IgA肾病伴贫血的临床病理特征研究

Clinical and Pathological Characteristics of Ig A Nephropathy with Anemia

目的探讨Ig A肾病伴贫血患者的临床病理特点。方法收集202例经肾活检明确诊断原发性Ig A肾病患者的临床病理资料。根据是否贫血分为两组,其中A组(贫血组)33例,B组(非贫血组)169例,比较两组临床和病理方面的差异。结果与B组比较,A组的Scr、BUN、24h-Upro明显增高,RBC、Hb、Alb下降,肾小球硬化、新月体形成及血管壁增厚的数目增多,差异具有统计学意义(P<0.05)。肾组织病理学参照Lee氏分级比较,贫血组病理Lee氏分级较重(P<0.05)。Spearman相关分析结果提示,Hb与小球硬化/肾小球总数、新月体/肾小球总数呈负相关,Scr、24h-Upro与小球硬化/肾小球总数、新月体/肾小球总数呈正相关。多因素Logistic回归分析表明女性、Scr、24h-Upro、新月体病变是是Ig AN合并贫血患者的独立危险因素。结论 Ig AN伴有贫血患者的临床病理改变重于Ig A肾病不伴有贫血的患者,即贫血可加重Ig A肾病患者的临床病理损伤。

Objective To analyze the clinical and pathological characteristics of IgA nephropathy with anemia patients. Methods Two hundred and two patients of IgA nephropathy with anemia diagnosed by renal biopsy were classified into two groups according to whether anemia：33 cases of IgA nephropathy with anemia （group A） and 169 cases of IgA nephropathy with non - anemic（ Group B）. The changes of the clinical and pathological features were studied between the group. Results Compared with group B,changes in group A, serum creatinine, blood urea nitrogen, 24 hours urinary protein were increased, red blood cell, serum hemoglobin, Serum albumin de- creased, the number of glomerular sclerosis, crescent formation and thickening of the vessel wall increased. Statistically significant differ- ences in these indexes（P 〈 0.05 ）. The pathology of Lee＇s classification is higher in group A （ P 〈 0.05 ）. Spearman correlation analysis indicated that glomerular sclerosis/glomerular number, crescent/glomerular number was negatively correlated with serum hemoglobin, but positively correlated with serum creatininc, 24 hours urinary protein. Multivariate Logistic regression analysis showed that female, serum creatinine, 24 hours urinary protein, crescentic lesions were independent risk factors of IgA nephropathy patients with anemia. Conclusion Clinical pathological changes are more serious in IgA nephropathy patients with anemia than with non - anemic, which anemia can ag- gravate clinical pathological in patients with IgA nephropathy.