Hepatorenal syndrome natural history, complications and prognosis
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aarti Narayan, M.B.B.S [2]
Overview
Hepatorenal syndrome progresses from pre-ascitic stage to frank ascites. Multiorgan system failure, infections and chronic renal failure are the most common complication of HPS. Type I HPS carries poorer prognosis compared to type II HPS.
Natural History
Pre-ascites Phase
Systemic vasodilatation causes kidneys to retain sodium and water, thereby overcoming the compensatory renal vasoconstriction. This prevents the drop in glomerular filtration rate and subsequent vasoconstriction of renal arterioles.[1][2]
Ascitic Phase
As the systemic vasodilatation worsens further, the kidney's are unable to compensate and renal arterioles undergo vasoconstriction. As a result, there is sodium and water retention from the renal tubules resulting in ascites. This ascites is responsive to diuretics. Further increase in renal sodium retention causes the ascites to become resistant to treatment with diuretics.[3][4][5]
Once the ascites progresses to a point where it is unresponsive to diuretics, even repeated paracentesis does not prevent progression to hepatorenal syndrome type I or II.[6][7]
Complications
Hepatorenal syndrome complications include:
- Bleeding
- Multiorgan system failure
- End-stage kidney disease
- Fluid overload with congestive heart failure or pulmonary edema
- Hepatic coma
- Secondary infections
- Death
Prognosis
- Type I HRS carries a very poor prognosis, usually of less than 50% over one month. Patients with type I hepatorenal syndrome are usually ill, may have low blood pressures, and may require therapy with inotropes, or intravenous drugs to maintain blood pressure.[8]
- It is typically associated with ascites that is unresponsive to diuretic medications, and also carries a poor, if somewhat longer (median survival ~6 months) outlook,[9] unless the patient undergoes liver transplantation.
References
- ↑ Sersté T, Lebrec D, Valla D, Moreau R (2008). "Incidence and characteristics of type 2 hepatorenal syndrome in patients with cirrhosis and refractory ascites". Acta Gastroenterol Belg. 71 (1): 9–14. PMID 18396743.
- ↑ Mathurin S, Jaimet C, Turletti C, Arosio A, González G, Kuzmicz G (2008). "[Renal failure in patients with cirrhosis and ascites: incidence, etiology and predictive factors]". Acta Gastroenterol Latinoam. 38 (2): 116–25. PMID 18697406.
- ↑ Mathurin S, Jaimet C, Turletti C, Arosio A, González G, Kuzmicz G (2008). "[Renal failure in patients with cirrhosis and ascites: incidence, etiology and predictive factors]". Acta Gastroenterol Latinoam. 38 (2): 116–25. PMID 18697406.
- ↑ Fabrizi F, Aghemo A, Messa P (2013). "Hepatorenal syndrome and novel advances in its management". Kidney Blood Press Res. 37 (6): 588–601. doi:10.1159/000355739. PMID 24356549.
- ↑ de Mattos ÁZ, de Mattos AA, Méndez-Sánchez N (2016). "Hepatorenal syndrome: Current concepts related to diagnosis and management". Ann Hepatol. 15 (4): 474–81. PMID 27236146.
- ↑ Wong F, Leung W, Al Beshir M, Marquez M, Renner EL (2015). "Outcomes of patients with cirrhosis and hepatorenal syndrome type 1 treated with liver transplantation". Liver Transpl. 21 (3): 300–7. doi:10.1002/lt.24049. PMID 25422261.
- ↑ Heemann U, Füeßl HS, Renders L (2015). "[The hepatorenal syndrome]". Dtsch Med Wochenschr. 140 (20): 1520–3. doi:10.1055/s-0041-105807. PMID 26445256.
- ↑ Pandey CK, Karna ST, Singh A, Pandey VK, Tandon M, Saluja V (2014). "Hepatorenal syndrome: a decade later". J Assoc Physicians India. 62 (8): 696–702. PMID 25856938.
- ↑ Blendis L, Wong F. The natural history and management of hepatorenal disorders: from pre-ascites to hepatorenal syndrome. Clin Med 2003 Mar-Apr;3(2):154-9. PMID 12737373