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researchers generally agree that increased procalcitonin ( pct ) synthesis is detrimental to the host because a high concentration of this calcitonine precursor reflects the severity of sepsis and is predictive of mortality ( bossink et al 1999 ) .
procalcitonin , a 116 amino acid peptide , is produced physiologically by thyroid c - cells and cleaved by specific protease .
this prohormone is found at low concentration ( < 0.1 ng / ml ) in healthy subjects and at high concentration in critically ill patients with a particular infection or shock .
although the role and production site of the pct are unclear , this peptide induced by tumor necrosis factor alpha ( tnf- ) is currently considered to be an effective inflammatory marker used to monitor septic shock , pancreatic necrosis , or burn injuries ( venet et al 2002 ) . recently ,
our research has focused on how pct is implicated in acute childhood pyelonephritis ( ap ) , followed in 30% of cases by renal fibrosis ( rf ) leading to chronic sequelae ( such arterial hypertension gravidic toxemy ) .
renal fibrosis results from functional parenchyma disorder consecutive to renal cell apotosis , usually mediated by lipopolysaccharide ( lps)-induced tnf- production . during the infection of the renal parenchyma ,
the bacterial lps of the membranes induces the release of tnf , interleukin-1 ( il1 ) , and il6 ( oberhoffer et al 1999 ) .
pro - inflammatory tnf- activates nitric oxide ( no ) release , which is catalyzed by nitric oxide synthase ( nos ) in the presence of ca / calmodulin .
thus intracellular calcium concentration is crucial for ca / calmodulin complex formation and nos activation - inducing apoptosis ( arena et al 2002 ) .
in fact , cell viability and apoptosis depends on the spatiotemporal organization of cytosolic ca leading to transmembrane polarization magnitude ( lang et al 2005 ) . in this context , the renal scintigraphy using the polar tc - dmsa complex allows parenchyma exploration and then monitoring of acute and chronic lesions due to membrane adsorption attenuation ( belhadj - tahar et al 2000 ) .
the aim of this work is to clarify the physiological role of pct in ap by monitoring the early and later renal lesions ( edema / fibrosis ) using tc - dmsa parenchyma exploration .
this prospective study enrolled 183 children . all subjects exhibited clinical and biological infectious syndrome , with abdominal or lumbar pains and positive urine culture before antibiotherapy administration .
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 antibiothrapy suited to antibiogram . on admission c - reactive protein ( crp ) , phospholipase a2 , and procalcitonin were measured by the following methods : crp turbidimetric immunoassay ( olympus diagnostica , gmbh ) pla2 : fluometric assay ( sfm 25 kontron instruments ) and pct : luminescent immunoassay ( brahms diagnostica gmbh ) .
scintigraphy monitoring with intravascular tc - dmsa ( cis bio international , france ) was performed according to mackenzie protocol ( mackenzie 1996 ) on day 4 and nine months after admission in the presence of persistent abnormalities .
the scintigraphic parenchyma lesions were classified into 4 categories : absence ( stage 0 ) , unique and focal ( stage ii ) , multiple but unilateral ( stage ii ) , and bilateral ( stage iii ) .
at day 4 , 78% ( 107/136 ) had scintigraphic parenchyma renal alterations and 30% ( 17/57 ) presented renal fibrosis at 9th month . on admission , except for crp , both pla2 and pct were significantly higher in patients with early scintigrahic alteration ( pct : 7.85 vs 2.36 g / l and pla2 : 72.1 vs 29.9 iu / l ) ( table 1 ) .
during the infection of the renal parenchyma , the bacterial lps of the membranes induces the release of tnf , il1 , and il6 .
these cytokines are capable of evoking fever , inflammation syndrome , and cell apoptosis followed by fibrosis ( figure 1 ) . in the acute phase , il1 and il6 induce hepatic production of crp and pla2 leukocyte release .
pla2 is directly implied in the inflammatory process including the prostaglandins production from arachidonic acid in the presence of cyclooxygenase ( diaz 1996 ) . whereas , procalcitonin crp and pla2 have weak discriminative power for predictive renal fibrosis regarding to their auc values below 0.65 ( see figure 1 ) .
we hypothesized that pct down - regulates nitric oxide ( no ) release produced by no - synthase activated by tnf- pro - inflammatory cytokine ( figure 2 ) .
indeed , pct was paradoxically significantly lower in the presence of chronic renal fibrosis ( 4.19  1.03 vs 7.59  3.45 gl ) .
we observe a significant pct increase in the favorable progress ( recovery 7.55  4.02 vs aggravation 3.34  1.09 ) and no difference between recovery and improvement evolution .
these results suggest the protective effect of pct against apoptosis resulting from down - regulation of nitric oxide release catalyzed by no - synthase ( figure 1 ) and corroborate the previous in vitro observations ( hoffmann et al 2003 ) .
our study shows that pct plays key role in the renal parenchyma protection against cell apopotosis and fibrosis caused by acute pyelonephritis .
this finding constitutes a original approach in the comprehension of apoptosis paradigm that causes parenchyma fibrosis .
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 : intra - vascular 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 gl1 ) . 
 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 .