Case:
A 49-year-old man with a history of retrobulbar optic neuritis was diagnosed with axial SpA since 2017. The diagnosis was made according to ASAS 2009 criteria (inflammatory chronic back pain over one year, positive C-Reactive-Protein (CRP) at 164mg/l and bilateral sacroiliitis on X ray (grade II)) (4). There was no extra-articular manifestation at the time of the disease diagnosis. He was treated with Non-Steroidal Anti-Inflammatory Drugs NSAIDs (diclofenac and indomethacin) for a period of two months. This treatment was quickly stopped upon the discovery of proteinuria at 0.3 g/24h. The patient was put on corticosteroid therapy (10 mg of Prednisone) and we decided to put him on biotherapy (Adalimumab).
The patient was lost to follow-up from 2017 to 2020. He consulted in December 2020 with edema of lower limbs, a hydrocele, and a bilateral pleural effusion of low abundance. His blood pressure was high (180-200 mmHg systolic). On osteoarticular examination, there were back stiffness and limitation in hips mobility. Moreover, there were no other articular involvement or abnormalities in the general examination.
Laboratory investigations showed: CRP at 51mg/l, normal level of urea and creatinine, the 24-hour urine protein was at 5.9 g/24h, the proteinemia was at 46g/l and the albuminemia was at 14.4g/l and there was not hématuria. In front of those clinical and biological data; we retained the diagnosis of impure nephrotic syndrome with arterial hypertension. Regarding SpA activity, the Bath Ankylosing Spondylitis Disease Activity score (BASDAI) was at 6.3, the Ankylosing Spondylitis Disease Activity Score (ASDAS CRP) was at 4.95. By questioning the patient, he affirmed that he self-administrated paracetamol and NSAIDs occasionally in case of pain.
To explore the impure nephrotic syndrome, a renal biopsy was indicated and the anatomopathological examination concluded to a FSGS involvement (Figure 1 ). After ruling out the causes of secondary FSGS (human immune-deficiency virus, hepatitis B virus, parvovirus B19, and Cytomegalovirus infections, drug / toxic origin, adaptive FSGS by nephronic reduction and glomerular hyperfiltration) we put the patient on corticosteroid therapy (prednisone) at a dose of 1 mg/kg/day in association with diuretics (furosemide and spironolactone) and an ACE inhibitor (ramipril) for a period of 3 months, five albumin infusions were also prescribed.
After three months of treatment, the edema as well as the nephrotic syndrome have almost disappeared. Regarding his SpA, the patient is currently awaiting a support agreement for Adalimumab from the social insurance funds. He only receives analgesic treatment.