After 3 days of treatment, the patient's fever resolved. The renal function returned to normal on day 12 (Table 1). The proteinuria decreased 1.02 g/L at third week (Table 2). Microscopic hematuria persisted after 24 weeks (Table 3). Conclusions: There was rapid improvement of the nephrotic proteinuria, normalization of renal function and persistent microscopic hematuria with our therapeutic approach. Discussion: Mycobacterium tuberculosis (MT) infection has already been reported as an infection related to the occurrence of IgA nephropathy in 10 cases between 1983 and 2016 [16]. Our case represents the 11th that described the discovery of Ig A nephropathy associated with pleural tuberculosis. The treatment of the majority of cases was anti-tubercoulous chemotherapy alone (Table 4). Referring to studies, the antigen of MT can stimulate ƴdT cell activation and proliferation on the human mucosal surface to secrete TGF-b1 wich stimulates B cells to produce defective IgA1 [22, 23, 24, 25, 26]. The IgA1 deposition in the mesangial cause IgAN. Whereas glucocorticoids can block TGF-b production [27], this medication could be useful for decreasing production of IgA1. Furthermore the antitubercoulous drugs can reduce the blood load in MT. These pathophysiological explications could explain the good evolution of our patient by using concomitantly anti-tuberculous chemotherapy with corticosteroids. Further studies are needed to evaluate this therapeutic approach.

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