IgA肾病患者合并高尿酸血症临床及病理特征分析

目的探讨IgA肾病高尿酸血症的临床病理特征及相关危险因素。 方法选取2010年1月至2015年7月于山西医科大学第二医院行经皮肾穿刺活检确诊为IgA肾病的188例患者，根据血尿酸水平将患者分为正常血尿酸组与高尿酸血症组，收集患者一般资料、尿蛋白定量、肾功能等临床生化指标以及病理指标，并对肾脏病理组织进行牛津病理分型。分析两组患者临床表现、肾脏病理特点，应用多元回归统计学方法分析高尿酸血症发生的影响因素。其他数据采用SPSS13.0软件进行统计分析。 结果本研究中心188例IgA肾病患者中合并高尿酸血症的患者有42例，高尿酸血症发生率为22.3%；高尿酸血症组中男性患者36例，女性患者6例；与正常血尿酸组(男性患者61例、女性患者85例)相比，高尿酸血症组男性患者明显增多(χ²＝25.2，P<0.001)。本组研究IgA肾病患者肾脏组织牛津病理分型以M1E1S0T0多见；与正常血尿酸组比较，高尿酸血症组患者肾小管－间质损伤重，差异有统计学意义(χ²＝5.056，P＝0.025)。肾组织免疫复合物IgA沉积于毛细血管袢者高尿酸血症发生率明显升高(χ²＝44.69，P<0.001)。IgA肾病患者合并高尿酸血症的相关因素为性别、体质量指数、甘油三酯、IgA沉积于毛细血管袢。 结论IgA肾病高尿酸血症的危险因素为男性、肥胖、高甘油三酯血症，并可能与IgA在毛细血管区沉积相关。

Clinical and pathological characteristics analysis in IgA nephropathy patients with hyperuricemia

ObjectiveTo investigate the clinical-pathological features and related risk factors in IgA nephropathy patients with hyperuricemia. MethodsBetween January 2010 and July 2015, a total of 188 IgA nephropathy patients were recruited, who were diagnosed IgA nephropathy by renal biopsy in the Second Hospital of Shanxi Medical University, and divided into high uric acid group and normal uric acid group. Collected were general data, urine protein amount, renal function, and other clinical biochemical as well as pathological indicators; and Oxford classification system was applied for the renal histopathology. Clinical manifestation and renal pathology features were analyzed for the two groups; and multiple regression statistical methods were applied to analyze the influencing factors for hyperuricemia occurrence. And other data were statistically analyzed with the SPSS13.0 software. ResultsOf the 188 IgA nephropathy patients, there were 42 patients with hyperuricemia (22.34%), among whom there were 36 males and 6 females; and compared with the normal uric acid group consisting of 61 males and 85 females, the high uric acid group consisted of more male patients (χ²=25.2, P<0.001). The Oxford classification system analysis showed that in the IgA nephropathy patients with hyperuricemia M1E1S0T0 was predominant. In the high uric acid group, tubulointerstitial lesions were more severe than those of the normal uric acid group (χ²=5.056, P=0.025), and there were more IgA deposits on capillary loops than in the normal uric acid group (χ²=44.69, P<0.001). In the IgA nephropathy patients with hyperuricemia, the relevant factors were male, obesity, hypertriglyceridemia, and deposition of IgA on the capillary loops. ConclusionThe risk factors for hyperuricemia in IgA nephropathy consists of maleness, obesity and hypertriglyceridemia, as well as deposition of IgA on the capillary loops.