title: Lower Blood Pressure-Induced Renal Hypoperfusion Promotes Cisplatin-Induced Nephrotoxicity.
abstract: OBJECTIVE
  Cisplatin-induced nephrotoxicity primarily occurs in the proximal tubules, and tubular injuries reduce glomerular filtration rates. Lower blood pressure causes renal hypoperfusion, which promotes ischemic acute kidney injury (AKI). Our study examined the relationship between lower blood pressure-induced renal hypoperfusion and cisplatin-induced nephrotoxicity.
  
  
  METHODS
  The relationship between cisplatin use and hypoalbuminemia is not clear. This study consisted of Japanese patients who received cisplatin as the first-line chemotherapy at Fujita Health University Hospital from April 2006 to December 2012. Hypoalbuminemia was defined as serum albumin levels ≤3.5 mg/dl.
  
  
  RESULTS
  Patients who experienced lower blood pressure during chemotherapy were included in the lower blood pressure group (n = 229), and those who did not were included in the normal blood pressure group (n = 743). Total cisplatin dose in the normal blood pressure and lower blood pressure groups was 58.9 ± 23.8 and 55.0 ± 20.4 mg/m2, respectively. The rate of severe nephrotoxicity was higher and overall survival was shorter in the lower blood pressure group than in the normal blood pressure group. In a multivariable analysis, lower blood pressure significantly correlated with hypoalbuminemia.
  
  
  CONCLUSIONS
  To prevent ischemic AKI, nutrition and cachexia controlling are important parts of cancer treatment.
authors.affiliation: Department of Analytical Pharmacology, Meijo University Faculty of Pharmacy, Nagoya, Japan.
authors.forename: Tomohiro
authors.initials: T
authors.lastname: Mizuno
authors.forename: Takahiro
authors.initials: T
authors.lastname: Hayashi
authors.forename: Yuka
authors.initials: Y
authors.lastname: Shimabukuro
authors.forename: Maho
authors.initials: M
authors.lastname: Murase
authors.forename: Hiroki
authors.initials: H
authors.lastname: Hayashi
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Ishikawa
authors.forename: Kazuo
authors.initials: K
authors.lastname: Takahashi
authors.forename: Yukio
authors.initials: Y
authors.lastname: Yuzawa
authors.forename: Shigeki
authors.initials: S
authors.lastname: Yamada
authors.forename: Tadashi
authors.initials: T
authors.lastname: Nagamatsu
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood / Q000139:chemically induced / Q000209:etiology*; D000368:Aged; D000970:Antineoplastic Agents / Q000008:administration & dosage / Q000009:adverse effects*; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure; D002945:Cisplatin / Q000008:administration & dosage / Q000009:adverse effects*; D015897:Comorbidity; D003404:Creatinine / Q000097:blood*; D005260:Female; D005919:Glomerular Filtration Rate; D006801:Humans; D007022:Hypotension / Q000150:complications*; D053208:Kaplan-Meier Estimate; D007668:Kidney / Q000098:blood supply* / Q000503:physiopathology*; D007677:Kidney Function Tests; D008297:Male; D008875:Middle Aged; D012189:Retrospective Studies; D012307:Risk Factors; D013997:Time Factors
chemical_list: D000970:Antineoplastic Agents; D015415:Biomarkers; D003404:Creatinine; D002945:Cisplatin