Renoprotective effects of long-term oral nicotine in a rat model of spontaneous proteinuria

Agarwal, Pramod Kumar; Born, Jacob van den; Goor, Harry van; Navis, Gerjan; Gans, Rijk O. B.; Bakker, Stephan J. L.

doi:10.1152/ajprenal.00507.2011

Cited by 10 publications

(12 citation statements)

References 52 publications

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“…In support of this hypothesis, COX-2 inhibition in vivo has been shown to reduce the pro-angiogenic and pro-atherosclerotic effects of nicotine[35]. Although the administration of nicotine resulted in worse kidney injury in the anti-Thy1 model of acute nephritis, in the Munich-Wistar-Frömter rat, a model of proteinuria-induced renal inflammation, the long-term administration of nicotine (20 to 100 μg/mL in the drinking water) resulted in improvements in proteinuria and renal function[72]. The plasma levels of cotinine varied from 139 ng/ml for the lower dose of nicotine to more than 500 ng/mL for the higher doses of nicotine.…”

Section: Biologic Effects Of Nicotinementioning

confidence: 99%

Nicotine signaling and progression of chronic kidney disease in smokers

Jain¹,

Jaimes²

2013

Biochemical Pharmacology

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The deleterious health effects of cigarette smoking are far reaching, and it remains the most important modifiable risk factor for improving overall morbidity and mortality. In addition to being a risk factor for cancer, cardiovascular disease and lung disease, there is strong evidence, both from human and animal studies, demonstrating a role for cigarette smoking in the progression of chronic kidney disease (CKD). Clinical studies have shown a strong correlation between cigarette smoking and worsening CKD in patients with diabetes, hypertension, polycystic kidney disease, and post kidney transplant. Nicotine, in addition to its role in the addictive properties of cigarette smoking, has other biological effects via activation of non-neuronal nicotinic acetylcholine receptors (nAChRs). Several nAChR subunits are expressed in the normal kidney and blockade of the α7-nAChR subunit ameliorates the effects of nicotine in animal models of CKD. Nicotine increases the severity of renal injury in animal models including acute kidney injury, diabetes, acute nephritis and subtotal nephrectomy. The renal effects of nicotine are also linked to increased generation of reactive oxygen species and activation of pro-fibrotic pathways. In humans, nicotine induces transitory increases in blood pressure accompanied by reductions in glomerular filtration rate and effective renal plasma flow. In summary, clinical and experimental evidence indicate that nicotine is at least in part responsible for the deleterious effects of cigarette smoking in the progression of CKD. The mechanisms involved are the subject of active investigation and may result in novel strategies to ameliorate the effects of cigarette smoking in CKD.

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Section: Biologic Effects Of Nicotinementioning

confidence: 99%

Nicotine signaling and progression of chronic kidney disease in smokers

Jain¹,

Jaimes²

2013

Biochemical Pharmacology

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“…The density of renal macrophages and myofibroblasts were reduced by nicotine and the level of renal inflammatory markers was also reduced. The authors suggested evaluating nicotine as a potential therapeutic option for treating proteinuric kidney disease [12]. A further study was performed to investigate the effect of nicotine in an experimental mouse model of injury to the skin and subsequent healing during the inflammatory phase of repair.…”

Section: Introductionmentioning

confidence: 99%

The Effects of Nicotine in the Treatment of Keloids: A Pilot Study

T¹

2017

MOJS

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To determine whether topically applied nicotine has an effect in preventing the return of keloids following excision. This would serve as a pilot study to indicate whether a beneficial effect was evident and further randomized control trials would be justified. Introduction BackgroundDermal keloids are an ongoing problem for genetically predisposed patients. Minor injuries may result in abnormal scarring. Surgical excision results in a return of keloids in 50%-80% of cases, and available treatment options, namely steroid injections, radiation therapy and silicone dressings, or pressure garments are not always feasible options. These methods are not hundred percent effective, cannot be used in all persons, have side effects (for instance pain on injection), and are not effective to treat large areas. Even dermal substitutes have resulted in keloid return [1,2]. The ideal treatment should be painless, have few side effects, should be useful in large areas (for instance post burn scars) and should be easy to use maximizing compliance. The cost of the intervention should render it affordable. Steroid injections are painful, cannot be used successfully in large areas or children and there are costs involved. Triamcinolone is not always available as other steroids are purchased in the primary care setting. Radiation cannot be used in large areas and various side effects are associated. It is not safe for use in the very young or fertile age groups. Pressure garments demonstrate inadequate results and compliance. Seldom is the right amount of pressure obtained and loose fitting garments are a problem. Dermal substitutes show high return rates at high cost [3]. The burden of keloids is an ongoing problem. Resources of staff, drugs and dressings are utilized repeatedly with unsatisfactory results for patients and staff alike. The psychological burden on patients, especially young people with keloids is tremendous, leading to loss of adequate social functioning. This in turn may lead to loss of productivity in the school or workplace [4,5]. The study sought to determine if a cream, painless and easy to apply, produced at very low cost may be the answer to this burden. Our hypothesis was that this cream may be applied to large areas post excision, leading to maintenance of normal skin texture. AbstractBackground: Dermal keloid scarring after minor injuries remain a problem in genetically predisposed individuals. Simple excision results in return of keloids within 4-6 months in more than 50%-80% of patients. Available treatment options, such as steroid injections and radiotherapy, are not a hundred percent effective and cannot be used in all persons. Nicotine influences wound healing by suppressing Vascular Endothelial Growth Factor (VEGF), thought to play a key role in keloid pathogenesis, as well as suppressing inflammatory processes and possibly Transforming Growth Factor Beta (TGF-Beta). The authors sought to investigate if a nicotine containing cream may influence return of keloids post excision.Methods: A prospective...

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“…Lower plasma cotinine levels may result in different effects and signals. In contrast to the adverse events of chronic nicotine, several studies reported anti-inflammatory effects of nicotinic acetylcholine receptor agonists in ulcerative colitis, sepsis, hypersensitivity pneumonitis, experimental type 1 diabetes and even in renal ischaemic-reperfusion injury [23][24][25]. In an experimental mouse model of lipopolysaccharide (LPS)-induced septic AKI, administration of nicotinic agonists significantly abrogated renal leucocyte infiltration and attenuated kidney injury.…”

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confidence: 99%

“…Long-term oral nicotine administration showed a preserved kidney function, a reduced proteinuria, a reduced renal inflammation and protected progression of renal structural damage in Munich Wistar Frömter rats with proteinuria. However, these renoprotective effects may be limited to the specific animal models in which they are described [23].…”

mentioning

confidence: 99%