Rare association of cutaneous vasculitis, IgA nephropathy and antiphospholipid antibody syndrome with tuberculous lymphadenitis

We read with great interest the article by Bueno Filho et al. entitled ‘‘Rare association of cutaneous vasculitis, IgA nephropathy and antiphospholipid antibody syndrome with tuberculous lymphadenitis’’ that was published in the esteemed journal Clinics. The authors presented an interesting case of cutaneous vasculitis, IgA nephropathy and antiphospholipid antibody syndrome with tuberculous lymphadenitis in a 45-year-old woman (1). I would like to mention a few points regarding this paper. A definitive pathologic IgA nephropathy diagnosis based on immunostaining assays requires the presence of dominant mesangial IgA depositions in the absence of significant C1q depositions to rule out lupus nephritis (2–5), which the authors should note. Moreover, the detection of significant fibrin deposition along with IgA deposits can help differentiate between primary IgA nephropathy and Henoch-Schönlein purpura nephropathy (2–5). Therefore, the authors should also discuss this point. Bueno Filho et al. classified the morphologic lesions of IgA nephropathy in renal biopsies as ‘‘focal and segmental sclerosis with mild focal and chronic tubulointerstitial damage’’. Indeed, as a result of the publication of the Oxford classification of IgA nephropathy in 2009 (2,5), it is necessary to describe the morphologic lesions of IgA nephropathy according to this classification system (6–8). Furthermore, figure 2C shows a normal glomerulus, which is in contrast to the described morphologic features. The authors reported the final diagnosis as a combination of tuberculous lymphadenitis, cutaneous leukocytoclastic vasculitis, primary IgA nephropathy and anti-phospholipid antibody syndrome. However, the presence of morphologic lesions upon renal biopsy suggests anti-phospholipid syndrome nephropathy and should have been reported (9–11). Anti-phospholipid antibody syndrome is a vaso-occlusive disease (12,13) that affects renal tissue and has various morphologic lesions, some of which are characteristic of the disease (14). Accurate documentation and reporting of such rare cases are necessary to determine the complete spectrum of this disorder and improve the understanding of its pathophysiology. Bueno Filho et al. merit compliments for bringing this interesting case to this journal for discussion. Such discussions may help increase awareness of antiphospholipid antibody syndrome among pathologists and nephrologists, particularly in developing countries.