To detect plasma levels of IL-1β and IL-18 in patients with urate nephropathy and explore their role in this disease.

Male patients were selected as subjects between July 2016 and December 2017 in the Affiliated Baoan Hospital of Shenzhen, Southern Medical University. According to the inclusion and exclusion criteria, the patients were divided into three groups (15 patients each): a hyperuricemia group, a urate nephropathy group, and a control group. Blood biochemical indicators were measured using a biochemical analyzer and urinary biochemical parameters were determined using a urine analyzer. Biochemical indicators included blood lipids (total cholesterol, triacylglycerol, low-density lipoprotein and high-density lipoprotein), renal function (creatinine and urea nitrogen), and uric acid. ELISA was used to detect the levels of IL-1β and IL-18 in plasma. The values are expressed as mean±SD. One-wayANOVA was used to compare the means of multiple groups and LSD-t test was adopted to compare the means between two groups. P-values<0.05 were considered to be significant.

Compared with the control group, the hyperuricemia group and urate nephropathy group had significantly decreased high density lipoprotein and significantly increased low density lipoprotein, total cholesterol, uric acid, creatinine, and blood urea nitrogen [(1.04±0.28) mmol/L, (1.11±0.38) mmol/L vs (1.73±0.37) mmol/L, t=-4.622, -5.162, P<0.001 for both; (4.32±1.15) mmol/L, (5.42±1.04) mmol/L vs (3.35±0.78) mmol/L, t=5.519, 2.443, P<0.001 and P=0.019; (3.08±0.96) mmol/L, (3.62±0.76) mmol/L vs (2.07±0.64) mmol/L, t=5.159, 3.466, P<0.001 and P=0.001; (65.82±28.37) μmol/L, (80.97±3.34) μmol/L vs (33.67±8.60) μmol/L,t=4.832, 3.810, P<0.001 for both; (5.55±1.64) mmol/L, (5.24±1.70) mmol/L vs (3.87±0.75) mmol/L,t=2.524, 3.197, P=0.015 and P=0.003; (487.13±140.91) μmol/L, (503.60±52.81) μmol/L vs (192.80±63.06) μmol/L, t=9.036, 8.557, P<0.001 for both]. Compared with the control group, the hyperuricemia group and urate nephropathy group had increased total triglycerides [(1.23±0.44) mmol/L vs (2.19±0.61) mmol/L vs (0.85±0.45) mmol/L], and there was a significant difference between the control and hyperuricemia groups (t=3.786, P<0.001). Compared with the control group and hyperuricemia group, the urate nephropathy group had significantly higher urine erythrocyte [(31.80±59.42)/HP vs (0.60±0.74)/HP,(2.13±1.92)/HP, t=1.933, 2.033, P=0.014, 0.017]. Compared with the control group, plasma IL-1β and IL-18 levels were significantly increased in the hyperuricemia group and urate nephropathy group [(81.20±17.63) ng/L, (55.19±16.79) ng/L vs (28.41±14.05) ng/L, t=4.519, 8.907, P<0.001 for both; (870.67±371.13) ng/L vs (718.16±211.42) ng/L vs (323.35±96.16) ng/L, t=4.290, 5.947, P<0.001 for both]. Plasma IL-1β level was significantly increased in the urate nephropathy group compared with the hyperuricemia group (t=4.387, P<0.001).

Plasma levels of IL-1β and IL-18 significantly increase in patients with urate nephropathy, which suggests that inflammatory factors play a vital role in the development of hyperuricemia-induced renal damage.