Table 1.

Changes of cardiovascular function and vasoactive systems from patients with spontaneous bacterial peritonitis to hepatorenal syndrome

	SBP Group-1	SBP Group-2	SBP Group-2	P value
	At diagnosis of infection	At diagnosis of infection	At diagnosis of HRS
Serum creatinine (mg/dL)	1.0 ± 0.3	1.3 ± 0.6	2.5 ± 0.4	< 0.02
MAP (mmHg)	83 ± 10	83 ± 7	73 ± 8	< 0.02
SVR (dyn•s/cm5)	893 ± 196	1137 ± 220a	1268 ± 320	NS
PAP (mmHg)	12.0 ± 2.0	13.2 ± 4.0	12.6 ± 3.7	NS
PCWP (mmHg)	5.9 ± 1.8	5.7 ± 4.0	7.4 ± 2.6	NS
Cardiac output (L/min)	7.4 ± 1.9	5.7 ± 0.9a	4.6 ± 0.7	< 0.02
Heart Rate (bpm)	87 ± 16	93 ± 13	87 ± 9	NS
Norepinephrine (pg/mL)	315.7 ± 172	797.3 ± 226.6a	1290.5 ± 415.3	< 0.02
PRA (ng/mL•h)	3.9 ± 3.6	18.4 ± 11.2a	28.3 ± 12.4	< 0.02

Data obtained from Ruiz-del-Árbol et al[146]. Renal failure in SBP is related to a deterioration of circulatory function. At baseline, there were no significant differences between groups in serum creatinine. At diagnosis of infection, patients in the SBP Group-2 showed lower cardiac output and higher levels of systemic vascular resistance, PRA and NE than patients in the SBP Group-1. Following resolution of infection, patients in the SBP Group-2 had severe renal failure and a further decrease in cardiac output, low arterial pressure, and extremely high levels of PRA and NE. There were no significant differences between groups in heart rate and cardiopulmonary pressures. SBP Group-1, Cirrhotic patients with spontaneous bacterial peritonitis that had not developed hepatorenal syndrome in the follow-up; SBP Group-2, Cirrhotic patients with spontaneous bacterial peritonitis that had developed hepatorenal syndrome in the follow-up.

^aP < 0.025 vs values at diagnosis of infection of SBP Group-1. Data are presented as mean ± SD. SBP: Spontaneous bacterial peritonitis; HRS: Hepatorenal Syndrome; NS: Not significant; MAP: Mean arterial pressure; PAP: Pulmonary artery pressure; PCWP: Pulmonary capillary wedged pressure; SVR: Systemic vascular resistance; PRA: Plasma renin activity.