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Glomerular presentations are rare in tubercular infections with the most common being IgA nephropathy, membranous nephropathy, amyloidosis, and membranoproliferative disease. Infection related glomerulonephritis is a rare presentation in patients diagnosed with tuberculosis. We hereby report an extremely rare case of pediatric pulmonary tuberculosis who presented with dialysis requiring rapidly progressive renal failure and was subsequently reversed using corticosteroids.
A 14 year old male presented with a history of fever, cough and weight loss for 4 weeks. Two weeks later he developed progressively decreased urine output and generalized body swelling. On evaluation he was found to have
· High blood pressure -170/100
· Advanced azotemia (serum urea/creatinine 256/7.1 mg/dl)
· Nephrotic syndrome -spot urine protein/creatinine ratio – 4.5 gm/gm , serum albumin- 2.1 gm/dl and deranged lipid profile.
· Active sediments with red blood cells and RBC casts in urine routine analysis.
· Low C3 levels and normal C4 value.
· Anti Nuclear Antibody (ANA), Extractable Nuclear Antigen (ENA) Anti Myeloperoxidase (MPO), Anti Proteinase- 3 (PR-3) and Anti Glomerular Basement Membrane (GBM) were negative.
· High Resolution CT of chest was done in view of chronic fever and cough which showed cavitating lesions in bilateral upper zone and sputum for Acid Fast Bacilli was strongly positive. Ultrasound of whole abdomen was normal.
In view of increased azotemia he received three sessions of hemodialysis and then underwent an uncomplicated renal biopsy. He was then started on pulse iv steroid (methylprednisolone 500 mg iv once daily for 3 days) followed by oral wysolone 1 mg/kg/day. He was also started on weight based renal modified anti-tubercular therapy – isoniazid, rifampicin, pyrazinamide and ethambutol. Renal biopsy showed diffuse proliferative glomerulonephritis without any crescents and a full house picture on immunofluorescence. He received 2 more hemodialysis sessions following which his urine output started to increase and no further sessions of hemodialysis were required. He was discharged with creatinine of 1.5 mg/dl. On follow up his creatinine became normal and steroid was tapered over the next 6 weeks. His antitubercular drugs were continued throughout the entire course.
We had a case of Infectious Related Glomerulonephritis (IRGN) secondary to primary pulmonary TB. We conclude this because of the timing of the clinical features, the histological features on renal biopsy and the exclusion of alternative aetiologies. Diffuse proliferative glomeurulonephritis with full house pattern on immunofluorescence with ANA negative and low C3 and normal C4 is diagnostic of Infectious Related Glomerulonephritis. IgA nephropathy in association with TB infection is well documented both with and without evidence of intra-renal TB infection. On the other hand, nephrotic nephritic syndrome with non-IgA nephropathy secondary to active extra-renal TB is a very rare occurrence. Only 5 cases of rapidly progressive glomerulonephritis have been reported in adolescent tubercular patients.
This is the first instance of Infection Related Glomerulonephritis occurring secondary to pulmonary tuberculosis in a pediatric population. Strong suspicion should be there specially in patients who present with nephritic nephrotic syndrome. Even more rare is the presentation of dialysis requiring IRGN and these phenotype of patients’ respond dramatically with steroids and treatment of the underlying cause, which in this case was anti tubercular therapy.
In conclusion, we present a rare case of immune mediated glomerulonephritis complicating pulmonary tuberculosis in an adolescent. Glomerulonephritis should be strongly considered in patients diagnosed with active tuberculosis who develop renal complications that appear unrelated to the primary focus of tuberculous infection since early initiation of immunosuppression in these patients can complete alter the renal course in these patients.
