432 J Nephrol Dialy Transplant Vol. 20 No. 5 Oct. 2011 acute kidney injury AKI 2008 8 ~ 2011 3 22 AKI AKI 1 22 13 9 20 ~ 70 44. 46 ± 11. 53 0. 5 ~ 0. 75g 2 /d 2 AKI 1d 0. 5h ~ 4d 54. 55% 22. 73% 22. 73% 13. 64% 13 59. 09% 7 31. 82% 16 72. 73% 3 13. 64% 1 4. 55% 3 16 72. 73% ~ 1 0. 44 ± 0. 35 g /24h 3 355 ~ 12 500 /ml1 100 /ml N- -β-d- C 81. 25% 13 /16 4 18 16 88. 89% 2 11. 11% 5 16 72. 73% 19 86. 36% 30 mg /d 6 13 7 ~ 14d 1 1 SCr 137 μmol /L SCr AKI AIN 70% Acute kidney injury associated with clindamycin XIE Hong-lang CHEN Hui-ping HU Yang-ling XU Shu-tian HE Qun-peng LIU Jin HU Wei-xin LIU Zhi-hong Research Institute of Nephrology Jinling Hospital Nanjing University Clinical School of Medicine Nanjing 210002 China Corresponding author LIU Zhi-hong E-mail zhihong--liu@ hotmail. com ABSTRACT 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 210002 E-mail zhihong--liu@ hotmail. com 2011
20 5 2011 10 433 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. Key words acute kidney injury clindamycin acute interstitial nephritis acute kidney injury AKI AKI Ali 1 AKI 2 147 7% 2 ICU 10. 8% ~ 67. 2% 3 AKI Uchino 4 ICU AKI 20% NSAIDs AKI NSAIDs AKI AKI 2008 8 ~ 2011 3 AKI 1 SCr 26. 52 37 AKIμmol /L 50% AKI 2 SCr 14 > 200% ~ 300% AKI 3 SCr 1 1 22 > 300% 353. 6 μmol /L 1 2 44. 2 μmol /L 140 mmhg AKI 3 90 mmhg AKI 3 H-TdR AKI 4 ml 6 1 AKI AKI AKIN 5 Hb 120 g /L Hb 110 g /L
434 J Nephrol Dialy Transplant Vol. 20 No. 5 Oct. 2011 18 B 10% COPD 1. 5 μm - HE shiff PAS 3 13. 64% 1 4. 55% PASM-Masson Masson 3 13. 64% 4 μmigg IgA IgM C3 C4 C1q Fibrin 13 59. 09% 7 31. 82% 13 59. 09% ± x 珋 ± SD 16 72. 73% 2B 22 AKI 13 9 20 ~ 70 44. 46 ± 11. 53 11 50% 2 1 1 / 13 /9 44. 46 ± 11. 53 /COPD 11 2 2 2 1 1 1 1 1 COPD AKI 85 /ml 100 /ml 1d 0. 5h ~ 4d 0. 5 ~ 0. 75g 2 /d AKI 2 54. 55% 22. 73% 22. 73% 13. 64% 2A 1 > 2 AKI 1 16 13 81. 25% COPD 2 A B 16 72. 73% ~ 1 2 AKI 1 20 90. 91% AKI 3 ~ 0. 44 ± 0. 35 g /24h 3 355 ~ 12 500 /ml 1 < 20 /ml AKI
20 5 2011 10 435 Hb g/l 2 珋 x ± SD 110 ~150 111. 3 ± 15. 8 85 ~ 143 120 ~160 <7. 00 2. 00 ± 1. 00 0 ~ 4. 00 % SCr μmol /L 45. 08 ~109. 62 671. 84 ± 312. 05 112. 27 ~ 1272. 96 CysC mg/dl 0. 45 ~1. 0 3. 01 ± 1. 17 1. 21 ~ 4. 9 0. 6 ~1. 18 g/24h 0. 4 0. 43 ± 0. 35 0. 1 ~ 1. 50 NAG U/ g cr 16. 5 43. 44 ± 32. 22 9. 3 ~ 151. 9 RBP mg/l 0. 5 14. 06 ± 17. 16 0. 2 ~ 42. 6 Lyso mg/l <1. 0 5. 23 ± 6. 40 0. 98 ~ 23. 3 CysC mg/l <0. 15 1. 48 ± 2. 41 0. 17 ~ 7. 5 NGAL μg/l <20 439. 8 ± 1 301. 3 4. 48 ~ 4 758. 6 KIM-1 μg/l <0. 4 4. 05 ± 6. 79 0. 15 ~ 26. 48 IL-18 ng/l <20 37. 88 ± 48. 22 2. 71 ~ 150. 1 Hb SCr CysC C NAG N- -β-d- RBP Lyso NGAL KIM-1 1 IL-18-18 2 44. 44% 66. 67% 33. 33% 100% 3 4 83. 33% 4 1 7 CD4 + CD8 + CD68 + 3 16 88. 89% AIN 2 11. 11% ATN 3 16 72. 73% 3 19 86. 36% 30 mg /d 7 ~ 16d 10. 43 ± 3. 96 d 18 10 19. 72 ± 12. 45 SCr 1 12 11 SCr 1 50% < 109. 62 μmol /L 1 SCr 137 μmol /L 2 3 SCr 110 μmol /L 104 μmol /L
436 J Nephrol Dialy Transplant Vol. 20 No. 5 Oct. 2011 AKI AIN 1966 Magerlein NSAID 7 14 AKI 90% AIN AIN 3 n = 7 15 CD4 + /mm 2 27. 2 ± 11. 3 239. 43 ± 166. 25 CD8 + /mm 2 20. 8 ± 7. 3 210. 29 ± 154. 42 CD4 + /CD8 + 1. 29 ± 1. 26 1. 15 ± 0. 18 44% CD68 + /mm 2 510. 29 ± 408. 29 80% SCr BUN 1 7 8 9 AIN ADR AKI 1 419 ADR 2 0. 36% 2 /3 10 11 108 SCr BUN 5 3. 53% 10% 2003 ~ 2008 ADR 107 4 19. 86% 1 12 13 1d AKI 90% AKI 3 22 AKI 70% 72. 73% 90% AKI 3 AKI AIN ATN AIN ADR ADR
20 5 2011 10 437 5 Mehta RL Kellum JA Care 2007 11 2 R31. 8% 6% Mazur 16 1994 3 2 70-76. 70 10% 17 0. 4% 7. therapy 40. P87-88. AKI 2009 149 3 246-250. 9 Lammintausta K 2002 146 4 10 AKI 141-142. 12 2010 29 7 963-965. 81. 25% AIN 70% 1 Ali T Khan I Simpson W Prescott G et al. Incidence and outcomes in acute kidney injury a comprehensive population-based study. Am Soc Nephrol 2007 18 4 1292-1298. 2 Nash K Hafeez A Hou S. Hospital-acquiredrenal insufficiency. Am J Kidney Dis 2002 39 5 930-936. 3 Srisawat N Hoste EE Kellum JA. Modern classification of acute kidney injury. Blood Purif 2010 29 3 300-307. 4 Uchino S Kellum JA Bellomo R et al. Acute renal failure in critically ill patients a multinational multicenter study. JAMA 2005 294 7 813-818. Shah SV et al. Acute Kidney Injury Network report of an initiative to improve outcomes in acute kidney injury. Crit 6.. The Sanford guide to antimicrobial Sanford JP.. 2010 8 Seitz CS Br cker EB Trautmann A. Allergy diagnostic testing in clindamycin-induced skin reactions. Int Arch Allergy Immunol 2009 Tokola R Kalimo K. Cutaneous adverse reactions to clindamycin results of skin tests and oral exposure. Br J Dermatol 643-658.. 419. 2010 16 1 51-54. 11. 108. 2010 7 2.. 13.. 2010 32 8 910-911. 14 Dennen P Douglas IS Anderson R. Acute kidney injury in the intensive care unit an update and primer for the intensivist. Crit Care Med 2010 38 1 261-275. 15 Praga M González E. Acute interstitial nephritis. Kidney Int 2010 77 11 956-961. 16 Mazur N Greenberger PA Regalado J. Clindamycin hypersensitivity appears to be rare. Ann Allergy Asthma Immunol 1999 82 5 443-445. 17 Klainer AS. Clindamycin. Med Clin North Am 1987 71 6 1169-1175. 2011-06-17