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.