The association of polymorphonuclears with humps in acute postinfectious glomerulonephritis

Vol. 53 No. 3 Suppl., 2012
This supplement was not sponsored by Outside Organizations.


E. Mandache, M. N. Penescu

It is currently considered that hump dense deposits developed during an acute poststreptococcal glomerulonephritis become finally dissolute by three hypothetical mechanisms: loosing their electron density, internalization and processing by podocytes and by incorporation in the glomerular basal lamina (GBM). Analyzing ultrastructurally the association of polymorphonuclear leukocytes and hump deposits, we emphasized features endorsing the hypothesis that the immune complexes of dense deposits are discharged in the circulation under the leukocytes activity. The active polymorphonuclear cells are melting the GBM in the area of contact by complement activation and by the NAPlr bound plasmin. The reversed flow of immune complexes from humps towards the blood circulation leaves fading, wrinkled shaped humps, before total dissolution.

Corresponding author: Eugen Mandache, MD, PhD; e-mail:

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M. Olteanu, Mimi Nitu, Andreea Golli

A 41-year-old female patient was admitted into Surgery Clinic accusing abdominal pain, diarrhea, fever and chills. Based on clinical, biological and imaging data, it was established a diagnosis of pelviperitonitis and it was initiated an antibiotic and anti-inflammatory treatment. As fever and abdominal pain continued, it was decided to go on with surgery that revealed suppurated and perforated mesenteric adenopathy. Pus was sampled for bacteriological exam and also biopsy was performed for pathological exam. The result of pathological exam was suggestive for a specific granulomatous lesion (TB lesion). It was established diagnosis of TB mesenteric adenopathy and it was initiated specific anti-TB treatment according to WHO guidelines. After three, respectively five months of treatment, patient developed a right laterocervical adenopathy that fistulized in both cases, despite the correct treatment administered. No resistant TB strain and no atypical mycobacteria was discovered.

Corresponding author: Mihai Olteanu, MD, PhD; e-mail:

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