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2017 ; 9
(5
): 2548-2566
Nephropedia Template TP
gab.com Text
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English Wikipedia
Impact of impaired cardiac function on the progression of chronic kidney
disease---role of pharmacomodulation of valsartan
#MMPMID28560004
Yang CC
; Yip HK
; Chen KH
; Sun CK
; Chen YT
; Chai HT
; Sung PH
; Chiang HJ
; Ko SF
; Chung SY
; Chen CH
; Lin KC
; Lin PY
; Sheu JJ
Am J Transl Res
2017[]; 9
(5
): 2548-2566
PMID28560004
show ga
Although chronic kidney disease (CKD) is known to aggravate cardiovascular
disease in the setting of cardiorenal syndrome (CRS), the impact of impaired
cardiac function on the progression of CKD has seldom been reported. This study
tested the impact of acute myocardial infarction on a rodent CKD model and the
therapeutic effect of valsartan in this setting. Adult male Sprague-Dawley rats
(n = 50) equally divided into group 1 (sham control), group 2 (CKD induced by 5/6
nephrectomy), group 3 (AMI by ligation of left coronary artery), group 4
(CKD+AMI), group 5 (CKD+AMI+valsartan, orally 10 mg/kg/day). By day 60, kidney
injury score, creatinine levels, and ratio of urine to creatinine were highest in
group 4 and lowest in group 1, significantly higher in group 4 than those in
groups 2 and 5, and significantly higher in group 5 than those in group 2 (all p
< 0.001). Protein expressions of inflammation (IL-1?/MMP-9), oxidative stress
(NOX-1/NOX-2/oxidized protein, angiotensin-II receptor), apoptosis (Bax, cleaved
caspase-3/PARP), fibrosis (Smad3/TGF-?), and kidney injured (KIM-1/FSP-1) markers
showed an identical pattern, whereas anti-fibrosis (Smad5/BMP-2) indices
exhibited an opposite pattern compared to that of creatinine level among all
groups (all p < 0.01). Cellular expressions of inflammation (CD14/CD68),
DNA-damage (?-H2AX, CD90/XRCC1) and proximal-renal tubule (KIM-1) biomarkers
displayed an identical pattern, whereas podocyte-integrity markers
(podocin/ZO-1/p-cadherin/synaptopodin) showed a pattern opposite to that of
creatinine level among all groups (all p < 0.001). In a rodent CKD setting, renal
function impairment and parenchymal damage further deteriorated after AMI but
were suppressed following valsartan treatment.
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