Tubular Handling of Sodium and Phosphate in Cirrhosis with Salt Retention

Rochman, Jose; Chaimovitz, Cidio; Szylman, P; Better, Ori S.

doi:10.1159/000181201

Cited by 7 publications

(1 citation statement)

References 7 publications

(9 reference statements)

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“…Ή ικανότης τοΰ νεφρικού σωληναρίου δια τήν όξινοποίησιν τών ουρών επηρεάζεται κυρίως έκ τής όξεοβασικής ισορροπίας τοΰ έξωκυτταρίου υγρού (Rector 1976), τών ερεθισμάτων δια τήν έπαναρρόφησιν τοΰ Να+ κατά μήκος τοΰ νεφρικοΰ σωληναρίου (Shear 1965, Papper 1958, Chaimowith 1972, Bet ter 1972, Rochman 1978, τής ικανότητος έπαναρροφήσεως τών ανιόντων (Bank 1960, Jamison 1976) καί τέλος τής ποσότητος τοΰ σπειραματικοΰ διηθήματος (Steinmetz καί συν. 1963) , καίτοι τούτο δεν φαίνεται να εχη σημασίαν εις τον βαθμον τής τελικής νατριουρήσεως.…”

Section: συζητησιςunclassified

Η Λειτουργια Του Νεφρικου Σωληναριου Επι Κιρρωσεως Του Ηπατος: Μελετη Δια Φορτωσεως Χλωριουχου Ασβεστιου. Η Εμφανισις Του Συνδρομου Της Νεφροσωληναριακης Οξεωσεως.

Βαγιωνάς¹

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Section: συζητησιςunclassified

Η Λειτουργια Του Νεφρικου Σωληναριου Επι Κιρρωσεως Του Ηπατος: Μελετη Δια Φορτωσεως Χλωριουχου Ασβεστιου. Η Εμφανισις Του Συνδρομου Της Νεφροσωληναριακης Οξεωσεως.

Βαγιωνάς¹

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Medical Treatment of Ascites in Cirrhosis

Angeli¹,

Gatta²

2005

Ascites and Renal Dysfunction in Liver Disease

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Medical treatment of cirrhotic ascites is essentially supportive, dictated by the patient's discomfort, impaired car-diovascular or respiratory function and potential for infection. Treatment of'simple' ascites (moderate fluid accumulation , serum albumin > 3.5 g/dl, serum creatinine < 1.5 mg/di, no electrolyte disturbance) is implemented sequentially. Only 10% of patients respond to dietary sodium restriction and bed rest; most require pharmacotherapy consisting of spironolactone, which increases the proportion of responding patients to 65% and loop diuretics, which may produce clinical improvement in an additional 20% (85% in all); in the remaining 15% of refractory patients, use of novel adjunctive therapies may be attempted. Patients with tense ascites, impaired renal function and electrolyte disturbances merit special consideration before diuretics are introduced. Spironolactone has long been a standard for the treatment of cirrhotic ascites because it directly antagonizes aldosterone. The loop diuretic most frequently added to spironolactone has been furosemide. However, there is preliminary evidence that torasemide may be more effective in some patients. Other investigational agents that may play a role in treatment of patients resistant to conventional drugs include ornipressin (a vasopressin analogue) and atrial natriuretic factor. A brief overview of the pathophysiology of ascites formation in hepatic cirrhosis (1) can facilitate understanding both of the available therapeutic options and of the rationale for development of new therapeutic approaches. Traditionally, the initiating event of renal sodium and water retention in cirrhosis was considered to be ascites formation (underfilling hypothesis) or primary renal dysfunction due to a hepatorenal reflex (overflow hypothesis) (2). The alterations of systemic, splanchnic and renal haemodynamics, as well as increases in circulating levels of substances that cause sodium retention (3-6), are compatible with a decrease in effective blood volume as suggested by the underfill-ing hypothesis. These alterations, however, precede ascites formation. The recently introduced vasodilation hypothesis (7) reconciles many aspects of the underfill-ing theory and the overflow theory; it proposes that peripheral arterial vasodilation is the initiating event leading to decreased effective blood volume and renal sodium retention (Table 1) and suggests that haemodynamic, hormonal and renal changes are augmented as liver disease becomes more severe. Peripheral arterial vasodilation leads to a decrease in effective arterial blood volume and, in compensation, increases in circulating levels of renin, aldosterone, noradrenaline and vasopressin, which result in renal vasoconstriction with sodium and water retention. With increasing severity of cirrhosis, the activation of these stimulants of sodium retention cannot restore effective blood volume. This, together with a decrease in plasma oncotic pressure due to hypoalbuminaemia and an increase in hydrostatic pressure in the splan...

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The Pathogenesis of Renal Sodium Retention and Ascites Formation in Laennec’s Cirrhosis

Pitts

Thiel

1986

Recent Developments in Alcoholism

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Tubular Handling of Sodium and Phosphate in Cirrhosis with Salt Retention

Cited by 7 publications

References 7 publications

Medical Treatment of Ascites in Cirrhosis

The Pathogenesis of Renal Sodium Retention and Ascites Formation in Laennec’s Cirrhosis

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