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Cardiac Tamponade-Associated Dense Deposit Disease: A Case Report and Review of the Literature
Saeed M Al Zabali1, Aljawharah K Rubaihan2, Madawi F Alnetaifat3
1Pediatric Nephrology, King Fahad Medical City, Riyadh, SAU.
Insights
Dense deposit disease (DDD), a rare kidney condition, can cause significant pericardial effusion, leading to cardiac tamponade risk. Early cardiac assessment is crucial for patients with DDD, especially those with nephrotic syndrome.
Area of Science:
- Nephrology
- Cardiology
- Complement System Biology
Background:
- Dense deposit disease (DDD) is a rare kidney disorder characterized by uncontrolled activation of the alternative complement pathway.
- Pericardial effusion, fluid accumulation in the pericardial cavity, can stem from diverse cardiac and non-cardiac conditions.
Observation:
- A seven-year-old male with biopsy-proven DDD presented with respiratory symptoms (shortness of breath, cough, fever) and cardiomegaly on chest X-ray.
- Echocardiography revealed massive pericardial effusion, left ventricle compression, and a risk of cardiac tamponade.
Findings:
- Pericardiocentesis successfully removed 450 ml of pericardial fluid.
- This case represents the first reported instance of significant pericardial effusion with cardiac tamponade risk linked to Dense Deposit Disease.
Implications:
- Highlights the critical need for cardiac evaluation in Dense Deposit Disease patients, particularly those with nephrotic-range proteinuria and cardiac symptoms.
- Underscores the potential for severe cardiac complications in rare kidney diseases due to complement pathway dysregulation.
Abstract:
Pericardial effusion is an abnormal accumulation of fluid in the pericardial cavity. It can be associated with various cardiac and non-cardiac disorders. Dense deposit disease (DDD) is a rare kidney disease caused by uncontrolled activation of the alternative complement pathway. We are reporting a seven-year-old male child who was diagnosed to have DDD approved by renal biopsy and presented with shortness of breath, cough, and fever. Chest X-ray displayed cardiomegaly. Thereafter, echocardiography showed massive pericardial effusion and left ventricle compression with a risk for cardiac tamponade. He subsequently underwent pericardiocentesis with the removal of 450 ml of pericardial fluid. The patient's edema was not correlated with the described amount of drained pericardial fluid. To the best of our knowledge, this is the first reported case of significant pericardial effusion carrying the risk of cardiac tamponade associated with DDD. With this report, we would like to highlight the importance of cardiac assessment in patients with DDD, in particular those with nephrotic range proteinuria who present with cardiac symptoms and cardiomegaly.
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