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).