Objective: To investigate the clinical and pathological manifestation of acute kidney injury ( AKI) following infusion of clindamycin. Methodology: From Aug, 2008 to Mar, 2011, twenty two patients were diagnosed as the infusion of clindamycin induced AKI. All of patients met the following three criteria; ( 1 ) No previous history of underlying chronic kidney disease; (2) the AKIN critieria of AKI soon after the infusion of clindamycin; (3) No obvious other cause of AKI, e. G. Volume insufficency, septic shock, urinary obstruction, etc. The clinical and pathological manifestations of these patients were investigated. Results-.They were 13 males and 9 females, with an average of (44. 46 ±11. 53 ) ( ranged from 20 to 70 ) years old. The reasons of clindmycin therapy were upper respiratory infection, toothache, and routine anti-infection therapy after minor operation with a usual dosage of 1. 0 ~ 1. 5 g/d. The median time between administration of drug and onset of AKI was one day (0. 5h ~4d). The most frequent chief complains were nausea and vomiting( 54. 55% ), lumbodynia ( 22. 73% ) , abdominal pain ( 22. 73% ) and edema ( 13. 64% ). Oliguria was in 13(59. 09% )and anuria in 7 patients(31. 82% ). Sixteen patients(72. 73% ) had episodes of gross hematuria, while only 3 patients(13. 64% ) encountered fever and one (4. 55% ) had skin rash. Laboratory examinations revealed anemia in 16 (72. 73% ) patients,but eosinophilia was not detected. Nineteen(90. 91% ) patients were diagnosed as AKI 3 stage, the others were as AKI 1 stage on admission. Urine analysis sowed mild proteinuria (0. 44 ± 0. 35) g/24h and severe tubular function injury. Urine eosinophilic cell was positive in only one case, and uniform microscopic hematuria was positive in 3 cases. Clindamycin lymphocyte transformation assay was positive in 13/16 (81. 25% ). Renal biopsy was performed in 18 of them. The histological diagnosis of acute interstitial nephritides( AIN)in 16 patients(88. 89% ) , acute tubular necrosis (ATN)in 2(11. 11%). The immunofluorescent examination was negative in all of cases. Continuous renal replacement therapy (CRRT) were delivered to 16 patients (72. 73% ), and prednisone (30 mg/d) was prescribed to 19 patients (86. 36% ). Urine volume increased 7 - 14 days later, all of patients discharged from the hospital and free of renal replacement therapy. The level of serum creatinine was elevated in only one after 4 weeks of discharge, and decreased to normal 6 months later. Conclusion: Most of the AKI associated with clindamycin was oliguria with episodes of gross hematuria, while the manifestations of fever, skin rash and eosinophilia were uncommon. The histological changes revealed AIN in most of the patients. The recent prognosis was relatively good but the long-term prognosis should be investigated.%回顾性分析克林霉素导致急性肾损伤(acute kidney injury,AKI)的临床和病理特征,旨在提高对克林霉素相关肾损害的认识.方法:2008年8月～2011年3月间,选取南京军区南京总医院全军肾脏病研究所22例克林霉素治疗后出现AK1患者,均无明确慢性肾脏疾病史,排除容量、感染、尿路梗阻等因素导致的AKI.结果:(1)一般情况:22例患者中男性13例,女性9例,年龄范围20～ 70岁,平均(44.46±11.53)岁,使用克林霉素治疗的病因包括上呼吸道感染、牙痛和无菌手术后常规预防性抗感染治疗等,通常剂量0.5～0.75g,2次/d.(2)临床表现:AKI发病距用药的中位时间为1d (0.5h～4d),常见首发症状包括:恶心、呕吐、上腹不适(54.55%),腰痛(22.73%),腹痛(22.73%)和水肿、胸闷(13.64%)等；少尿和无尿患者分为13例(59.09%)和7例(31.82%),16例(72.73%)有发作性肉眼血尿,仅3例(13.64%)和1例(4.55%)用药后有发热和皮疹.(3)辅助检查:16例(72.73%)有轻～中度贫血,无1例嗜酸细胞增多.尿检以少量蛋白尿(0.44 ±0.35) g/24h为特点,3例存在大量均一型血尿( 355～12 500) 万/ml,仅1例尿嗜酸细胞增多(100个/ml).肾小管功能受损的指标包括N-乙酰-β-D-氨基葡萄糖苷酶、视黄醇结合蛋白、溶菌酶、胱抑素C等均明显升高.克林霉素淋巴细胞转化试验阳性率为81.25%(13/16).(4):肾活检病理:18例接受肾活检者肾组织免疫荧光检查均阴性,组织学示肾小球病变轻微,但肾间质单核细胞浸润和肾小管炎明显；16例(88.89%)患者病理诊断急性间质性肾炎,2例(11.11%)则诊断急性肾小管坏死.(5)治疗:16例(72.73%)接受连续性肾脏替代治疗,19例(86.36%)短期口服泼尼松(30 mg/d).(6)预后:13例少尿患者在7～14d后尿量增多,出院时均摆脱肾脏替代治疗.出院后1个月除1例血清肌酐(SCr)仍异常外(137 μmol/L),其余恢复正常,半年后复查SCr全部患者均正常.结论:克林霉素导致肾脏损害的临床突出表现为发作性肉眼血尿和少尿性AKI,罕见以往认为常见的发热、皮疹及嗜酸细胞增多等临床表现,肾小管功能损伤明显,淋巴细胞转化试验阳性率高.多数患者肾活检组织学改变符合AIN,70%患者需要肾脏替代治疗,但近期肾功能恢复良好,其对远期预后的影响尚有待长期随访观察.
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