A 58-year-old woman with a personal history of depressive syndrome and lumbar canal stenosis. Diagnosed with B27-positive ankylosing spondylitis in 2005 and on treatment with adalimumab since 2008. Before starting treatment, a positive tuberculin skin test required isoniazid prophylaxis for nine months. His regular medications included non-steroidal anti-inflammatory drugs, tramadol, antidepressants and proton pump inhibitors.
At a routine rheumatology check-up, a significant deterioration of her renal function was noted and she was requested to undergo a nephrology assessment. The patient was asymptomatic. On initial physical examination, there was no oedema, no palpable laterocervical or retroauricular lymphadenopathy and cardiopulmonary auscultation was normal.
In view of the analytical findings, a renal ultrasound was performed, showing kidneys measuring 10 and 12 cm, respectively, with good corticomedullary differentiation. There was no evidence of renal lithiasis or pyelocaliceal dilatation. The hypodense lesions in the spleen suggested possible lymphomatous involvement, at which point the patient was admitted for further studies.
The thoraco-abdomino-pelvic computed tomography (CT) scan showed multiple pulmonary nodules (predominantly in the upper lobes with a peribronchovascular pattern) and mediastinal adenopathies. No splenic lesions were observed.
A cervical adenopathy was biopsied, showing granulomatous epithelioid inflammation with extensive caseous necrosis. Ziehl-Nielsen staining showed few bacilli.
In view of these findings, it was decided to perform fibrobronchoscopy, in which no macroscopic lesions were observed in the airway. Bronchoalveolar lavage showed a moderate number of lymphocytes, bronchial lavage was negative and a transbronchial fine needle aspiration of a mediastinal adenopathy identified the existence of granulomas. Ziehl's staining was initially reported as negative, with a second observation revealing a single acid-fast bacillus. Following fibrobronchoscopy, an interferon gamma release assay for tuberculosis (quantiFERON) was performed, which was positive. Based on these tests, it was decided to start anti-tuberculosis treatment.
As part of the nephrological work-up, antinuclear antibody (ANA), anti-neutrophil cytoplasmic antibody (ANCA), anti-DNA and anti-glomerular basement membrane antibodies were negative. Viral serology was negative for human immunodeficiency virus and hepatitis B and C viruses. Complement was normal. Urine analysis initially showed a microalbuminuria/creatininuria index of 261.9 mg/g and proteinuria/creatininuria 1.1 without nephrotic syndrome. The only notable finding in the proteinogram was a monoclonal IgM peak, with a serum concentration of 305 mg/dl and a negative urine light chain concentration.
During her evolution on the ward, the patient presented sustained arterial hypertension with no evidence of water overload or other symptoms of note.
Given the clinical findings (severe renal failure), radiological findings (kidneys of normal size and echostructure) and analytical findings (anaemia, proteinuria and microhaematuria), a renal biopsy was performed in which interstitial inflammation was detected at the expense of lymphocytes, accompanied by histiocytes that formed granulomas at several points. Multinucleated Langhans-type giant cells were present in one of them. The glomeruli were normal. In the tubules, the lumen was occupied with granular material and flattening of the epithelium. No microorganisms were observed in PAS and Ziehl-Nielsen staining.
After the renal biopsy, the patient was discharged on treatment with prednisone at a dose of 40 mg/day, erythropoietin and complete antituberculosis treatment (rifampicin, isoniazid, ethambutol and pyrazinamide).
The patient progressed towards slow but progressive improvement of renal function. She persisted with anaemia and high erythropoietin requirements, hypertension treated with two drugs and hyperuricaemia resolved with allopurinol.
