G. Wensing et al., URINARY SODIUM-BALANCE IN PATIENTS WITH CIRRHOSIS - RELATIONSHIP TO QUANTITATIVE PARAMETERS OF LIVER-FUNCTION, Hepatology, 26(5), 1997, pp. 1149-1155
The relationship between the impairment in hepatic and renal function
in cirrhosis has not been well established. This study investigated ur
inary sodium excretion in comparison with quantitative parameters of l
iver function in 75 patients with various degrees of cirrhosis kept on
a constant salt diet of 120 mmol/d for 5 days before the start of the
study, The aminopyrine breath test (ABT), indocyanine green (ICG) eli
mination, galactose elimination capacity (GEC), and hepatic sorbitol e
limination (HSE) served as quantitative parameters of liver function,
Results for the quantitative tests were compared with those for the Ch
ild-Pugh score. Urinary sodium excretion showed a significant nonlinea
r relationship to ABT (r = .70; P < .0001). Less-significant correlati
ons were observed for ICG (r = .60), the Child-Pugh score (r = -.57),
GEC (r = .44), and HSE (r = .34), Because a number of significant corr
elations were observed between the different liver function tests, mul
tivariate analysis was used to further elucidate the relationship betw
een hepatic function and sodium excretion, Only one independent predic
tor of urinary sodium excretion could be identified, and that was the
ABT (P < .02). More than half of the nonascitic patients showed a urin
ary sodium excretion of less than 80% of dietary sodium intake, indica
ting impaired renal sodium handling in pre-ascitic cirrhosis. Based on
the 95% confidence interval (CI) for ABT of nonascitic patients with
normal (mean ABT 0.56% dose X kg/mmol CO2; 95% CI: 0.44 to 0.69) and r
educed urinary sodium excretion (mean ABT 0.26% dose X kg/mmol CO2; 95
% CI: 0.18 to 0.35), a threshold level of ABT of about 0.4 (% dose X k
g/mmol CO2) for conservation of normal urinary sodium excretion in cir
rhosis can be defined. This ABT value reflects an approximate 50% redu
ction in function compared with the mean of cirrhotic patients with no
rmal liver and kidney function (0.81% dose x kg/mmol CO2). The presenc
e of ascites was also associated with a reduction in ABT to below 0.4
(% dose X kg/mmol CO2), while, for all other parameters, either the cu
t-off point was close to the lower limit of normal or no cut-off level
could be detected. In conclusion, the results of the present study pr
ovide further evidence that the impairment in urinary sodium excretion
in cirrhosis is related to hepatic function, The data suggest a nonli
near relationship. Because AB-T has been shown to reflect functional h
epatocellular mass, the occurrence of sodium retention and ascites app
ears to be related to a threshold of an approximate 50% reduction in f
unctional liver cell mass.