Effects of low-dose captopril on renal hemodynamics and function in patients with cirrhosis of the liver

Geñtilini, Paolo; Romanelli, Roberto Giulio; Villa, Giorgio La; Maggiore, Q; Pesciullesi, E; Cappelli, G; Raggi, Vincenzo Casini; Foschi, Marco; Marra, Fabio; Pinzani, Massimo; Buzzelli, G

doi:10.1016/0016-5085(93)90431-b

Cited by 84 publications

(34 citation statements)

References 27 publications

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“…7,8 In experimental animals, the administration of ANG II to perfuse cirrhotic liver leads to an increase in intrahepatic vascular resistance by the direct contraction of stellate cells. 9 Gentilini et al 10 used captopril to study the influence of ANG II in renal function in patients with cirrhosis. However, it has been shown that a significant hypotensive effect produced by captopril, enhances the release of bradykinin and prostaglandin, and the inhibition of aldosterone secretion by captopril interferes with the recognition of the true effects of ANG II in renal hemodynamics.…”

Section: Introductionmentioning

confidence: 99%

One-week losartan administration increases sodium excretion in cirrhotic patients with and without ascites

Yang

Lee

et al. 2002

J Gastroenterol

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Section: Introductionmentioning

confidence: 99%

One-week losartan administration increases sodium excretion in cirrhotic patients with and without ascites

Yang

Lee

et al. 2002

J Gastroenterol

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“…29 Inhibition of angiotensin II action by inhibiting the angiotensinconverting enzyme with captopril or blocking type 1 angiotensin receptors with losartan or irbesartan may induce marked arterial hypotension and vasodilation of postglomerular arterioles, causing prerenal failure in patients with cirrhosis and ascites. [30][31][32] Intrinsic Renal Failure Acute Tubular Necrosis. Injury to the renal tubules may be ischemic or toxic in origin.…”

Section: Prerenal Failurementioning

confidence: 99%

Acute renal failure in patients with cirrhosis: Perspectives in the age of MELD

2003

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In patients with cirrhosis, acute renal failure is mainly due to prerenal failure (caused by renal hypoperfusion) and tubular necrosis. The main causes of prerenal failure are "true hypovolemia" (induced by hemorrhage or gastrointestinal or renal fluid losses), sepsis, or type 1 hepatorenal syndrome (HRS). The frequency of prerenal failure due to the administration of nonsteroidal anti-inflammatory drugs or intravascular radiocontrast agents is unknown. Prerenal failure is rapidly reversible after restoration of renal blood flow. Treatment is directed to the cause of hypoperfusion, and fluid replacement is used to treat most cases of "non-HRS" prerenal failure. In patients with type 1 HRS with very low short-term survival rate, liver transplantation is the ideal treatment. Systemic vasoconstrictor therapy (with terlipressin, noradrenaline, or midodrine [combined with octreotide]) may improve renal function in patients with type 1 HRS waiting for liver transplantation. MARS (for molecular adsorbent recirculating system) and the transjugular intrahepatic portosystemic shunt may also improve renal function in these patients. In patients with cirrhosis, acute tubular necrosis is mainly due to an ischemic insult to the renal tubules. The most common condition leading to ischemic acute tubular necrosis is severe and sustained prerenal failure. Little is known about the natural course and treatment (i.e., renal replacement therapy) of cirrhosis-associated acute tubular necrosis. (HEPATOLOGY 2003;37:233-243.)

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“…Angiotensin-converting enzyme inhibitors and angiotensin receptor blockers should be avoided in patients with cirrhosis and ascites even in low doses as they can induce arterial hypotension and renal failure [60,61]. If used, blood pressure and renal function must be monitored carefully [7].…”

Section: Drugs To Be Avoided or Used With Cautionmentioning

confidence: 99%

Pharmacological Therapy of Ascites

Ajlan¹,

Al–Hamoudi²,

Elsiesy³

2017

Ascites - Physiopathology, Treatment, Complications and Prognosis

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Ascites refer to accumulation of fluids in the peritoneal cavity. Ascites is caused by multiple causes, among which liver cirrhosis is the commonest. Confirming the etiology is the first and most important step toward proper management. Assuming that ascites is always caused by cirrhosis can lead to unnecessarily sending patients with different etiologies for liver transplantation, particularly patients with non-cirrhotic portal hypertension. Calculating serum albumin ascitic gradient is important in differentiating ascites due to portal hypertension from other etiologies. The first-line therapy for ascites in cirrhosis is low salt diet and diuretics. It is important to avoid nonsteroidal anti-inflammatory drugs (NSAIDs) and nephrotoxic medications in these patients.

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Effects of low-dose captopril on renal hemodynamics and function in patients with cirrhosis of the liver

Cited by 84 publications

References 27 publications

One-week losartan administration increases sodium excretion in cirrhotic patients with and without ascites

One-week losartan administration increases sodium excretion in cirrhotic patients with and without ascites

Acute renal failure in patients with cirrhosis: Perspectives in the age of MELD

Pharmacological Therapy of Ascites

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