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Renal and hepatic functions are interrelated. Acute and chronic advanced liver disease is often complicated by renal dysfunction that typically worsens with prolonged time on the waiting list for liver transplantation.


Renal failure is common in patients with acute liver failure (ALF). The etiology of this process relates to circulatory disturbances similar to those causing hepatorenal syndrome (HRS) in cirrhosis (reduced systemic vascular resistance with high cardiac output and renal vasoconstriction). On the other hand, the lack of significant portal hypertension in most patients with ALF and a prominent systemic inflammatory response syndrome make this process more similar to renal failure secondary to sepsis than to HRS associated with cirrhosis.

Other factors contributing to renal failure in ALF include hypovolemia, administration of nephrotoxic drugs, infection, and disseminated intravascular coagulation (Figs. 102-1 and 102-2).

FIGURE 102-1

Normal renal cortex. Most of the cortical tissue is composed of proximal convoluted tubules with abundant pink (eosinophilic) tall cytoplasm; the lumina of the proximal tubules are inconspicuous (virtual). The remaining structures represent distal convoluted tubules lined by cuboidal epithelium with more basophilic cytoplasm and glomeruli.

FIGURE 102-2

Acute tubular necrosis in a patient with cirrhosis and hepatorenal syndrome. The kidney injury resulted from severe hypovolemia due to bleeding of esophageal varices. This complication also resulted in the patient's death. The renal tubular epithelium shows flattening (simplification) with luminal dilatation, marked cytoplasmic vacuolization, and cellular dropout loss. Note the loss of nuclear profiles. Incipient protein cast formation is marked by an asterisk.

In patients with ALF due to acetaminophen toxicity, the renal failure is often associated with concurrent direct nephrotoxicity leading to acute tubular necrosis (Fig. 102-3).

FIGURE 102-3

Acute tubular injury in a patient who developed acute renal failure 3 days after ingesting a toxic dose of acetaminophen. The epithelium lining the renal tubules appears flattened, and the nuclei are irregularly distributed due to the loss of scattered renal tubular cells, leaving a denuded tubular basement membrane. Liver toxicity was seen concurrently, consisting of hepatocyte necrosis around the central veins.


Hepatorenal Syndrome

HRS, which is potentially reversible, is caused by portal hypertension leading to systemic and splanchnic arterial vasodilatation with hyperdynamic circulation and secondary renal vasoconstriction. HRS is characterized by the absence of significant structural changes in the renal parenchyma despite severe renal dysfunction and markedly decreased glomerular filtration rate (GFR). The diagnosis of HRS is based on well-defined criteria and requires exclusion of other causes of renal failure such as ...

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