title: Ionic contrast media induced more apoptosis in diabetic kidney than nonionic contrast media.
abstract: BACKGROUND
  Contrast-induced nephropathy is a major cause of hospital-acquired acute renal failure, and its risk is significantly increased in patients with diabetes mellitus. This study aimed to examine both the role of apoptosis in low-osmolar contrast media-induced kidney injury in normal and diabetic rats and the difference in the induced kidney injury between ionic and nonionic contrast media.
  
  
  METHODS
  Normal and streptozotocin-induced diabetic Wistar rats were administered with ionic low-osmolar ioxaglate, nonionic low-osmolar iopromide or normal saline injection. Apoptosis in kidney tubular cells was determined by the presence of positive terminal deoxynucleotidyl transferase-mediated dUTP in situ nick end-labeling (TUNEL) stain.
  
  
  RESULTS
  At 24 hours after administration, both ioxaglate and iopromide injections induced more apoptosis in diabetic (49.7% vs. 25.3% for ioxaglate; 37.7% vs. 25.3% for iopromide; both p<0.001) and normal (36.2% vs. 27.4%, p=0.002, for ioxaglate; 33.6% vs. 27.4%, p=0.029, for iopromide) kidney tubular cells than normal saline injections. Additionally, ioxaglate induced more apoptotic tubular cells in diabetic kidneys than in normal kidneys (p<0.001). Moreover, ioxaglate significantly induced more apoptotic cells than iopromide in diabetic kidneys, but not in normal kidneys (p<0.001, for diabetic rats; p=0.345, for normal rats).
  
  
  CONCLUSIONS
  Ionic low-osmolar contrast media induced more apoptosis in tubular cells in diabetic kidneys than in normal kidneys. Notably, ionic contrast media induced more apoptosis than nonionic contrast media in diabetic kidneys.
authors.affiliation: Division of Cardiology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung - Taiwan.
authors.forename: Hsiang-Chun
authors.initials: HC
authors.lastname: Lee
authors.forename: Jan-Gowth
authors.initials: JG
authors.lastname: Chang
authors.forename: Hsueh-Wei
authors.initials: HW
authors.lastname: Yen
authors.forename: I-Hsin
authors.initials: IH
authors.lastname: Liu
authors.forename: Wen-Ter
authors.initials: WT
authors.lastname: Lai
authors.forename: Sheng-Hsiung
authors.initials: SH
authors.lastname: Sheu
mesh_terms: D051698:Activating Transcription Factor 2 / Q000378:metabolism; D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D003287:Contrast Media / Q000009:adverse effects / Q000494:pharmacology*; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000473:pathology*; D007472:Iohexol / Q000009:adverse effects / Q000031:analogs & derivatives* / Q000494:pharmacology; D007477:Ions; D007485:Ioxaglic Acid / Q000009:adverse effects / Q000494:pharmacology*; D007684:Kidney Tubules / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D008297:Male; D009994:Osmolar Concentration; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin / Q000009:adverse effects
chemical_list: D051698:Activating Transcription Factor 2; C497107:Atf2 protein, rat; D003287:Contrast Media; D007477:Ions; D007472:Iohexol; D013311:Streptozocin; C038192:iopromide; D007485:Ioxaglic Acid