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NDT Advance Access published online on January 26, 2008
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm937
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© The Author [2008]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org


Elevated urinary plasmin activity resistant to {alpha}2-antiplasmin in acute poststreptococcal glomerulonephritis

Takashi Oda1, Kikuko Tamura2, Nobuyuki Yoshizawa3, Tetsuzo Sugisaki4, Koichi Matsumoto5, Motoshi Hattori6, Toshihiro Sawai7, Tamehachi Namikoshi1, Muneharu Yamada1, Yuichi Kikuchi1, Shigenobu Suzuki1 and Soichiro Miura1

1 Department of Internal Medicine, National Defense Medical College, Saitama, Japan 2 Department of Pediatrics, National Hospital Organization, Nishisaitama Chuo National Hospital, Saitama, Japan 3 Department of Medicine, Hirose Hospital, Saitama, Japan 4 Department of Nephrology, Showa University School of Medicine, Tokyo, Japan 5 Department of Nephrology, Nihon University School of Medicine, Tokyo, Japan 6 Department of Pediatric Nephrology, Tokyo Women's Medical College, Tokyo, Japan 7 Department of Pediatrics, Shiga University of Medical Science, Shiga, Japan

Correspondence and offprint requests to: Takashi Oda, Department of Internal Medicine, National Defense Medical College, 3-2 Namiki, Tokorozawa-shi, Saitama 359-8513, Japan. Tel: +81-4-2995-1609; Fax: +81-4-2996-5201; E-mail: takashio{at}ndmc.ac.jp



  Abstract

Background. A pathogenic role of intraglomerular plasmin bound to nephritogenic antigen (nephritis-associated plasmin receptor, NAPlr) and resistant to physiologic inhibitors such as {alpha}2-antiplasmin ({alpha}2-AP) has recently been proposed in acute poststreptococcal glomerulonephritis (APSGN). To confirm this concept, we analysed the urinary profile of plasmin cascade in APSGN patients.

Methods. Urine samples from 10 patients with APSGN, 12 patients with IgA nephropathy (IgAN), 10 patients with streptococcal infection without nephritis (SI) and 10 healthy control subjects were analysed. The {alpha}2-AP-resistant plasmin activity was assessed by a chromogenic assay after {alpha}2-AP was added to each urine sample. Urinary plasminogen activator (PA) and plasmin were further analysed by polyacrylamide gel zymography. Urinary NAPlr was assessed by western blot analysis in selected samples.

Results. Urinary {alpha}2-AP-resistant plasmin activity corrected for creatinine concentration (units/g · creatinine) was significantly higher in patients with APSGN (2.99 ± 0.63) than in patients with IgAN (1.02 ± 0.20, P < 0.01), SI (0.79 ± 0.17, P < 0.01), or in healthy control subjects (0.73 ± 0.18, P < 0.01). This tendency was confirmed by casein gel zymography. However urinary PA activity assessed by plasminogen–casein gel zymography did not differ between groups. NAPlr was detected in the urine of APSGN patients.

Conclusions. We found elevated urinary plasmin activity resistant to {alpha}2-AP, which may be due to urinary excretion of NAPlr in patients with APSGN. This result supports the pathogenic role of the NAPlr–plasmin complex in the development of APSGN. Furthermore, {alpha}2-AP-resistant urinary plasmin activity may be useful as a diagnostic marker for APSGN.

Keywords: acute poststeptococcal glomerulonephritis; {alpha}2-antiplasmin; nephritis-associated plasmin receptor; plasmin; zymography

Received for publication: 13. 5.07
Accepted in revised form: 18.12.07


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