Urinary heat shock protein-72 excretion in clinical and experimental renal ischemia

Mueller, Thomas
Bidmon, Bettina
Pichler, Patrick
Arbeiter, Klaus
Ruffingshofer, Dagmar
VanWhy, Scott K.
Aufricht, Christoph

¹Department of Pediatrics, Kinderdialyse, AKH Wien, Waehringer Guertel 18-20, 1090 Vienna, Austria
²Department of Pediatrics, Medical College of Wisconsin, 8701 W. Watertown Plank Road, Milwaukee, WI 53226-4901, USA
³Universitaetsklinik fuer Kinder und Jugendheilkunde, Kinderdialyse, AKH Wien, Waehringer Guertel 18-20, 1090 Vienna, Austria

Received: 29 May 2002 / Revised: 3 October 2002 / Accepted: 8 October 2002 / Published online: 19 December 2002

Thomas Mueller and Bettina Bidmon contributed equally to the study

Tel.: +43-1-404003257, Fax: +43-1-404003189

Pediatric Nephrology 18(2):p 97-99, 2003. | DOI: 10.1007/s00467-002-1037-5

Abstract

Renal ischemia not only causes injury but also induces repair mechanisms, such as the cellular induction of the 72-kilodalton heat shock protein HSP-72. The aim of this study was to determine whether HSP-72 is excreted in urine after ischemic renal injury. The first urine of six pediatric allograft recipients was examined for proteinuria and urinary HSP-72 excretion. Sprague-Dawley rats were treated with renal ischemia or hyperthermia and renal cortex and urinary HSP-72 levels were determined. HSP-72 was excreted in the first urine of renal allografts. In rats, renal HSP-72 was induced both by renal ischemia or hyperthermia. However, only renal ischemia resulted in urinary excretion of HSP-72. Urinary excretion of HSP-72 indicates an increased renal stress response and loss of tubular cell integrity after clinical and experimental renal ischemia.