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Updated: May 6, 2026

Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock
Published on: June 6, 2011
Diffuse hepatic calcification as a sequela to shock liver
Insights
A patient on chronic hemodialysis developed liver calcification following a shock state. This hepatic calcification may be linked to ischemic liver injury or uremia-related calcium-phosphorus imbalances.
Area of Science:
- Nephrology
- Hepatology
- Pathology
Background:
- Chronic hemodialysis is a life-sustaining treatment for end-stage renal disease.
- Patients undergoing hemodialysis are at risk for various complications, including cardiovascular and metabolic disturbances.
- Hepatic complications in uremic patients, though less common, can significantly impact morbidity and mortality.
Observation:
- A 31-year-old woman on chronic hemodialysis developed intractable congestive heart failure.
- She experienced a shock state due to ventricular tachycardia and gastrointestinal bleeding, leading to elevated transaminases.
- Abdominal radiography revealed diffuse hepatic calcification four months after the shock episode.
Findings:
- Autopsy showed liver parenchymal necrosis and diffuse calcification.
- Microscopic examination identified calcifications in the central to midzonal areas of hepatic lobules.
- The hepatic calcification was associated with ischemic liver injury following a prolonged shock state.
Implications:
- Hepatic calcification may be a consequence of severe ischemic liver injury in patients with chronic kidney disease.
- Disturbances in intracellular calcium homeostasis or elevated calcium-phosphorus product in uremia could contribute to calcification.
- This case highlights a rare but significant hepatic complication in the context of chronic hemodialysis and shock.
Abstract:
A 31-yr-old Japanese woman who was on chronic hemodialysis for 3 yr died of intractable congestive heart failure. Three years before death, the patient was in a state of shock for 48 h due to ventricular tachycardia and gastrointestinal bleeding, which was followed by marked elevation of serum transaminase. Four months later, abdominal plain radiography demonstrated diffuse hepatic calcification. At autopsy, microscopic examination of the liver revealed parenchymal necrosis and tiny calcifications in the central to midzonal area of the lobule. Calcification in the degenerative area of the hepatic lobule occurred subsequent to parenchymal ischemia after overt shock that lasted for 2 days. Although a definitive explanation for the calcification was not obtained, it may be related to the disturbances of intracellular Ca2+ homeostasis as a result of ischemic liver injury or it may be related to an elevated calcium-phosphorus product in the uremic state.
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