Kidney Function and Tobacco Smoke Exposure in US Adolescents

García‐Esquinas, Esther; Loeffler, Lauren F.; Weaver, Virginia M.; Fadrowski, Jeffrey J.; Navas‐Acien, Ana

doi:10.1542/peds.2012-3201

Cited by 56 publications

(43 citation statements)

References 55 publications

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“…In a study investigating risk factors for CKD in over 3500 CKD patients, the Chronic Renal Insufficiency Cohort (CRIC) study also demonstrated a moderate association between cigarette smoking and lower eGFR[13]. Similar deleterious results have been noted in a study evaluating the effects of smoking, as well as second hand cigarette smoking exposure among adolescents[14]. Median (IQR) eGFR in participants unexposed to tobacco was 99.1 (88.1–111.0) mL/minute per 1.73 m2 compared with 96.8 (85.0–109.0) mL/minute per 1.73 m2 among participants exposed to secondhand smoke and 90.1 (81.3–100.9) mL/minute per 1.73 m2 among active smokers.…”

Section: Role Of Cigarette Smoking In Human Subjectsmentioning

confidence: 76%

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: Role Of Cigarette Smoking In Human Subjectsmentioning

confidence: 76%

Nicotine signaling and progression of chronic kidney disease in smokers

Jain¹,

Jaimes²

2013

Biochemical Pharmacology

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“…[164][165][166][167] Cigarette Smoking Both active and passive cigarette smoking have been found to be independent risk factors for the de novo development of CKD in healthy subjects. [168][169][170][171][172][173][174][175][176] Cigarette smoking is also a major risk factor for the initial development or worsening of preexisting CKD in patients with human immunodeficiency virus infection, chronic obstructive pulmonary disease, diabetes, diabetic nephropathy, hypertension, autosomal polycystic kidney disease, primary glomerulopathies, lupus nephritis, and those who are obese or who have undergone a lung transplant. [177][178][179][180][181][182][183][184][185][186][187] In addition, smoking by either the donor or recipient has been shown to adversely influence the function and survival of transplanted kidneys and overall patient survival.…”

Section: Hypertensionmentioning

confidence: 99%

“…[177][178][179][180][181][182][183][184][185][186][187] In addition, smoking by either the donor or recipient has been shown to adversely influence the function and survival of transplanted kidneys and overall patient survival. 170,171,188,189 Allograft survival and function both worsen with increasing pack-years smoked. The number of cigarettes smoked correlates directly with the severity of renal dysfunction and the likelihood that either CKD will develop or a kidney allograft will fail.…”

Section: Hypertensionmentioning

confidence: 99%

Hypoxia: The Force that Drives Chronic Kidney Disease

Colgan

Shelley

2016

Clinical Medicine & Research

129

111

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In the United States the prevalence of end-stage renal disease (ESRD) reached epidemic proportions in 2012 with over 600,000 patients being treated. The rates of ESRD among the elderly are disproportionally high. Consequently, as life expectancy increases and the baby-boom generation reaches retirement age, the already heavy burden imposed by ESRD on the US health care system is set to increase dramatically. ESRD represents the terminal stage of chronic kidney disease (CKD). A large body of evidence indicating that CKD is driven by renal tissue hypoxia has led to the development of therapeutic strategies that increase kidney oxygenation and the contention that chronic hypoxia is the final common pathway to end-stage renal failure. Numerous studies have demonstrated that one of the most potent means by which hypoxic conditions within the kidney produce CKD is by inducing a sustained inflammatory attack by infiltrating leukocytes. Indispensable to this attack is the acquisition by leukocytes of an adhesive phenotype. It was thought that this process resulted exclusively from leukocytes responding to cytokines released from ischemic renal endothelium. However, recently it has been demonstrated that leukocytes also become activated independent of the hypoxic response of endothelial cells. It was found that this endothelium-independent mechanism involves leukocytes directly sensing hypoxia and responding by transcriptional induction of the genes that encode the β2-integrin family of adhesion molecules. This induction likely maintains the long-term inflammation by which hypoxia drives the pathogenesis of CKD. Consequently, targeting these transcriptional mechanisms would appear to represent a promising new therapeutic strategy.

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“…, and kidney and endocrine dysfunction (García-Esquinas et al, 2013) in young children. Indeed, it has been reported that the annual excess mortality in children aged 5 years or younger due to SHS exposure may be higher than that due to all other causes (Florescu et al, 2009).…”

mentioning

confidence: 99%