Systemic lupus erythematosus (SLE) is a complex autoimmune disease. The underlying pathogenesis still needs to be elucidated.
To investigate interleukin-32 (IL-32) (rs28372698) and interleukin-37 (IL-37) (rs3811047) genetic variations, measure their serum levels in SLE patients, and evaluate their relation with disease parameters.
This work included 46 SLE patients and 43 matched controls. The SLE disease activity index (SLEDAI) and SLE damage index (SDI) were recorded. Genetic variations were assessed by real-time polymerase chain reaction (RT-PCR), and serum levels of IL-32 and IL-37 were measured by enzyme-linked immune-sorbent assay (ELISA).
The mean age of the patients was 29.2 ± 6.1 years, and the female: male ratio was 45:1. IL-37 genetic variation (rs3811047) GG was significantly more frequent in SLE patients (24/46,52.2 %) (p = 0.024), those with lupus nephritis (LN)(18/27,66.7 %) (p = 0.038), and active disease (15/21,68.2 %) (p = 0.002). The IL-37 G allele was significantly more represented in lupus patients (68/92,73.9 %)(p = 0.008), with IL-37 serum levels significantly increased in SLE patients (855.7 ± 465.4) compared to the control (504.1 ± 553.8) (p = 0.002). Although serum IL-32 was significantly higher in patients who received cyclophosphamide (CYC),and significantly correlated with total cholesterol, on regression analysis neither CYC nor cholesterol were significant factor for serum IL-32. The area under the curve for IL-37 serum levels to distinguish SLE patients from controls was 0.71, (CI 0.601–0.827; p = 0.001).
The IL-37 genetic variation (rs3811047) GG was significantly elevated in SLE, LN, and active patients. G allele was significantly more represented in lupus patients. IL-37 serum levels were significantly increased in SLE patients.
To determine the frequency of and risk factors for renal impairment in patients with axial spondyloarthritis (axSpA).
Fifty axSpA patients participated in this study. In accordance with the Kidney Disease Outcomes Quality Initiative (K/DOQI) criteria, patients were split into two groups: group 1comprised renal impairment and group 2 comprised non-renal impairment. The ankylosing spondylitis (AS) disease activity score (ASDAS), Bath AS disease activity index (BASDAI) and estimated glomerular filtration rate were assessed.
The mean age of patients was 38.9 ± 11.7 years, males were 54 % and the disease duration was 11.36 ± 6.1 years. The mean ASDAS score was 5.58 ± 1.38 and BASDAI was 5.18 ± 1.55. The eGFR was 76.4 ± 36.2 ml/min/1.73 m2 and 28 % had positive human leucocytic antigen (HLA-B27). 80 % were receiving biologic therapy. Nephropathy by ultrasound and renal impairment were detected in 34 % and 52 % of the cases respectively. The cumulative dose of non-steroidal anti-inflammatory drugs (NSAIDs), C-reactive protein, erythrocyte sedimentation rate, low density cholesterol, blood urea nitrogen, creatinine, proteinuria, ASDAS and BASDAI were significantly higher in those with renal impairment(p = 0.0001, p = 0.0001, p = 0.001, p = 0.035, p = 0.0001, p = 0.0001, p = 0.0001, p = 0.001, p = 0.001 respectively) while the eGFR and high density lipoprotein were significantly lower (p = 0.001and p = 0.02). Only the cumulative dose of NSAIDs was a significantly independent variable influencing the development of renal impairment (OR=1.01, CI; 1.001–1.02, p = 0.024) at cut-off level > 1166.3 g.
Renal impairment is frequent in axSpA patients with decreased eGFR and high disease activity. The cumulative dose of NSAIDs is a significant predictor of renal impairment.

