1. Hepatorenal syndrome in cirrhosis: Pathogenesis and treatment
Vicente Arroyo, Mónica Guevara, Pere Ginès 
Gastroenterology 
Volume 122, Issue 6, Pages (May 2002)
DOI: /gast
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2. Fig. 1
Glomerular filtration rate and urinary excretion of prostaglandin E2 (mean ± standard error of the mean) before and after the IV injection of 450 mg of lysine acetylsalicitate in 19 patients with cirrhosis and ascites. Patients are divided in 2 groups according to whether they developed renal insufficiency (II, 11 patients) or not (I, 8 patients) after the administration of the drug. C1 and C2 represent 2 30-minute periods before the administration of lysine acetylsalicilate. LAS1, LAS2, and LAS3 represent 3 30-minute periods after the administration of lysine acetylsalicylate. Values of plasma noradrenaline correspond to those of samples obtained before lysine acetylsalicylate injection. Reprinted with permission.30
Gastroenterology  , DOI: ( /gast )
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3. Fig. 2
Renal plasma flow in baseline conditions (B) after prostaglandin inhibition with lysine acetylsalicylate (LAS), after nitric oxide inhibition with l-nitro-arginine (NNA), and after the administration of both inhibitors in rats with cirrhosis and ascites. Reprinted with permission.87
Gastroenterology  , DOI: ( /gast )
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4. Fig. 3
Renal plasma flow and renal vascular resistance in control (solid line) and cirrhotic rats with ascites (dotted line) under baseline conditions and at 30, 60, and 90 minutes after administration of a specific antagonist of endogenous natriuretic peptide receptors. Significance denoted in the figure is versus baseline values. *P < Reprinted with permission.88
Gastroenterology  , DOI: ( /gast )
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5. Fig. 4
Course of renal function in a cirrhotic patient admitted to hospital for the treatment of an episode of tense ascites. The patient had type 2 HRS and refractory ascites. He was treated with repeated therapeutic paracentesis. In the follow-up, the patient developed signs of spontaneous bacterial peritonitis (SBP) and was treated with cefotaxime. Despite resolution of spontaneous bacterial peritonitis, a rapid deterioration of renal function (Type-1 HRS) developed. The patient died 3 weeks after infection diagnosis.
Gastroenterology  , DOI: ( /gast )
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6. Fig. 5
Probability of survival of patients with severe HRS. Reprinted with permission.113
Gastroenterology  , DOI: ( /gast )
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7. Fig. 6
Possible mechanisms of type 1 (right) and type 2 (left) HRS. SNS, sympathetic nervous system; RAAS, renin-angiotensin-aldosterone system; ADH, antidiuretic hormone.
Gastroenterology  , DOI: ( /gast )
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8. Fig. 7
Central blood volume and mean transit time of central circulation in healthy subjects and patients with compensated cirrhotic patients and patients with ascites. Reprinted with permission.114
Gastroenterology  , DOI: ( /gast )
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9. Fig. 8
Relationship between the decrease in mean arterial pressure (MAP) after angiotensin II blockade with saralasin and the baseline plasma renin activity (PRA). Reprinted with permission.41
Gastroenterology  , DOI: ( /gast )
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10. Fig. 9
Resistive index (RI) in the mean cerebral artery (A) and in the arcuate or interlobar intrarenal artery (B) in healthy subjects, patients with compensated cirrhosis and patients with ascites. C illustrates the relationship between both measurements in the patients with cirrhosis. Reprinted with permission.137
Gastroenterology  , DOI: ( /gast )
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11. Fig. 10
Changes in plasma renin activity (PRA), plasma aldosterone, and norepinephrine (NE) concentration, and GFR (inulin clearance) in patients with HRS treated with ornipressin (2 U/h the first day, 4 U/h the second day, and 6 U/h the third day) plus IV albumin infusion. There was a marked suppression of the neurohormonal systems without clinically significant increase in GFR. Reprinted with permission.72
Gastroenterology  , DOI: ( /gast )
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12. Fig. 11
Evolution of serum creatinine in patients with HRS treated by terlipressin (0.5–2 mg/4 h) and IV albumin infusion. Reprinted with permission.172
Gastroenterology  , DOI: ( /gast )
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