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Plasma human atrial natriuretic peptide levels in patients with liver cirrhosis
K Uemura1, H Oguchi, K Kiyosawa
1Second Department of Internal Medicine, Shinshu University School of Medicine, Matsumoto, Japan.
Insights
Plasma levels of human atrial natriuretic peptide (hANP) are elevated in liver cirrhosis patients with ascites. The kidney
Area of Science:
- Nephrology
- Hepatology
- Endocrinology
Background:
- Liver cirrhosis often leads to fluid retention and electrolyte imbalances.
- Human atrial natriuretic peptide (hANP) plays a role in regulating sodium and water balance.
Purpose of the Study:
- To investigate plasma hANP levels in liver cirrhosis patients.
- To explore the relationship between plasma hANP and factors like ascites, electrolytes, and the renin-angiotensin-aldosterone system.
Main Methods:
- Measured plasma hANP levels in patients with and without ascites.
- Assessed correlations with urine electrolytes, blood volume, and hormonal factors.
- Evaluated liver function tests.
Main Results:
- Plasma hANP levels were significantly higher in patients with ascites.
- hANP levels decreased with ascites resolution.
- Urine sodium excretion correlated with hANP in non-ascites patients but not in those with ascites.
- No correlation found between hANP and blood volume, hormonal levels, or liver function tests.
Conclusions:
- Elevated plasma hANP in cirrhosis, particularly with ascites, suggests a compensatory mechanism.
- The kidney's natriuretic response to hANP may be impaired in cirrhotic patients with ascites.
Abstract:
Plasma levels of human atrial natriuretic peptide (hANP) were investigated in patients with liver cirrhosis, and the relationships between plasma hANP levels and the following factors were studied: presence of ascites, serum and urine electrolytes, plasma renin activity, angiotensin I and II, aldosterone, catecholamines, prostaglandin derivatives, conventional liver function tests and circulating blood volume. Plasma hANP level was significantly (P less than 0.05) elevated in patients with ascites (mean = 58.6 pg/mL, s.e.m. = 8.8) compared with cases without ascites (mean = 36.6 pg/mL, s.e.m. = 2.6). With the disappearance of ascites, the level fell to normal in most cases. Urine sodium excretion was positively correlated with plasma hANP in patients without ascites, but not in patients with ascites. The plasma hANP level was disproportionately high for the rate of urinary Na excretion in cirrhotics with ascites. The plasma hANP level was not correlated with any of the other factors such as blood volume, renin-angiotensin-aldosterone levels, catecholamines and liver function tests. These results suggest that plasma hANP levels are elevated in cirrhotic patients especially with ascites, but the natriuretic response of the kidney to this raised hANP level can be impaired in patients with liver cirrhosis and ascites.