Discussion:
SpA is a chronic inflammatory rheumatism predominantly affecting young men. Its prevalence is estimated between 0.3 and 2% of the general population (1). It can be responsible for axial, peripheral articular and enthesitic involvement.
Renal involvement is rare in SpA, its frequency varies between 4.3 and 35%(2). This impairment is often underestimated because of its late onset (with an average of 6.6 to 19.4 years) (2) and the decrease in its incidence mainly explained by the reduction in the use of NSAIDs after the introduction of biotherapies in management of SpA (3).
The main circumstances of discovery of renal involvement during SpA are edema, proteinuria, hematuria, increased blood pressure, urolithiasis, deterioration of renal function and nephrotic syndrome (2,5,6).
Data from the literature report renal involvement in SpA to three main etiologies represented by AA amyloidosis, IgA nephropathy and urolithiasis. These different etiologies vary according to studies. Ninety per cent of kidney damage are explained by amyloidosis (62%) and IgA nephropathy (30%) (2,5–7). Literature data on other etiologies (less than 8%) are limited to case reports. Cases of extra-membranous glomerulonephritis, mesangial glomerulonephritis with C3 and IgM deposits, and membrano-proliferative glomerulonephritis have been reported rarely (8–11). Rare cases of SpA-FSGS association have also been reported, including 3 cases in 3 Tunisian series (2,6,12,13). To the best of our knowledge, the present case is the fourth reported one with no other identifiable cause of secondary FSGS.
Given the paucity of data in the literature, it seems difficult to determine whether this association is etiological or a simple coincidence. In our patient, before adopting an association between SpA and FSGS, we excluded the causes of secondary FSGS (viral infections, drug / toxic origin, adaptive FSGS by nephronic reduction and glomerular hyperfiltration). Knowing that our patient had NSAIDs to control his SpA activity, the presence of FSGS could be either due to previous medication with NSAIDs or associated with his SpA.
A review of the literature showed that renal damage due to NSAIDs are mainly acute interstitial nephritis (AIN), acute tubular injury (ATI), minimal change disease (MCD), papillary necrosis (PN) and, rarely membranous nephropathy (MN) (13,14). Literature data about the relationship between NSAIDs and FSGS are controversial, an association has been reported by some authors even in topical NSAIDs (15,16). However Markowitz et al and Paueksakon et al in more recent study assert that available data do not support a relationship between NSAIDs and FSGS (14,17). Those data may support that FSGS in our patient can be related to SpA. In summary, there is no study, as well as epidemiologic evidence, that directly demonstrate the causal relationship between SpA and FSGS. The role of NSAIDs, which are the main treatments for SpA, as the cause of FSGS remains unclear. Since that, having eliminated the other possible causes is in favor of SpA and FSGS association.
Our patient will be put on Adalinumab. This later has been used since 2006 for the treatment of SpA (18). It has also been used in refractory cases of FSGS since 2014, it reduces proteinuria and protect kidney function from degradation, it has also been reported as an alternative in cases of resistance or allergy to rituximab in FSGS (19,20).