Membranous Glomerulonephritis, Antiphospholipid Syndrome, and Persistent Low C3 Levels Associated with Meningococcal Disease

Abstract

A young male patient with a recent history of meningococcemia was referred to our hospital in his recovery period. He had signs suggesting deep venous thrombosis in the legs but no other abnormalities on physical examination at admission. Laboratory results showed proteinuria (3.1 g/day), prolonged activated partial thromboplastin time (56.3 s), low level of C3c (0.19 g/l), high titers of both IgM (27.04 MPLU/ml) and IgG (74.88 GPLU/ml) anticardiolipin antibodies and recanalized thrombotic changes in the deep veins of the lower extremities on venography. Histopathological diagnosis of the kidney disease was membranous glomerulonephritis. He was started on an angiotensin-converting enzyme inhibitor to reduce proteinuria and an oral anticoagulant to prevent thromboembolic events. Since no reduction in proteinuria was observed at the 10th month of therapy, the angiotensin-converting enzyme inhibitor was discontinued. On his last follow-up, approximately 1.5 years after meningococcemia, he had no complaints and no abnormal findings on physical examination. While both IgM and IgG anticardiolipin antibody titers returned to the normal range, he still had persistent proteinuria and hypocomplementemia.

The environment and antiphospholipid syndrome

“…Infections with Treponema pallidum, 18 leishmaniasis 18 , Leptospiara interrogans, 18 Neisseria, 19 Plasmodium species, 20 Streptococcus Pyogenes, 21 Helicobacter pylori, 22 Mycoplasma pneumoniae 23 and other microorganisms are associated with an increased prevalence of aPL.…”