ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on Twitter

Kidney Week

Abstract: TH-PO524

Membranoproliferative Glomerulonephritis Associated With Tuberculosis, "the Great Imitator": Case Report

Session Information

Category: Glomerular Diseases

  • 1303 Glomerular Diseases: Clinical‚ Outcomes‚ and Trials


  • Moreno, Rodolfo Alejandro, Centro Medico Militar, Guatemala, Guatemala, Guatemala
  • Navarro Blackaller, Guillermo, Hospital Civil de Guadalajara Unidad Hospitalaria Fray Antonio Alcalde, Guadalajara, Jalisco, Mexico
  • Natareno, Angel D., Centro Medico Militar, Guatemala, Guatemala, Guatemala
  • De león, Werner, SERPAT, Guatemala, Guatemala, Guatemala
  • Sierra, Mario, Centro Medico Militar, Guatemala, Guatemala, Guatemala
  • Chavez, Jonathan, Hospital Civil de Guadalajara Unidad Hospitalaria Fray Antonio Alcalde, Guadalajara, Jalisco, Mexico

Tuberculosis (TB) is a multisystemic disease of pulmonary predominance caused by Mycobacterium tuberculosis; the kidney can be affected in different ways but as Membranoproliferative glomerulonephritis (MPGN) its an unusual presentation.

Case Description

A 19-year-old Guatemalan male patient with a 3-day history of malaise and fever. No previous medical history. On evaluation at the ER presented with hypertension and AKI with progressive elevation of SCr (admission 2.54mg/dl, max 6.45mg/dl) associated with proteinuria and hematuria. Laboratories: hypoalbuminemia (2.5g/dl), proteinuria 12g/day, hypocomplementemia (C3 0.04, C4 normal) ANAs, ANCAs HIV, HBV, HCV, urine culture negative, Kinyoun stain in urine with BAAR (+). Renal biopsy was performed, that reported MPGN with 50% of globally sclerosed glomeruli, 3 cellular crescents, mesangial proliferation, endocapillary hypercellularity, basement membranes with formation of double contours and "wire loops". IF: IgM (+++), C4d (+++) with diffuse granular pattern in glomerular basement membranes and subendothelium, tubulointerstitium with lymphocytic infiltrates. The patient received methylprednisolone pulses for 3 doses, oral prednisone (1mg/kg/day) and tapered until suspended and 4-drug anti-TB regimen with improvement in SCr to 3.9m/dl and normalization of complement C3 at 10 days.


The pathogenesis of TB-associated MPGN is unknown. Histopathologically it can mimic different types of glomerulopathies (IgAN, collapsing, mesangiocapillary, membranous, crescentic GN, membranoproliferative and PIGN). Antibodies against M. tuberculosis activate the complement pathway generating the formation of antigen-antibody complexes that generate MPGN. The specific treatment is not yet known due to the rarity of the presentation, but antifimics and steroids are suggested in case of crescents.