Analysis of the association between Mycobacterium tuberculosis infection and Immunoglobulin A nephropathy by early secreted antigenic target 6 detection in renal biopsies: a prospective study

Objectives: Immunoglobulin A nephropathy (IgAN) is the most frequent cause of primary renal disease, and clarifying the pathogenesis of IgAN is of great importance for its diagnosis and treatment. It is well known that Mycobacterium tuberculosis (MTB) can infect the urinary tract and result in the typical symptoms of cystitis. However, MTB can also affect the kidney more insidiously. Patients may present with glomerular disease, and sometimes with advanced renal failure. This study was to investigate the association between MTB infection and IgA nephropathy (IgAN), and the early diagnosis of MTB-mediated IgAN by means of early secreted antigenic target 6 (ESAT-6) detection in renal biopsies. Methods: One hundred and twenty patients were divided into 3 groups: a renal tuberculosis (RTB) group, a glomerulonephritis without MTB infection (GN-TBI) group and a glomerulonephritis with MTB infection (GN+TBI) group. Morning urine samples were collected for MTB culture. Immunohistochemistry for ESAT-6 expression in renal tissues was performed. Results: The incidence rate of IgAN in the GN+TBI group was 66.7%, which was significantly higher than that of the GN-TBI group. In the GN+TBI group, the ESAT-6 expression was positively associated with IgAN incidence. There was a statistical association between the positive expression of ESAT-6 and the incidence of IgAN. The sensitivity and specificity of urine MTB culture in diagnosing renal MTB infection was 23.3% and 100% respectively, while the sensitivity and specificity of ESAT-6 detection was 100% and 91.1% respectively. Compared with urine MTB culture, the sensitivity of ESAT-6 detection was significantly increased. Conclusion: MTB infection might be associated with the occurrence of IgAN, and ESAT-6 detection in renal tissues may be helpful for the early diagnosis of MTB-mediated IgAN.