الفهرس 
Strucure of ANPOnly 14 pages are availabe for public view
 |  | from | 146 |  |  |
| | | from | 146 | | |
Abstract
SUMMARY & CONCLUSION
This study was conducted on 47 subjects divided into 2
groups:
Group 1 : Included 10 well cross matched healthy
volunteers.
* Group 2 : Included 37 patients with liver cirrhosis,
divided into 2 groups:
- Group (A): Cirrhotic non ascitic patients (12
patients)
- Group (B): Cirrhotic ascitic patients (25
patients)
This group were subdivided into 2
subgroups:
(1)Patients with preserved renal
function (10 patients)
(2)Patients with impaired renal function i.e hepato-renal syndrome.
(15 patients)
Every case was subjected to the following
investigations:
-Liver function tests.
-Serum and urine creatinine.
-Urinary and serum Na+ level.
-Plasma level of ANP. The following had been reported in this work:
103
* All biochemical liver function tests with exception of total proteins were deranged in cirrhotic patients when
compared to control group (Table 1).
* All biochemical liver function tests were significantly impaired in cirrhotic ascitic patients when compared to
cirrhotic non ascitic patients
*Patients with hepato-renal syndrome showed significant impaired biochemical liver function test when compared to other groups (Table 3, 5, 6, & 7).
*Serum creatinine was significantly higher in patients with hepato-renal syndrome when compared to all groups (Table 3,
5 & 6).
*All our patients with high serum creatinine had fractional
excretion filtered sodium less than 1, proving that renal
impairment in them was due to hepato-renal syndrome rather
than intrinsic renal diseases (Table 7).
*Serum Na4- and urinary Na+ did not change significantly in cirrhotic non ascitic patients.
*Serum Nat and urinary Na+ showed significant reduction in cirrhotic ascitic patients when compared to either control group or cirrhotic non ascitic group.
*Patients with hepato-renal syndrome showed significant reduction in both urinary and serum sodium when compared to cirrhotic ascitic patients with preserved kidney function (Table 6).
104
The plasma ANP level did not change significantly in cirrhotic non ascitic patients when compared to control
group (Table 1).
* The plasma ANP level was not significantly high in cirrhotic ascitic patients when compared to either cirrhotic non ascitic or control group (Table 2 & 4).
* Patients with hepato-renal syndrome had a significant rise in plasma ANP level when compared to cirrhotic ascitic patients with preserved kidney function (Table 6).
* The high level of ANP is caused by hypervolemia and increased level of renin, angiotensin II and norepinephrin.
* The elevated concentration of ANP in cirrhotic patients possibly particepates in the pathogenesis of hepato-renal syndrome through reduction of renal blood flow and this is mediated through its vasodilater effect and antagonism of the action of renin, angiotensin II and norepinephrine. Also, through change in intra-renal distribution of the blood flow by diverting it amay from the renal cortex, a phenomenon which already exists in cirrhotic patients, thus reducing glomerular filtration rate (GFR).