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Procalcitonin implication in renal cell apoptosis induced by acute pyelonephritis in children

Authors Hafid Belhadj-Tahar, Yvon Coulais, Mathieu Tafani, François Bouissou

Published Date August 2008 Volume 2008:1 Pages 17—20


Published 12 August 2008

Hafid Belhadj-Tahar1,2, Yvon Coulais2, Mathieu Tafani2, François Bouissou3

1Groupe Santé Recherche, Toulouse, France; 2EA 3033 Université Paul Sabatier III, Toulouse, France; 3Service de Néphrologie Pédiatrique, CHU Purpan, Toulouse, France

Abstract: The aim of this biomedical trial was to clarify the physiological role of procalcitonin (PCT) in renal parenchyma apoptosis and fibrosis caused by acute childhood pyelonephritis. This prospective study enrolled 183 children. All children were treated with bi-therapy according to the French consensus on acute pyelonephritis treatment dated November 16, 1990: intravascular administration of ceftriaxone 50 mg/kg/day and netromicine 7 mg/kg/day during the first 48 hours, followed by specific antibiotherapy suited to antibiogram. On admission, PCT, C-reactive protein, and phospholipase A2 were quantified in serum. Scintigraphy monitoring with 99mTc-DMSA was performed on day 4 and 9 months later, in the presence of persistent abnormalities. On day 4, 78% presented renal parenchyma alterations and 30% renal fibrosis 9 months after admission. Paradoxically, PCT level was significantly lower in the presence of renal fibrosis due to cell apoptosis (4.19 vs 7.59 µgL-1). A significant increase in PCT indicated favorable progress (recovery 7.55 vs aggravation 3.34) and no difference between recovery and improvement. This result suggests the protective effect of PCT against apoptosis by nitric oxide down-regulation.

Keywords: acute pyelonephritis, procalcitonin, apoptosis, fibrosis, technetium-DMSA

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