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J Investig Med. 1999 May;47(5):183-202.

Pathogenesis of ascites and renal salt retention in cirrhosis.

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Department of Medicine, University of Texas Southwestern Medical School, Dallas 75235, USA.


The sequence in which the various therapies discussed above are instituted can be viewed as a continuum that parallels the severity of the underlying cirrhotic state (Figure 6). In the earliest stages of the disease urinary sodium excretion is plentiful and negative salt balance can be achieved by simply lowering dietary sodium intake. As the disease advances neurohumoral effectors become more activated initially resulting in more intense renal salt retention and later in a progressive decline in renal function. Eventually, the filtered load of sodium becomes completely reabsorbed by the tubule and the final urine becomes virtually devoid of salt. If some component of the filtered load reaches the collecting duct or beyond, spironolactone will be effective in increasing urinary sodium excretion. Once sodium reabsorption is complete, proximal to the collecting duct, then thiazides and later loop diuretics will have to be added to spironolactone to increase urinary sodium excretion. Eventually, the filtered load is completely reabsorbed proximal to the thick ascending limb of Henle. At this point the patient is resistant to the effects of diuretics and requires more invasive procedures such as repetitive large volume paracentesis to remain in salt balance. In the terminal stages of the disease the glomerular filtration rate falls to such a degree that oliguria, azotemia, and eventually uremia are present and the patient is clinically diagnosed with hepatorenal syndrome. Vasoconstrictive input focused on the kidney is severe and irreversible. Renal failure is functional in nature; however, restoration of near normal renal function can be obtained following a liver transplant.

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