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Systemic lupus erythematosus is an autoimmune disease of unknown etiology, The hallmark of SLE is the presence of serum autoantibodies directed to nuclear constituents (i.e., antinuclear antibodies, ANA). Lupus nephritis is one of the common manifestations of SLE. . ANA is the most sensitive test for SLE and is present in more than 90% of patients but not specific for SLE. Anti dsDNA is a more specific but less sensitive marker of SLE. High titre of anti dsDNA correlates with disease activity and especially with lupus nephritis. Serum levels of complements C3 and C4 are usually decreased in active SLE and in active lupus nephritis. Most of the patients with active proliferative lupus nephritis have high titre of anti dsDNA and low C3 and C4 levels.
A PROSPECTIVE STUDY. Sample size- 32. CENTER: Nephrology departmentt,GMKMCH, Salem
In our study 32patients were female patients were included and All patients had proteinuria in our study. In our study (19) 60% had Class IV lupus nephritis. (5) 15% Class V lupus nephritis. (6)19 % both Class IV and Class V. (2) 6% Class II lupus nephritis.Only 22 patients (68%) of LN had microscopic hematuria. 15 of 19 patients (48%) with class IV, 3 of 6 patients (50%) with class IV&V, 1 of 2 patients (50%) with class II and 3 of 5 patients (60%) with class V LN had microscopic hematuria.Of 32 patients with LN, 26(82%) had anti dsDNA positivity. 17 of 19 patients (90%) with class IV, all the 6 patients (100%) with class IV&V, 3 of 5 patients (60%) with class V LN had anti dsDNA positivity. Totally 26 of 32 patients (83.2%) with proliferative LN had anti dsDNA positivity (P Value < 0.001).Of 32 patients with LN, 16 (50%) had low C3 level in serum. 16 of 19 patients (84.21%) with class IV, all the 6 patients (100%) with class IV&V and 2 of 5 patients (40%) with class V LN had low C3 level in serum. But none of the patients with class II LN had low C3 level. Totally 30 of 32 patients (93.75%) with proliferative LN had low C3 level (P Value < 0.001). Of 32 patients with LN, 22(70%) had low C4 level in serum. 17 of 19 patients (89.4%) with class IV, all the 6 patients (100%) with class IV&V and 4 of 5 patients (80%) with class V LN had low C4 level in serum. But none of the patients with class II LN had low C4 level. Totally 27 of 30 patients (81%) with proliferative LN had low C4 level (P Value < 0.001)
In our study, serological profile of SLE had significant correlation with histopathology of lupus nephritis. Anti dsDNA, low C3 and low C4 had significant independent correlation (p<0.05) with proliferative LN (class IV, IV&V). Positive predictive value of all these three serological markers put together for proliferative LN was 97.4%. None of the patients with class II or class V LN had the combination of anti dsDNA positivity, low C3 and low C4 levels.
So, we may suggest that serology alone is sufficient to predict the proliferative LN and there can be a case for starting immunosuppressive therapy without biopsy in a known SLE patient with evidence of LN and positive serology