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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Physiol+Renal+Physiol
2013 ; 304
(11
): F1358-65
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C-reactive protein exacerbates renal ischemia-reperfusion injury
#MMPMID23535585
Pegues MA
; McCrory MA
; Zarjou A
; Szalai AJ
Am J Physiol Renal Physiol
2013[Jun]; 304
(11
): F1358-65
PMID23535585
show ga
Renal ischemia-reperfusion injury (IRI) is a common cause of acute kidney injury
(AKI), occurring with hypotension and cardiovascular surgery and inevitably
during kidney transplantation. Mortality from AKI is high due to incomplete
knowledge of the pathogenesis of IRI and the lack of an effective therapy.
Inflammation accompanies IRI and increases the blood level of C-reactive protein
(CRP), a biomarker of worsened outcomes in AKI. To test if CRP is causal in AKI
we subjected wild-type mice (WT) and human CRP transgenic mice (CRPtg) to
bilateral renal IRI (both pedicles clamped for 30 min at 37°C then reperfused for
24 h). Serum human CRP level was increased approximately sixfold after IRI in
CRPtg (10.62 ± 1.31 ?g/ml at baseline vs. 72.01 ± 9.41 ?g/ml at 24 h) but was not
elevated by sham surgery wherein kidneys were manipulated but not clamped.
Compared with WT, serum creatinine, urine albumin, and histological evidence of
kidney damage were increased after IRI in CRPtg mice. RT-PCR analysis of mRNA
isolated from whole kidneys of CRPtg and WT subjected to IRI revealed that in
CRPtg kidneys 1) upregulation of markers of macrophage classical activation (M1
markers) was blunted, 2) downregulation of markers of macrophage alternative
activation (M2 markers) was more robust, and 3) expression of the activating
receptor Fc?RI was increased. Our finding that CRP exacerbates IRI-induced AKI,
perhaps by shifting the balance of macrophage activation and Fc?R expression
towards a detrimental portfolio, might make CRP a promising therapeutic target
for the treatment of AKI.
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