Clinical significance of tubular and podocyte biomarkers in acute kidney injury

Clinical significance of tubular and podocyte biomarkers in acute kidney injury

  • نوع فایل : کتاب
  • زبان : انگلیسی
  • مؤلف : Katsuomi Matsui Atsuko Kamijo-Ikemori Masanori Hara Takeshi Sugaya Takamitsu Kodama Sigeki Fujitani Yasuhiko Taira Takashi Yasuda Kenj
  • چاپ و سال / کشور: 2011

Description

Background Acute kidney injury (AKI) is a common complication in critically ill patients. Urinary excretion of liver-type fatty acid-binding protein (L-FABP), which is expressed in the proximal tubules, reflects the presence of tubular injury. Urinary excretion of podocalyxin (PCX), a glycoprotein prominently expressed on podocytes, is associated with podocyte injury. Our aims were to evaluate the utility of urinary L-FABP for the early detection of AKI and to examine whether podocyte injury is present in AKI patients using the biomarker of urinary PCX. Methods Patients admitted to the intensive care unit (ICU) were divided into the AKI group (n = 14) and non- AKI group (n = 11), according to the occurrence of AKI during hospitalization in the ICU. Changes in various biomarkers were evaluated. Results In the AKI group, elevation of urinary L-FABP level [maximum value of L-FABP, 199.0 (92.5–433.6) lg/g creatinine, median (25–75% interquartile range)], which reflects tubular injury (area under the curve 0.95, cut-off value 44.1 lg/g Cr), occurred between -30 and 0 h before the occurrence of AKI (i.e., the time at which serum creatinine peaked), and elevation of urinary PCX level [maximum value of PCX, 389.5 (267.0–501.0) lg/g creatinine; upper limit of reference value, 160 lg/g creatinine] occurred during the time of recovery from AKI when serum creatinine levels were decreasing between 34.0 and 72.0 h after the occurrence of AKI. Furthermore, a parameter with the primary large AUC for predicting the onset of AKI was urinary L-FABP. Conclusions Our study suggests that L-FABP is a useful biomarker for early detection of AKI and that podocyte injury was induced during the recovery phase of AKI.
Clin Exp Nephrol (2011) 15:220–225 Received: 27 May 2010 / Accepted: 10 November 2010 / Published online: 14 December 2010  Japanese Society of Nephrology 2010
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