Cigarette Smoking and Other Inhaled Toxins in Anti-GBM Disease

Herody, M.; Duvic, C.; Lh, Noël; Nédélec, G; Grünfeld, Jean‐Pierre

doi:10.1159/000060046

Cited by 10 publications

(5 citation statements)

References 13 publications

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“…A causative relationship between active smoking and Goodpasture’s syndrome has been proposed in several previous studies based on the fact that a high proportion of patients with lung hemorrhage were active smokers. They suggested the possibility that cigarette smoke could increase the permeability of lung capillaries to allow preformed circulating antibodies to reach the alveolar basement membrane (ABM), or that smoking and other inhaled toxins could alternatively change antigenic determinants in the ABM, inducing formation of anti-ABM antibodies or enabling them to cross-react with anti-glomerular basement membrane (anti-GBM) antibodies [ 26 , 27 ]. Moreover, similar to the former mechanism, some preclinical studies have shown that a high concentration of inspired oxygen or hydrocarbon fumes can induce permeability changes in lung capillaries [ 28 – 30 ].…”

Section: Discussionmentioning

confidence: 99%

Clinical significance of cigarette smoking and dust exposure in pulmonary alveolar proteinosis: a Korean national survey

et al. 2017

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BackgroundThis study aimed to investigate clinical characteristics of Korean PAP patients and to examine the potential risk factors of PAP.MethodsWe retrospectively reviewed medical records of 78 Korean PAP patients diagnosed between 1993 and 2014. Patients were classified into two groups according to the presence/absence of treatment (lavage). Clinical and laboratory features were compared between the two groups.ResultsOf the total 78 PAP patients, 60% were male and median age at diagnosis was 47.5 years. Fifty three percent were ever smokers (median 22 pack-years) and 48% had a history of dust exposure (metal 26.5%, stone or sand 20.6%, chemical or paint 17.7%, farming dust 14.7%, diesel 14.7%, textile 2.9%, and wood 2.9%). A history of cigarette smoking or dust exposure was present in 70.5% of the total PAP patients, with 23% having both of them. Patients who underwent lavage (n = 38) presented symptoms more frequently (38/38 [100%] vs. 24/40 [60%], P < 0.001) and had significantly lower PaO2 and DLCO with higher D(A-a)O2 at the onset of disease than those without lavage (n = 40) (P = 0.006, P < 0.001, and P = 0.036, respectively). Correspondingly, the distribution of disease severity score (DSS) differed significantly between the two groups (P = 0.001). Based on these, when the total patients were categorized according to DSS (low DSS [DSS 1–2] vs. high DSS [DSS 3–5]), smoking status differed significantly between the two groups with the proportion of current smokers significantly higher in the high DSS group (11/22 [50%] vs. 7/39 [17.9%], P = 0.008). Furthermore, current smokers had meaningfully higher DSS and serum CEA levels than non-current smokers (P = 0.011 and P = 0.031), whereas no difference was found between smokers and non-smokers. Regarding type of exposed dust, farming dust was significantly associated with more severe form of PAP (P = 0.004).ConclusionA considerable proportion of PAP patients had a history of cigarette smoking and/or dust exposure, suggestive of their possible roles in the development of PAP. Active cigarette smoking at the onset of PAP is associated with the severity of PAP.

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Section: Discussionmentioning

confidence: 99%

Clinical significance of cigarette smoking and dust exposure in pulmonary alveolar proteinosis: a Korean national survey

et al. 2017

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“…Second, the risk of pulmonary hemorrhage in anti-glomerular basement membrane (GBM)-disease, i.e. for the Goodpasture syndrome, is highly increased in smokers [ 95 , 96 ].…”

Section: Adverse Renal Effects Of Smoking In Patients With Renal Disementioning

confidence: 99%

Cigarette smoking: an important renal risk factor – far beyond carcinogenesis

Orth¹

2003

Tob. Induced Dis.

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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 clearly shown that the risk for high-normal urinary albumin excretion and microalbuminuria is increased in smoking compared to non-smoking subjects of the general population. Data from the Multiple Risk Factor Intervention Trial (MRFIT) indicate that at least in males, 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 show to reduce the rate of progression of renal failure both in patients with renal disease or a renal transplant. The mechanisms of smoking-induced renal damage are only partly understood and comprise acute hemodynamic (e.g., increase in blood pressure 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 mellitus on hemodialysis is abysmal. In the present review article the current state of knowledge about the renal risks of smoking is reviewed. It is the aim of the article to point out that smoking not only increases the risk of renal cell carcinoma or uroepithelial cell carcinoma, but also the risk of a faster decline of renal function. The latter is a relatively new negative aspect which has not been widely recognized.

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“…Other pulmonary symptoms may include cough and dyspnea, and chest X-ray discloses pulmonary infiltrates. Patients with known lung injury due to smoking, cocaine abuse, or hydrocarbon exposure will have more extensive pulmonary damage [12]. Renal manifestations include acute renal failure with urinary findings of hematuria, nonnephrotic range proteinuria, dysmorphic red cells, and red cell and granular casts.…”

Section: Discussionmentioning

confidence: 99%

Crescentic Glomerulonephritis with Anti-GBM and p-ANCA Antibodies

Javed

Vohra

2012

Case Reports in Nephrology

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We are presenting a case of renal failure with anti-GBM and p-ANCA antibodies positive. Patients with dual antibodies are considered to be a vasculitis-variant of anti-GBM antibody nephritis. These patients may have atypical presentation and it may delay diagnosis and treatment. Recurrence rate is higher in these patients. We reviewed the literature of cases and studies on cresenteric glomerulonephritis with anti-GBM and p-ANCA positive patients. We recommend that patients suspected with pulmonary-renal syndrome should be checked for anti-GBM and p-ANCA antibodies, should undergo renal biopsy and should should have close long term follow up to watch for recurrence.

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Cigarette Smoking and Other Inhaled Toxins in Anti-GBM Disease

Cited by 10 publications

References 13 publications

Clinical significance of cigarette smoking and dust exposure in pulmonary alveolar proteinosis: a Korean national survey

Clinical significance of cigarette smoking and dust exposure in pulmonary alveolar proteinosis: a Korean national survey

Cigarette smoking: an important renal risk factor – far beyond carcinogenesis

Crescentic Glomerulonephritis with Anti-GBM and p-ANCA Antibodies

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