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Relation between severity of liver disease and renal oxygen consumption in patients with cirrhosis
  1. A Gadano,
  2. R Moreau,
  3. J Heller,
  4. C Chagneau,
  5. F Vachiéry,
  6. C Trombino,
  7. A Elman,
  8. C Denié,
  9. D Valla,
  10. D Lebrec
  1. Laboratoire d’Hémodynamique Splanchnique et de Biologie Vasculaire, INSERM and Service d’Hépatologie, Hôpital Beaujon, Clichy, France
  1. Dr R Moreau, INSERM, Hôpital Beaujon, 92118, Clichy, France.

Abstract

BACKGROUND Worsening cirrhosis may lead to increased renal O2 metabolism caused by activation of neurohumoral antinatriuretic substances.

AIMS To evaluate the relation between the severity of liver disease, sodium excretion, and neurohumoral antinatriuretic substances on the one hand and renal O2 metabolism on the other in patients with cirrhosis.

METHODS Renal O2 consumption and haemodynamics as well as plasma concentrations of noradrenaline, renin, and aldosterone were measured. Investigations were performed in 14 patients with Pugh’s grade A, 43 with grade B, and 29 with grade C liver disease.

RESULTS Renal O2 consumption significantly increased with the severity of cirrhosis (grade A, 8.9 (1.6); grade B, 15.5 (1.3); grade C, 18.0 (1.5) ml/min/m2). Plasma concentrations of noradrenaline, renin, and aldosterone significantly increased while mean arterial presssure and systemic vascular resistance significantly decreased with the severity of the disease. A significant inverse correlation was found between renal O2 consumption and sodium excretion. A significant direct correlation was found between plasma levels of noradrenaline and aldosterone on the one hand and renal O2consumption on the other. Renal blood flow and the glomerular filtration rate did not differ significantly between patients with grade C and grade A or B disease.

CONCLUSIONS This study shows for the first time that, in patients with cirrhosis, worsening of the disease is associated with an increase in renal O2consumption. The results suggest that increased renal O2consumption is due to renal tubular sodium retention caused by increased levels of neurohumoral antinatriuretic substances. This neurohumoral activation is related to cirrhosis induced vasodilation.

  • antinatriuretic hormones
  • cirrhosis
  • kidney
  • haemodynamics
  • O2 consumption
  • sodium retention
  • Abbreviations used in this paper

    Na+/K+ ATPase
    sodium/potassium dependent adenosine triphosphatase
    PAH
    p-aminohippurate
    Po2
    O2 tension
    So2
    oxyhaemoglobin saturation
    ANP
    atrial natriuretic peptide
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  • Abbreviations used in this paper

    Na+/K+ ATPase
    sodium/potassium dependent adenosine triphosphatase
    PAH
    p-aminohippurate
    Po2
    O2 tension
    So2
    oxyhaemoglobin saturation
    ANP
    atrial natriuretic peptide
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