a vasoconstrictor agent in patients with hepatorenal syndrome (HRS). This new medical perspective was compared with a traditional medical approach for HRS, such as the infusion of nonpressor doses of dopamine to produce renal vasodilation. Thirteen patients with type 1 HRS were enrolled in the study. Five of them were treated with the oral administration of midodrine and the parenteral administration of octreotide. In addition, the patients received 50 to 100 mL of 20% human albumin solution daily for 20 days. Midodrine and octreotide were dosed to obtain a stable increase of at least 15 mm Hg of mean arterial pressure. Eight patients were treated with the intravenous administration of nonpressor doses of dopamine (2-4 micrograms/kg/min) and the same daily amount of albumin. After 20 days of treatment with midodrine and octreotide, an impressive improvement in renal plasma flow (RPF), glomerular filtration rate, and urinary sodium excretion was observed in patients. This was accompanied by a significant reduction in plasma renin activity, plasma vasopressin, and plasma glucagon. No side effects were observed. Three patients were discharged from the hospital. One of them successfully underwent liver transplantation. One of the two remaining patients is still alive after 472 days with a preserved renal function, and the other died from terminal liver failure after 76 days. One of the two patients who were not discharged from the hospital successfully underwent liver transplantation, and the other died from pneumonia after 29 days. Seven out of eight patients who were treated with dopamine experienced a progressive deterioration in renal function and died during the first 12 days. Only one patient recovered renal function and underwent liver transplantation. In conclusion, the long-term administration of midodrine and octreotide seems to be an effective and safe treatment of type 1 HRS in patients with cirrhosis.
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              Hepatorenal syndrome.

              Hepatorenal syndrome (HRS) is a common complication of advanced cirrhosis, characterised by renal failure and major disturbances in circulatory function. Renal failure is caused by intense vasoconstriction of the renal circulation. The syndrome is probably the final consequence of extreme underfilling of the arterial circulation secondary to arterial vasodilatation in the splanchnic vascular bed. As well as the renal circulation, most extrasplanchnic vascular beds are vasoconstricted. The diagnosis of HRS is currently based on the exclusion of other causes of renal failure. The prognosis is very poor, particularly when there is rapidly progressive renal failure (type 1). Liver transplantation is the best option in patients without contraindications to the procedure, but it is not always possible owing to the short survival expectancy. Therapies introduced during the past few years, such as vasoconstrictor drugs (vasopressin analogues, alpha-adrenergic agonists) or the transjugular intrahepatic portosystemic shunt, are effective in improving renal function. Nevertheless, liver transplantation should still be done in suitable patients even after improvement of renal function because the outcome of HRS is poor. Finally, recent findings suggest that the risk of developing HRS in the setting of spontaneous bacterial peritonitis may be reduced by the administration of albumin together with antibiotic therapy, and that of HRS occurring in severe alcoholic hepatitis can be lowered by administration of pentoxifylline. Although these findings need to be confirmed, these two strategies represent innovative approaches to lower the frequency of HRS in clinical practice.

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                September 2008
                18 September 2008
                : 109
                : 4
                : p73-p79
                INSERM U773, Centre de Recherche Biomédicale Bichat-Beaujon CRB3, and Service d’Hépatologie, Hôpital Beaujon, Clichy, France
                142939 Nephron Physiol 2008;109:p73
                © 2008 S. Karger AG, Basel

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                Page count
                Figures: 1, Tables: 1, References: 35, Pages: 1


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