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Abstract: TH-PO658

Combined Diagnosis of Proliferative Lupus Nephritis and Tuberculosis Infection: A Treatment Dilemma

Session Information

Category: Glomerular Diseases

  • 1402 Glomerular Diseases: Clinical, Outcomes, and Trials


  • Atemnkeng, Francis Njukeng, Westchester Medical Center, Valhalla, New York, United States
  • Kirk, Michelle Lee, Westchester Medical Center, Valhalla, New York, United States
  • Pullman, James M., Montefiore Medical Center, New York, New York, United States
  • Klein, Michael D., Westchester Medical Center, Valhalla, New York, United States
  • Chugh, Savneek S., Westchester Medical Center, Valhalla, New York, United States
  • Gupta, Sanjeev, Westchester Medical Center, Valhalla, New York, United States

The treatment of tuberculosis (TB) infection (previously termed latent TB) during the induction phase of treatment for proliferative lupus nephritis (LN) is challenging. The use of high dose immunosuppression (IS) can cause TB disease. Rifamycin-based treatment for TB infection can also lead to major drug-drug interaction as rifampin can reduce the serum levels of mycophenolate mofetil (MMF), hence the level of IS.

Case Description

A 38-years-old Mexican male who presented with lower limb edema. Initial labs showed leukocytosis and acute kidney injury with nephrotic syndrome. Blood cultures grew Streptococcus pyogenes. Workup for glomerulonephritis (GN) revealed a positive ANA and hypocomplementemia, consistent with immune complex mediated GN. He received antibiotics for a total of 14 days. The urine protein/creatinine ratio (UPCr) one week later increased to 36.9 g/g from 3.2 g/g. Kidney biopsy demonstrated class III+V LN with 5/22 globally sclerosed glomeruli, 4 with segmental endocapillary hypercellularity with 2 cellular crescents on light microscopy and full house staining on immunofluorescence. Electron microscopy demonstrated mesangial, intramembranous, and sup-epithelial electron dense deposits and extensively effaced foot processes. The patient was discharged on conservative anti proteinuric therapy, as well as MMF. Routine TB screening with Quantiferon was positive, so he was started on rifampin and isoniazid. Follow-up 1 month later demonstrated UPCr of 1.76 g/g with no signs of TB disease.


The term latent TB was changed to TB infection because these patients are infected with viable mycobacteria in various stages of containment by the host immune system. Therefore, during the induction phase of treatment of LN, with use of high dose IS, the presence of TB infection presents a high risk of progression to TB disease. We found no case reports of simultaneous diagnosis of proliferative LN and TB infection. Treatment literature is obtained from transplant patients diagnosed with TB infection, where rifampin was found to lower the level of MMF. Therefore, we suggest close follow-up of these patients to rule out TB disease and non-response to LN treatment during each visit.