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Vol. 57. Núm. S2.
Hiponatremia y síndrome de secreción inadecuada de ADH (SIADH)
Páginas 15-21 (Mayo 2010)
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Vol. 57. Núm. S2.
Hiponatremia y síndrome de secreción inadecuada de ADH (SIADH)
Páginas 15-21 (Mayo 2010)
Acceso a texto completo
Hiponatremia en la cirrosis hepática: patogenia y tratamiento
Hyponatremia in liver cirrhosis: pathogenesis and treatment
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35529
Mónica Guevara, Pere Ginès
Autor para correspondencia
jcomin@hospitaldelmar.cat

Autor para correspondencia.
Servei d’Hepatologia, Hospital Clínic de Barcelona, Universitat de Barcelona, Institut d’Investigacions Biomèdiques August-Pi-Sunyer (IDIBAPS), Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas (CIBEREHD), Barcelona, España
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Resumen

La hiponatremia es la alteración hidroelectrolítica más común en los pacientes con cirrosis. La hiponatremia puede ser consecuencia de una pérdida importante de líquido extracelular, “hiponatremia vera o hipovolémica”, o presentarse en el contexto de un aumento del volumen de líquido extracelular y en ausencia de pérdidas importantes de sodio, situación que ocurre en los pacientes con cirrosis avanzada, “hiponatremia dilucional o hipervolémica”. En la hiponatremia dilucional o hipervolémica la concentración sérica de sodio está disminuida, el volumen plasmático aumentado (aunque el volumen plasmático efectivo está disminuido debido a una marcada vasodilatación arterial en la circulación esplácnica) y el volumen de líquido extracelular aumentado, con ascitis y edemas en ausencia de signos de deshidratación. Esto es consecuencia del deterioro marcado en la excreción renal de agua libre de solutos, que condiciona una retención renal de agua desproporcionada con relación a la retención de sodio. La hiponatremia vera representa un 10% de todas las hiponatremias que presentan los pacientes con cirrosis; por tanto, y debido a que la hiponatremia hipervolémica es por mucho la más frecuente, este capítulo se dedica específicamente a la hiponatremia hipervolémica en la cirrosis.

Palabras clave:
Cirrosis
Hiponatremia
Ascitis
Vaptanes
Hormona antidiurética
Abstract

Hyponatremia is the most common electrolyte disorder in patients with cirrhosis. This disorder can be a result of substantial loss of extracellular fluid “hypotonic or hypovolemic hyponatremia” or develop in the context of an increase in extracellular fluid volume and in the absence of major sodium losses; this situation occurs in patients with advanced cirrhosis and is known as “dilutional or hypervolemic hyponatremia”. In dilutional or hypervolemic hyponatremia, serum sodium concentration is reduced, plasma volume is increased (although the effective plasma volume is decreased due to marked arterial vasodilation in the splanchnic circulation) and extracellular fluid volume is increased, with ascites and edema in the absence of signs of dehydration. This is a result of the marked deterioration in renal excretion of solute-free water, leading to disproportionate water retention in relation to sodium retention. Hypotonic hyponatremia represents 10% of all hyponatremias in patients with cirrhosis. Since hypervolemic hyponatremia is by far the most frequent form of this disorder, the present chapter will concentrate specifically on hypervolemic hyponatremia in cirrhosis.

Keywords:
Cirrhosis
Hyponatremia
Ascites
Vaptans
Vasopressin
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Bibliografía
[1.]
P. Ginès, J. Rodès.
Clinical disorders of renal function in cirrhosis with ascites.
Ascites and liver dysfunction in liver disease, pp. 36-62
[2.]
P. Angeli, F. Wong, H. Watson, P. Ginès.
Hyponatremia in cirrhosis: results of a patient population survey.
Hepatology, 44 (2006), pp. 1535-1542
[3.]
R.W. Schrier, V. Arroyo, M. Bernardi, M. Epstein, J.H. Henriksen, J. Rodès.
Peripheral arterial vasodilation hypothesis — a proposal for the initiation of renal sodium and water-retention in cirrhosis.
Hepatology, 8 (1988), pp. 1151-1157
[4.]
V. Arroyo, J. Claria, J. Salo, W. Jiménez.
Antidiuretic-hormone and the pathogenesis of water-retention in cirrhosis with ascites.
Seminars in Liver Disease, 14 (1994), pp. 44-58
[5.]
M. Epstein.
Derangements of renal water handling in liver disease.
Gastroenterology, 89 (1985), pp. 1415-1425
[6.]
M. Epstein.
Deranged sodium homeostasis in cirrhosis.
Gastroenterology, 76 (1979), pp. 622-635
[7.]
V. Arroyo, J. Rodès, M.A. Gutierrezlizarraga, L. Revert.
Prognostic value of spontaneous hyponatremia in cirrhosis with ascites.
Am J Dig Dis, 21 (1976), pp. 249-256
[8.]
S. Ishikawa, R.W. Schrier.
Arginine vasopressin in cirrhosis, pp. 220-230
[9.]
G.L. Robertson, T. Berl.
Pathophysioloy of water metabolism: water retaining disorders.
The Kidney, 5th ed.,
[10.]
T. Berl, R.W. Schrier.
Disorder of water metabolism.
Renal and electrolyte disorders, 5th ed., pp. 1-71
[11.]
M.A. Knepper, S. Nielsen, C.L. Chou, S.R. DiGiovanni.
Mechanism of vasopressin action in the renal collecting duct.
Semin Nephrol, 14 (1994), pp. 302-321
[12.]
S. Nielsen, C.L. Chou, D. Marples, E.I. Christensen, B.K. Kishore, M.A. Knepper.
Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane.
Proc Natl Acad Sci USA, 92 (1995), pp. 1013-1017
[13.]
M.A. Knepper.
The aquaporin family of molecular water channels.
Proc Natl Acad Sci USA, 91 (1994), pp. 6255-6258
[14.]
S. Nielsen, P. Agre.
The aquaporin family of water channels in kidney.
Kidney Int, 48 (1995), pp. 1057-1068
[15.]
J. Ros, G. Fernández-Varo, J. Muñoz-Luque, V. Arroyo, J. Rodès, J.W. Gunnet, et al.
Sustained aquaretic effect of the V2-AVP receptor antagonist, RWJ-351647, in cirrhotic rats with ascites and water retention.
Br J Pharmacol, 146 (2005), pp. 654-661
[16.]
W. Jiménez, C.S. Gal, J. Ros, C. Cano, P. Cejudo, M. Morales-Ruiz, et al.
Long-term aquaretic efficacy of a selective nonpeptide V(2)-vasopressin receptor antagonist, SR121463, in cirrhotic rats.
J Pharmacol Exp Ther, 295 (2000), pp. 83-90
[17.]
G.C. Serradeil-Le, J. Wagnon, C. García, C. Lacour, P. Guiraudou, B. Christophe, et al.
Biochemical and pharmacological properties of SR 49059, a new, potent, nonpeptide antagonist of rat and human vasopressin V1a receptors.
J Clin Invest, 92 (1993), pp. 224-231
[18.]
P. Ginès, G. Fernández-Esparrach, V. Arroyo.
Ascites and renal functional abnormalities in cirrhosis. Pathogenesis and treatment.
Baillieres Clinical Gastroenterology, 11 (1997), pp. 365-385
[19.]
R.M. Pérez-Ayuso, V. Arroyo, J. Camps, A. Rimola, J. Gaya, J. Costa, et al.
Evidence that renal prostaglandins are involved in renal water metabolism in cirrhosis.
Kidney International, 26 (1984), pp. 72-80
[20.]
J. Orloff, J.S. Handler, S. Bergstrom.
Effect of prostaglandin (Pge-1) on the permeability response of toad bladder to vasopressin, theophylline and adenosine 39’,59’-monophosphate.
Nature, 205 (1965), pp. 397-398
[21.]
H.J. Adrogue, N.E. Madias.
Hyponatremia.
N Engl J Med, 342 (2000), pp. 1581-1589
[22.]
P. Ginès, M. Guevara.
Hyponatremia in cirrhosis: pathogenesis, clinical significance, and management.
Hepatology, 48 (2008), pp. 1002-1010
[23.]
D. Haussinger, A.T. Blei.
Hepatic encephalopathy.
Text Book of Hepatology. From basic science to clinical practise, pp. 728-760
[24.]
D. Haussinger.
Low grade cerebral edema and the pathogenesis of hepatic encephalopathy in cirrhosis.
Hepatology, 43 (2006), pp. 1187-1190
[25.]
G. Kircheis, M. Cohnen, F. Miese, H.J. Wittsack, F. Wenserski, J. Hemker, et al.
Low-grade cerebral edema in hepatic encephalopathy (HE): correlation of magnetization transfer ratio (MTR), apparent diffusion coefficient (ADC), and critical flicker frequency (CFF) in patients with alcoholic and non-alcoholic induced cirrhosis.
J Hepatol, 40 (2004), pp. 61
[26.]
M.E. Baccaro, M. Guevara, A. Torre, E. Arcos, M. Martín-Llahí, C. Terra, et al.
Hyponatremia predisposes to hepatic encephalopathy in patients with cirrosis. Results of a prospectiive study with time-dependent analysis abstract.
Hepatology, 44 (2006), pp. 233A
[27.]
O. Riggio, S. Angeloni, F.M. Salvatori, S.A. De, F. Cerini, A. Farcomeni, et al.
Incidence, natural history, and risk factors of hepatic encephalopathy after transjugular intrahepatic portosystemic shunt with polytetrafluoroethylene-covered stent grafts.
Am J Gastroenterol, 103 (2008), pp. 2738-2746
[28.]
M. Guevara, M.E. Baccaro, A. Torre, B. Gómez-Ansón, J. Ríos, F. Torres, et al.
Hyponatremia is a risk factor of hepatic encephalopathy in patients with cirrhosis: a prospective study with time-dependent analysis.
Am J Gastroenterol, 104 (2009), pp. 1382-1389
[29.]
M.C. Londoño, A. Cardenas, M. Guevara, L. Quinto, H.D. De Las, M. Navasa, et al.
MELD score and serum sodium in the prediction of survival of patients with cirrhosis awaiting liver transplantation.
Gut, 56 (2007), pp. 1283-1290
[30.]
S.W. Biggins, H.J. Rodríguez, P. Bacchetti, N.M. Bass, J.P. Roberts, N.A. Terrault.
Serum sodium predicts mortality in patients listed for liver transplantation.
Hepatology, 41 (2005), pp. 32-39
[31.]
D.M. Heuman, S.G. Bou-Assi, A. Habib, L.M. Williams, R.T. Stravitz, A.J. Sanyal, et al.
Persistent ascites and low serum sodium identify patients with cirrhosis and low MELD scores who are at high risk for early death.
Hepatology, 40 (2004), pp. 802-810
[32.]
A.E. Ruf, W.K. Kremers, L.L. Chavez, V.I. Descalzi, L.G. Podesta, F.G. Villamil.
Addition of serum sodium into the MELD score predicts waiting list mortality better than MELD alone.
Liver Transpl, 11 (2005), pp. 336-343
[33.]
W.R. Kim, S.W. Biggins, W.K. Kremers, R.H. Wiesner, P.S. Kamath, J.T. Benson, et al.
Hyponatremia and mortality among patients on the liver-transplant waiting list.
N Engl J Med, 359 (2008), pp. 1018-1026
[34.]
M.C. Londoño, M. Guevara, A. Rimola, M. Navasa, P. Taura, A. Mas, et al.
Hyponatremia impairs early posttransplantation outcome in patients with cirrhosis undergoing liver transplantation.
Gastroenterology, 130 (2006), pp. 1135-1143
[35.]
B.S. Kim, S.G. Lee, S. Hwang, K.M. Park, K.H. Kim, C.S. Ahn, et al.
Neuro logic complications in adult living donor liver transplant recipients.
Clin Transplant, 21 (2007), pp. 544-547
[36.]
F.H. Saner, S. Koeppen, M. Meyer, M. Kohnle, S. Herget-Rosenthal, G.C. Sotiropoulos, et al.
Treatment of central pontine myelinolysis with plasmapheresis and immunoglobulins in liver transplant patient.
Transpl Int, 21 (2008), pp. 390-391
[37.]
R.W. Schrier, P. Gross, M. Gheorghiade, T. Berl, J.G. Verbalis, F.S. Czerwiec, et al.
Tolvaptan, a selective oral vasopressin V2-receptor antagonist, for hyponatremia.
N Engl J Med, 355 (2006), pp. 2099-2112
[38.]
A.L. Gerbes, V. Gulberg, P. Gines, G. Decaux, P. Gross, H. Gandjini, et al.
Therapy of hyponatremia in cirrhosis with a vasopressin receptor antagonist: a randomized double-blind multicenter trial.
Gastroenterology, 124 (2003), pp. 933-939
[39.]
P. Ginès, F. Wong, H. Watson, S. Milutinovic, L.R. Del Árbol, D. Olteanu.
Effects of satavaptan, a selective vasopressin V(2) receptor antagonist, on ascites and serum sodium in cirrhosis with hyponatremia: a randomized trial.
Hepatology, 48 (2008), pp. 204-213
[40.]
F. Wong, A.T. Blei, L.M. Blendis, P.J. Thuluvath.
A vasopressin receptor antagonist (VPA-985) improves serum sodium concentration in patients with hyponatremia: a multicenter, randomized, placebo-controlled trial.
Hepatology, 37 (2003), pp. 182-191
[41.]
F. Wong, M. Bernardi, Y. Horsmans, Z. Cabrijan, H. Watson, P. Ginès.
Effects of satavaptan, a selective V2 receptor antagonist, on management of ascites and morbidity in liver cirrhosis in a long-term placebo controlled study. [abstract].
Hepatology, (2009), pp. 102S
[42.]
T.D. Boyer.
Tolvaptan and hyponatremia in a patient with cirrhosis.
Hepatology, 51 (2010), pp. 699-702
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