Chylopericardial tamponade secondary to superior vena cava thrombosis in a child with nephrotic syndrome

Suri, Deepti; Gupta, Neeraj; Morigeri, Chandrashekara; Saxena, Akshay Kumar; Manoj, Rohit

doi:10.1007/s00467-008-1115-4

Cited by 8 publications

(2 citation statements)

References 13 publications

(13 reference statements)

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“…The main reason is probably multifactorial, including the associated hyperlipidemia (12), hypertension, tendency to thrombosis (13,14), and use of immunosuppressive medications. SRNS is also associated with increased endothelial markers, such as soluble thrombomodulin, plasminogen activator inhibitor-1, tissue plasminogen activator, and von-Willebrand factor (15), all of which are related to endothelial activation.…”

Section: Discussionmentioning

confidence: 99%

Endothelial Dysfunction in Children with Steroid-Resistant Nephrotic Syndrome

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Endothelial Dysfunction in Children with Steroid-Resistant Nephrotic Syndrome

et al. 2017

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“…Pericardial effusion can occur in idiopathic nephrotic syndrome and systemic lupus erythematosus (SLE) [ 15 , 8 ]. Pericardial tamponade is an extremely rare but serious complication of nephrotic syndrome with only a few documented cases in the literature [ 8 , 10 , 16 , 17 ]. Table 2 summarizes some cases reported for nephrotic syndrome patients with pericardial tamponade.…”

Section: Discussionmentioning

confidence: 99%

Cardiac Tamponade-Associated Dense Deposit Disease: A Case Report and Review of the Literature

Zabali¹,

Rubaihan²,

Alnetaifat³

et al. 2022

Cureus

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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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