2014
DOI: 10.1038/pr.2014.148
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Maternal nicotine exposure during gestation and lactation induces kidney injury and fibrosis in rat offspring

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Cited by 26 publications
(25 citation statements)
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“…While there was high nicotine exposure as evidenced by the increased cotinine levels, the amount of other toxins in the condensate may have been less than in our model. A more recent study also found that smoke exposure in utero has pro-fibrotic influences on offspring kidneys (Chen et al, 2015). Although we did not detect any renal histological changes at any time point (data not shown) nor an increase in serum creatinine, we propose that our findings of mitochondrial alterations at birth and adulthood may put offspring at increased risk for renal pathology especially in the setting of additional insults, such as sepsis or toxins.…”
Section: Discussioncontrasting
confidence: 41%
“…While there was high nicotine exposure as evidenced by the increased cotinine levels, the amount of other toxins in the condensate may have been less than in our model. A more recent study also found that smoke exposure in utero has pro-fibrotic influences on offspring kidneys (Chen et al, 2015). Although we did not detect any renal histological changes at any time point (data not shown) nor an increase in serum creatinine, we propose that our findings of mitochondrial alterations at birth and adulthood may put offspring at increased risk for renal pathology especially in the setting of additional insults, such as sepsis or toxins.…”
Section: Discussioncontrasting
confidence: 41%
“…In the present studies, due to potential differences in susceptibility of adverse in utero conditions between each sibling within a litter, individual offspring were used as an experimental unit (Chen et al 2015; Ngo et al 2014). Effects on birth weights, litter size, organ weights, area under the curve, hormone concentrations, differences in mRNA expression, and open arm entries in the EPM were analyzed using a one-way ANOVA with Proc GLM in SAS (version 9.2; SAS Institute, Cary, NC, USA).…”
Section: Methodsmentioning
confidence: 99%
“…All these observations point out that chronic profibrotic or vascular effects rather than immunological effects might play a role in previous smokers. In rats, nicotine stimulates the epithelial–mesenchymal transition (EMT) and connective tissue growth factor (CTGF) expression in kidney epithelium and induces neonatal kidney fibrosis after exposure to pregnant animals . In line with this, despite comparable kidney function, native kidney biopsies of current or historical smokers show a higher degree of glomerulosclerosis and arteriolar hyalinosis than in people who never smoked .…”
Section: Discussionmentioning
confidence: 84%
“…In mice, chronic nicotine exposure potentiates acute kidney injury by potentiating ischaemia/reperfusion‐related oxidative stress . Other proposed mechanisms include stimulation of renal nicotinic acetylcholine receptors and the renin–angiotensin system, increased sympathetic activity and finally direct hemodynamic effects leading to reduced glomerular filtration rate and renal plasma flow .…”
Section: Introductionmentioning
confidence: 99%