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

Belhadj-Tahar H, Coulais Y, Tafani M, Bouissou F - Infect Drug Resist (2008)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Groupe Santé Recherche, 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: 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 (99m)Tc-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.

No MeSH data available.


Related in: MedlinePlus

Physiopathology of pyelonephritis.Abbreviations: IL, interleukin; NO, nitric oxide; NOS, NO synthase; PCT, procalcitonin; PLA2, phospholipase A2; CRP, C-reactive protein; FGF, fibroblast growth factor; TNF, tumor necrosis factor.
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f2-idr-1-017: Physiopathology of pyelonephritis.Abbreviations: IL, interleukin; NO, nitric oxide; NOS, NO synthase; PCT, procalcitonin; PLA2, phospholipase A2; CRP, C-reactive protein; FGF, fibroblast growth factor; TNF, tumor necrosis factor.

Mentions: We hypothesized that PCT down-regulates nitric oxide (NO) release produced by NO-Synthase activated by TNF-α 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 μgL−1). 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).


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

Belhadj-Tahar H, Coulais Y, Tafani M, Bouissou F - Infect Drug Resist (2008)

Physiopathology of pyelonephritis.Abbreviations: IL, interleukin; NO, nitric oxide; NOS, NO synthase; PCT, procalcitonin; PLA2, phospholipase A2; CRP, C-reactive protein; FGF, fibroblast growth factor; TNF, tumor necrosis factor.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3108721&req=5

f2-idr-1-017: Physiopathology of pyelonephritis.Abbreviations: IL, interleukin; NO, nitric oxide; NOS, NO synthase; PCT, procalcitonin; PLA2, phospholipase A2; CRP, C-reactive protein; FGF, fibroblast growth factor; TNF, tumor necrosis factor.
Mentions: We hypothesized that PCT down-regulates nitric oxide (NO) release produced by NO-Synthase activated by TNF-α 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 μgL−1). 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).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Groupe Santé Recherche, 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: 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 (99m)Tc-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.

No MeSH data available.


Related in: MedlinePlus