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Logo of nihpaAbout Author manuscriptsSubmit a manuscriptHHS Public Access; Author Manuscript; Accepted for publication in peer reviewed journal;
Surg Forum. Author manuscript; available in PMC 2010 November 4.
Published in final edited form as:
Surg Forum. 1973; 24: 348–350.
PMCID: PMC2972734


Inasmuch as the kidney failure of the hepatorenal syndrome (1) is believed to be secondary to hepatic dysfunction, replacement of the diseased liver should improve renal function. This objective was realized in three patients with the hcpatorcnal syndrome treated by orthotopic liver transplantation.


The patients, who were 34, 42, and 44 yr old, suffered from cirrhosis. They had massive ascites and edema and two of them were in stage III or IV coma. All had had normal renal function documented within a few weeks of transplantation, but progressive renal failure had then supervened with azotemia and oliguria. Two patients had a preoperative urine sodium concentration of less than 1 mEq/liter, while in case 3 it was 40 mEq/liter. The degree of combined renal and hepatic failure can be seen in Table 1.

Table 1
Renal and Hepatic Function in Three Patients With Hepatorenal Syndrome and Orthotopic Liver Transplantation


Hepatic function in all three patients steadily improved after liver replacement (Table 1), but the course of recovery of kidney function varied. In cases 1 and 3 the characteristic urine findings, including oliguria, high specific gravity, and low sodium content persisted for several days. However, in case 2 a massive diuresis and natriuresis were immediately established. Within ten days all three patients had regained adequate although subnormal renal function (Table 1).

Subsequently, one patient (case 2), who died of extensive bronchopneumonia on the 42nd day, had mild terminal deterioration of hepatic and renal function. Another (case 3) died on the 124th day from severe hepatic failure, caused by rejection, ten days after a second liver transplantation; mild renal dysfunction developed terminally. At autopsy, these two patients had essentially normal kidneys. The third patient (case 1) is alive after nine months but with abnormal liver function, probably due to chronic rejection; renal function remains normal.

Berkowitz et al (2) have suggested that in hepatic failure, renin substrate, synthesized by the liver, is deficient, thereby causing renal blood flow aberrations with secondary kidney failure. This hypothesis was tested in case 3. Before transplantation the plasma renin activity was high, 11.9 ng angiotensin I/ml/hr (normal 0.2-3.6), and renin substrate was low, 110.7 ng angiotensin I/ml (normal > 800). Both became normal (renin 1.5 and substrate 808.2) soon after operation. However, renal improvement was delayed for several more days after these corrections.


The hepatorenal syndrome is completely reversible by liver transplantation, but the recovery of renal function may be slow. Improvement of liver function probably corrects an abnormality of renal blood flow, but the precise mechanism remains unknown.


Supported by the Veterans Administration, National Institutes of Health grants AI-AM-08898 and AM-07772, and Division of Research Resources grants RR-00051 and RR-00069.


1. Hecker R, Sherlock S. Electrolyte and circulatory changes in terminal liver failure. Lancet. 1956;2:1121–1125. [PubMed]
2. Berkowitz HD, Galvin C, Miller LD. Significance of altered renin substrate in the hepatorenal syndrome. Surg Forum. 1972;23:342–343. [PubMed]