Hepatorenal syndrome pathophysiology: Difference between revisions

Jump to navigation Jump to search
(Created page with "__NOTOC__ {{Hepatorenal syndrome}} {{CMG}} ==Overview== ==Pathophysiology== The pathology involved in the development of hepatorenal syndrome is thought to be an alteration ...")
 
No edit summary
Line 15: Line 15:


[[Image:Hepatorenal_syndrome.jpg|thumb|300 px|center|Liver pathology is altered in HRS while kidney histology is normal. The image is a trichrome stain of cirrhosis of the liver, the most common cause of HRS.]]
[[Image:Hepatorenal_syndrome.jpg|thumb|300 px|center|Liver pathology is altered in HRS while kidney histology is normal. The image is a trichrome stain of cirrhosis of the liver, the most common cause of HRS.]]
==Differentiating Hepatorenal Syndrome from other Diseases==
Many other diseases of the kidney are associated with liver disease and must be excluded before making a diagnosis of hepatorenal syndrome.  They include the following:
*[[Renal failure|Pre-renal failure]]:  Pre-renal failure usually responds to treatment with intravenous fluids, resulting in reduction in serum [[creatinine]] and the excretion of sodium.<ref name=IAC/>
*[[Acute tubular necrosis]] (ATN): This can be difficult to confidently diagnose.  It may be an inability to concentrate the urine, if any is being produced. The urine sediment should be bland, microscopy may show [[hyaline cast]]s. ATN may recover with supportive treatment only or progress to [[end-stage renal failure]]. In cirrhosis, urinary sodium is not a reliable guide to the development of ATN, as [[fractional sodium excretion]] may stay below 1 percent, due to the gradual worsening of renal [[ischaemia]].
*Other causes may include [[glomerulonephritis|glomerular disease]] secondary to [[Hepatitis B]] or [[Hepatitis C]],<ref>Han SH.  Extrahepatic manifestations of chronic hepatitis B.  ''Clin Liver Dis.'' 2004 May;8(2):403-18.  PMID 15481347</ref> drug toxicity (notably [[gentamicin]]) or [[Radiocontrast|contrast nephropathy]].


==References==
==References==

Revision as of 13:24, 28 September 2012

Hepatorenal syndrome Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Causes

Differentiating Hepatorenal syndrome from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

Electrocardiogram

Chest X Ray

CT

MRI

Ultrasound

Other Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

Hepatorenal syndrome pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hepatorenal syndrome pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hepatorenal syndrome pathophysiology

CDC on Hepatorenal syndrome pathophysiology

Hepatorenal syndrome pathophysiology in the news

Blogs on Hepatorenal syndrome pathophysiology

Directions to Hospitals Treating Hepatorenal syndrome

Risk calculators and risk factors for Hepatorenal syndrome pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

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 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]

Microscopic Pathology

Liver pathology is altered in HRS while kidney histology is normal. The image is a trichrome stain of cirrhosis of the liver, the most common cause of HRS.

References

  1. 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.
  2. Gines P, Arroyo V. Hepatorenal syndrome. J Am Soc Nephrol 1999 Aug;10(8):1833-9. PMID 10446954
  3. 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
  4. 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.
  5. 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
  6. 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

Template:WH Template:WS