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Abstract: FR-PO627

Lupus Nephritis Complicated by Multi-Organ Arterial Thrombosis

Session Information

Category: Glomerular Diseases

  • 1302 Glomerular Diseases: Immunology and Inflammation


  • Bazerbashi, Noor, Houston Methodist, Houston, Texas, United States
  • Gandhi, Nisarg, Houston Methodist, Houston, Texas, United States
  • Ewing, Elise, Houston Methodist, Houston, Texas, United States
  • Edwards, Angelina, Houston Methodist, Houston, Texas, United States

Thrombosis is a known complication of Nephrotic Syndrome (NS) and results in significant morbidity and mortality. While thrombotic events (TE) in Lupus Nephritis (LN) are often related to antiphospholipid syndrome, an imbalance between thrombotic and antithrombotic factors in those with nephrotic-range proteinuria (NRP) leads to NS-related hypercoagulability. Here, we report an unexpected case of multi-organ arterial thrombosis in a patient (pt) with LN.

Case Description

A 23-year-old woman with active systemic lupus erythematosus underwent kidney biopsy for evaluation of 7.7 g proteinuria on 24-hour urine collection. While serum creatinine was stable at 0.73 mg/dL, her serum albumin was low at 2.7 g/dL, and autoimmune markers including anti-nuclear antibody, anti-dsDNA antibody, ribonucleoprotein, and anti-smith antibody were reactive. Outpatient kidney biopsy showed Class IV and V LN, with global diffuse proliferative and membranous lesions with crescentic formation.
Before initiation of therapy, she presented with sudden onset of diffuse abdominal pain, headache, and positional chest discomfort. CT abdomen pelvis with contrast showed multifocal splenic and renal infarcts, and CT head showed lacunar infarcts. Evaluation of chest pain showed no valvular lesions on transthoracic echocardiogram, but further assessment with transesophageal echocardiogram showed a large thrombus in the descending aorta, confirming the embolic source. A comprehensive hypercoagulable workup was collectively unrevealing. The hypercoagulable state was thought to be secondary to underlying inflammatory disease and likely acquired protein C/S deficiency in the setting of NRP. Anticoagulation therapy was initiated, and aggressive management of LN was pursued. Follow-up imaging showed resolution of the thrombus, and the pt continues to show reduction in proteinuria and improvement in serum albumin.


Venous TE is well-described in NS, but arterial TE is rare and more reported in membranous glomerulonephritis. The cumulative effect of imbalance of antithrombin III, protein C/S, fibrinolytic activity, fibrinogen, and von Willebrand factor increases thrombotic risk. Initiation of thrombotic prophylaxis with appropriate risk stratification guided by pt’s serum albumin level is recommended to prevent these detrimental complications.