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Abstract: SA-PO677

A Heavy Heart and Grieving Kidneys: C3 Glomerulonephritis Complicated With Cardiac Tamponade

Session Information

Category: Glomerular Diseases

  • 1302 Glomerular Diseases: Immunology and Inflammation


  • Pedreira, Wilfredo M., VA Caribbean Healthcare System, San Juan, Puerto Rico
  • De Jesus Ramos, Charlynne, VA Caribbean Healthcare System, San Juan, Puerto Rico
  • Bosques, Jaymilitte, VA Caribbean Healthcare System, San Juan, Puerto Rico
  • Cortes, Carlos, VA Caribbean Healthcare System, San Juan, Puerto Rico
  • Robles-Franceschini, Mario J., VA Caribbean Healthcare System, San Juan, Puerto Rico

C3 glomerulopathies are rare complemented-mediated kidney diseases classified as Dense Deposit Disease or C3 Glomerulonephritis (GN) based on structural manifestations on electron microscopy (EM), both which result after complement cascade dysregulation. Most common clinical presentations are proteinuria, hematuria, altered kidney function & hypertension. We herein present a case of C3GN with nephrotic syndrome (NS) & a rare complication.

Case Description

66 y/o man recently hospitalized due to uncontrolled hypertension, new-onset NS, atrial fibrillation, & pneumonia developed involuntary movements, hypoxemia & hypotension days after discharge. Kidney biopsy results were pending & had been started on apixaban at discharge. POCUS: large pericardial effusion with right ventricular collapse during diastole. He was intubated & pericardiocentesis performed. Pericardial fluid: blood & inflammatory cells, other laboratories negative. Serum Cr: 2.58mg/dL BUN: 59.0mg/dL Alb:2.5g/dL Urine Prot/Cr: 6.37g. Kidney biopsy’s light microscopy: diffuse mesangial & endocapillary cell proliferative GN with crescents. Immunofluorescence: IgM & kappa light chains: trace, C1q: +1, C3: +2, others: negative. EM: Small sub-endothelial deposits, no sub-epithelial nor mesangial deposits, & foot process effacement. Labs: decreased C3 & C4, increased ESR & CRP, rheumatologic, hematologic (including monoclonal gammopathy) & infectious (except IgG mycoplasma) workup negative. Patient met criteria for C3GN. Patient improved & was later discharged, currently on immunosuppressive therapy.


Few reports of cardiac tamponade secondary to GN are present in the literature & to our knowledge, none related to C3GN. Although no mechanism has been explained in these patients, one could elucidate that circulatory congestion from NS could lead to formation of a pericardial effusion. Although recently started on apixaban, there is no evidence of increased risk of cardiac tamponade in anticoagulated patients compared with non-anticoagulated. Timely recognition of this unusual & lethal complication of Nephrotic Syndrome may prevent deaths.