Pharmacokinetics of nicotine in kidney failure

Molander, Lars; Hansson, Anna; Lunell, Erik; Alainentalo, Lisbeth; Hoffmann, Mikael; Larsson, Robert

doi:10.1067/mcp.2000.109006

Cited by 46 publications

(36 citation statements)

References 28 publications

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“…According to the manufacturer, bupropion does not accumulate in renal failure. In contrast, nicotine accumulates in renal failure (58), which has to be taken into consideration when treating patients with nicotine replacement therapy. Unfortunately, to date, no controlled information on the success of a modern smoking cessation strategy in renal patients is available.…”

Section: Resultsmentioning

confidence: 99%

Effects of Smoking on Systemic and Intrarenal Hemodynamics

Orth¹

2004

Journal of the American Society of Nephrology

117

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Abstract. In recent years, it has become apparent that smoking has a negative impact on renal function, being one of the most important remediable renal risk factors. It has been shown clearly that the risk for high-normal urinary albumin excretion and microalbuminuria is increased in smoking compared with nonsmoking subjects of the general population. Data from the Multiple Risk Factor Intervention Trial indicate that at least in men, smoking increases the risk to reach end-stage renal failure. Smoking is particularly "nephrotoxic" in older subjects, subjects with essential hypertension, and patients with preexisting renal disease. Of interest, the magnitude of the adverse renal effect of smoking seems to be independent of the underlying renal disease. Death-censored renal graft survival is decreased in smokers, indicating that smoking also damages the renal transplant. Cessation of smoking has been shown to reduce the rate of progression of renal failure both in patients with renal disease and in patients with a renal transplant. The mechanisms of smoking-induced renal damage are only partly understood and comprise acute hemodynamic (e.g., increase in BP and presumably intraglomerular pressure) and chronic effects (e.g., endothelial cell dysfunction). Renal failure per se leads to an increased cardiovascular risk. The latter is further aggravated by smoking. Particularly, survival of smokers with diabetes on hemodialysis is abysmal.Smoking has profound effects on systemic and intrarenal hemodynamics. A smoking-induced increase in BP and heart rate had first been reported in 1907 by Hesse (1). Although others had even found an association between smoking and renal damage (2), this has only been confirmed in 1979 in patients with type 1 diabetes (3), and it was not until 1997 (4) that nephrologists became aware of smoking being a major renal risk factor.The effects of smoking on BP were a matter of debate in the 1980s. Large epidemiologic studies had found that smokers are not more frequently hypertensive than nonsmokers (5). These studies, however, did not perform ambulatory BP measurement, which besides that smokers weigh less than their more obese nonsmoking counterparts explains these false-negative results (6). More recent studies using ambulatory BP measurement clearly document that smokers have higher BP than nonsmokers, i.e. an increase of approximately 3 to 12 mmHg in mean arterial pressure (MAP). This has been shown in several studies including healthy subjects, hypertensive subjects, patients with type 1 and type 2 diabetes, and patients with primary renal disease (for review, see reference 7). With an increase of 12 mmHg in MAP, patients with renal disease seem to be particularly prone to the effect of smoking on BP. There is some evidence, at least in hypertensive patients, that elderly subjects (Ͼ50 to 60 yr of age) are more affected than younger subjects (8,9). A recent population-based cross-sectional study investigated 12,417 men who were screened for a routine check-up in France (9). The preval...

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Section: Resultsmentioning

confidence: 99%

Effects of Smoking on Systemic and Intrarenal Hemodynamics

Orth¹

2004

Journal of the American Society of Nephrology

117

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“…[7] These "RLnI" reagents have been investigatedi nanumber of organic and inorganic transformations during the past years. [5,6,[8][9][10] Due to the low thermal stability of the LnÀC s-bond, [11] isolation of pseudo-Grignard products derived from the iodides has been a challenge, but has been assisted by the use of bulky ligands. Only af ew complexes have been prepared and structurally characterised.…”

Section: Introductionmentioning

confidence: 99%

Lanthanoid Pseudo‐Grignard Reagents: A Major Untapped Resource

Ali

Deacon

Junk

et al. 2017

Chemistry A European J

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Pseudo-Grignardr eagents PhLnI (Ln = Yb, Eu), readily prepared by the oxidative addition of iodobenzene to ytterbium or europium metal at À78 8Cint etrahydrofuran (THF) or 1,2-dimethoxyethane (DME), react with ar ange of bulky N,N'-bis(aryl)formamidines to generate an extensive series of Ln II or more rarely Ln III complexes,n amely [Eu(Dipp-, and [Yb(XylForm) 2 I(dme)]·dme (7b){ (Form = ArNCHNAr;X ylForm (Ar = 2,6-Me 2 C 6 H 3 ), MesForm (Ar = 2,4,6-Me 3 C 6 H 2 ), DippForm (Ar = 2,6-iPr 2 C 6 H 3 )}. Reaction of PhEuI and MesFormH in DME consistently gave 2, and reactionw ith XylFormH in THF gave 4.E uropium complexes 1 and 3a are seven-coordinate divalent monomers, whilst 3b is as even-coordinate dme-bridged polymer.C omplex 5a of the smaller Yb II is as ix-coordinate monomer,b ut the related 6 and 7a are six-coordinatei odide-bridged dimers. 4 is at rivalent seven-coordinate hydroxide-bridged dimer,w hereas complexes 5b and 7b are seven-coordinate monomeric Yb III derivatives. Ac haracteristic structural feature is that iodide ligands are cisoid to the formamidinate ligand.T oi llustrate the synthetic scope of the pseudoGrignardr eagents,[ Yb(Ph 2 pz)I(thf) 4 ]( Ph 2 pz = 3,5-diphenylpyrazolate) was oxidised with 1,2-diiodoethane to afford seven-coordinate monomeric pyrazolato-ytterbium (III)

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“…Although nicotine is a desirable biomarker for smoking status, there are limitations to its utility: a short half-life, complex measurement, and variability in plasma levels (which might be higher in subjects with impaired kidney excretion function) (Molander et al, 2000). Cotinine, a metabolite of nicotine, can be measured in saliva, plasma, and urine.…”

Section: Introductionmentioning

confidence: 99%

Can Urinary Cotinine Predict Nicotine Dependence Level in Smokers?

Jung

Kim²,

Son³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Background: Although nicotine dependence plays a role as a main barrier for smoking cessation, there is still a lack of solid evidence on the validity of biomarkers to determine nicotine dependence in clinical settings. This study aimed to investigate whether urinary cotinine levels could reflect the severity of nicotine dependence in active smokers. Materials and Methods: Data regarding general characteristics and smoking status was collected using a self-administered smoking questionnaire. The Fagerström test for nicotine dependence (FTND) was used to determine nicotine dependence of the participants, and a total of 381 participants were classified into 3 groups of nicotine dependence: low (n=205, 53.8%), moderate (n=127, 33.3%), and high dependence groups (n=49, 12.9%). Stepwise multiple linear regression model and receiver operating characteristic (ROC) curves analyses were used to determine the validity of urinary cotinine for high nicotine dependence. Results: In correlation analysis, urinary cotinine levels increased with FTND score (r=0.567, P<0.001). ROC curves analysis showed that urinary cotinine levels predicted the high-dependence group with reasonable accuracy (optimal cut-off value=1,000 ng/mL; AUC=0.82; P<0.001; sensitivity=71.4%; specificity=74.4%). In stepwise multiple regression analysis, the total smoking period (β=0.042, P=0.001) and urinary cotinine levels (β=0.234, P<0.001) were positively associated with nicotine dependence, whereas an inverse association was observed between highest education levels (>16 years) and nicotine dependence (β=-0.573, P=0.034). Conclusions: The results of this study support the validity of using urinary cotinine levels for assessment of nicotine dependence in active smokers.

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Pharmacokinetics of nicotine in kidney failure

Abstract: Progressive kidney failure is associated with a gradual decrease of renal and nonrenal elimination of nicotine.

Cited by 46 publications

References 28 publications

Effects of Smoking on Systemic and Intrarenal Hemodynamics

Effects of Smoking on Systemic and Intrarenal Hemodynamics

Lanthanoid Pseudo‐Grignard Reagents: A Major Untapped Resource

Can Urinary Cotinine Predict Nicotine Dependence Level in Smokers?

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