A 58-year-old woman with a history of depressive syndrome and lumbar canal stenosis.
She was diagnosed with ankylosing spondylitis B27 positive in 2005 and treated with adalimumab since 2008.
Before starting treatment, a skin tuberculin skin test positive for isoniazid prophylaxis was performed for nine months.
Nonsteroidal anti-inflammatory drugs include tramadol, antidepressants and proton pump inhibitors.
In a routine rheumatology review, a significant deterioration of renal function was observed and the patient was requested to be assessed by nephrology.
The patient was asymptomatic.
In the initial physical examination there were no edemas or isolated cervical or retroauricular lymphadenopathies and the cardiopulmonary auscultation was normal.
Because of the analytical findings, a renal ultrasound was performed, showing kidneys of 10 and 12 cm, respectively, with good corticomedullary differentiation.
There were no data on renal stones or footlocalization dilatation.
Hypodense lesions in the spleen suggested a possible lymphomatous involvement, when the patient was admitted to hospital to continue the studies.
1.
The computed tomography (CT) scan revealed multiple pulmonary nodules (predominantly in the upper lobes with a peribronchovascular pattern) and mediastinal adenopathies.
Splenic lesions were not observed.
Biopsy of a cervical adenopathy revealed epithelioid granulomatous inflammation with extensive caseous necrosis.
Ziehl-Nielsen stain showed few bacilli.
1.
Given these findings, we decided to perform fiberoptic bronchoscopy, in which no gross lesions were observed in the airway.
Bronchoalveolar lavage revealed a moderate quantity of lymphocytes, bronchial lavage was negative, and transbronchial needle aspiration of mediastinal adenopathy identified the existence of granulomas.
Ziehl stain was reported as negative at the beginning, and a single resistant acid bacillus was identified in a second observation.
After fiberoptic bronchoscopy, a positive gamma interferon release assay for tuberculosis (quantiFERON) was performed.
Based on these tests, it was decided to start tuberculosis treatment.
As part of the nephrological study, antinuclear antibodies (ANA), antineutrophil cytoplasmic antibodies (ANCA), anti-DNA and basal glomerular anthymia were negative.
Viral serology was negative for human immunodeficiency virus and hepatitis B and C viruses. Complement was normal.
The urine study initially showed a microalbuminuria/creatinine index of 261.9 mg/g and proteinuria/creatinine ratio 1.1 without nephrotic syndrome.
Only a monoclonal IgM peak could be highlighted in the proteinogram, with a serum concentration of 305 mg/dl and a negative urine concentration of light chains.
During her evolution on the ward, the patient presented sustained arterial hypertension without data of fluid overload or other symptoms to be highlighted.
associated with various clinical findings (severe renal failure), interstitial findings (size and normal echostructure), and laboratory findings (anemization, proteinuria and microhematuria) were observed in patients with renal granuloma
One of them had Langhans type multinucleated giant cells.
The glomeruli were normal.
In the tubules, there was occupation of light with granular material and flattening of the epithelium.
No microorganisms were observed in PAS and Ziehl-Nielsen stains.
1.
After renal biopsy, the patient was discharged on treatment with prednisone at a dose of 40 mg/day, erythropoietin and complete anti-tuberamide treatment (rifampicin, isoniazid, pernambuco).
The patient recovered slowly but progressively.
He remained with anemia and high requirements of erythropoietin, hypertension treated with two drugs and hyperuricemia resolved with allopurinol.
