Hepatorenal syndrome pathophysiology
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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]; Sunny Kumar MD [3]
Overview
The major pathophysiologic mechanism responsible for the clinical manifestation of hepatorenal syndrome is renal vasoconstriction. The hemodynamic disturbances include increased cardiac output, systemic vasodilatation and low arterial blood pressure. Thus, renal vasoconstriction occurs even with a normal blood volume and increased cardiac output.
Pathophysiology
The pathology involved in the development of hepatorenal syndrome is thought to be an alteration in blood flow and blood vessel tone in the circulation that supplies the intestines (the splanchnic circulation) and the circulation that supplies the kidney.[1] It is usually indicative of an end-stage of perfusion, or blood flow to the kidney, due to deteriorating liver function. Patients with hepatorenal syndrome are very ill, and, if untreated, the condition is usually fatal.
- The characteristic fall in systemic vascular resistance and increase in renal vasoconstriction also occurs in other conditions like sepsis and anaphylaxis.
- Doppler studies have proved that the reduced blood pressure in the splanchnic circulation is primarily responsible for the drop in systemic vascular resistance.
- The renal failure in hepatorenal syndrome is believed to arise from abnormalities in blood vessel tone in the splanchnic circulation (which supplies the intestines).[2]
- It is known that there is an overall decreased systemic vascular resistance in hepatorenal syndrome, but that the measured femoral and renal fractions of cardiac output are respectively increased and reduced, suggesting that splanchnic vasodilation is implicated in the renal failure.[3]
- There is activation of the renin-angiotensin-aldosterone system (RAAS) and the sympathetic nervous system, and profound vasoconstriction of the kidneys.[4]
- Many vasocontrictor chemicals have been hypothesized as being involved in this pathway, including vasopressin,[5] prostacyclin, thromboxane A2,[6] and endotoxin.[1]
- The prostaglandins antagonize the effects of the vasoconstrictors and maintain the blood flow into the glomerulus.
- The dominant effect of vasoconstrictors over vasodilators is exaggerated in hepatorenal syndrome.
Splanchnic vasodilatation
The vasodilator NO is thought to be responsible for the fall in arterial resistance of the splanchnic circulation and under-filling of the capillary bed. This along with portal hypertension and pooling of a part of blood volume in the form of ascitic fluid results in activation of the renin - angiotensin system, aldosterone and vasopressin causing vasoconstriction of systemic vessels.
| Cirrhosis | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Portal hypertension | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| splanchnic/systemic vasodilation | increased cardiac output | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| deceased arterial blood effective volume | high output cardiac failure | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| activation of nurohormonal system RAAS/SNS/ADH | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Sodium and water retention | Renal vasoconstriction | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Ascities and low sodium | Decereased renal blood flow | ||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Hepatorenal syndrome | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Systemic Vasoconstriction
All systemic arteries including those of the kidneys, brain and muscles constrict under the influence of vasoconstrictors. However, the splanchnic vessels remain resistant to the effect of vasoconstrictors because of over production of NO.
In early stages of cirrhosis and ascites, renal vasodilators maintain the inflow of blood into the glomerulus. As the disease progresses and splanchnic arterial pressure falls further, the effect of vasoconstrictors predominate and cause sodium and water retention with dilutional hyponatremia.
References
- ↑ 1.0 1.1 Arroyo V, Guevara M, Gines P. Hepatorenal syndrome in cirrhosis: pathogenesis and treatment. Gastroenterology 2002 May;122(6):1658-76. PMID 12016430.
- ↑ Gines P, Arroyo V. Hepatorenal syndrome. J Am Soc Nephrol 1999 Aug;10(8):1833-9. PMID 10446954
- ↑ Fernandez-Seara J, Prieto J, Quiroga J, Zozaya JM, Cobos MA, Rodriguez-Eire JL, Garcia-Plaza A, Leal J. Systemic and regional hemodynamics in patients with liver cirrhosis and ascites with and without functional renal failure. Gastroenterology 1989 Nov;97(5):1304-12. PMID 2676683
- ↑ Gines A, Escorsell A, Gines P, et al. Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites. Gastroenterology 1993 Jul;105(1):229-36. PMID 8514039.
- ↑ Lenz K, Hortnagl H, Druml W, Reither H, Schmid R, Schneeweiss B, Laggner A, Grimm Gm Gerbes AL. Ornipressin in the treatment of functional renal failure in decompensated liver cirrhosis. Effects on renal hemodynamics and atrial natriuretic factor. Gastroenterology 1991 Oct;101(4):1060-7. PMID 1832407
- ↑ Moore K, Ward PS, Taylor GW, Williams R. Systemic and renal production of thromboxane A2 and prostacyclin in decompensated liver disease and hepatorenal syndrome. Gastroenterology 1991 Apr;100(4):1069-77. PMID 2001805