Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients
Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolle...
Ausführliche Beschreibung
Autor*in: |
Perticone, Maria [verfasserIn] |
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E-Artikel |
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Sprache: |
Englisch |
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2022 |
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Anmerkung: |
© The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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Übergeordnetes Werk: |
Enthalten in: Internal and emergency medicine - Milan : Springer Milan, 2006, 18(2022), 1 vom: 18. Okt., Seite 105-112 |
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Übergeordnetes Werk: |
volume:18 ; year:2022 ; number:1 ; day:18 ; month:10 ; pages:105-112 |
Links: |
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DOI / URN: |
10.1007/s11739-022-03123-5 |
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Katalog-ID: |
SPR049166271 |
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520 | |a Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions. | ||
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700 | 1 | |a Andreozzi, Francesco |4 aut | |
700 | 1 | |a Sesti, Giorgio |4 aut | |
700 | 1 | |a Perticone, Francesco |4 aut | |
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10.1007/s11739-022-03123-5 doi (DE-627)SPR049166271 (SPR)s11739-022-03123-5-e DE-627 ger DE-627 rakwb eng Perticone, Maria verfasserin aut Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions. COPD (dpeaa)DE-He213 Renal function (dpeaa)DE-He213 e-GFR (dpeaa)DE-He213 Arterial hypertension (dpeaa)DE-He213 Maio, Raffaele aut Tripepi, Giovanni aut Abelardo, Domenico aut Andreucci, Michele aut Imbalzano, Egidio aut Toscani, Alfredo Francesco aut Sciacqua, Angela aut Andreozzi, Francesco aut Sesti, Giorgio aut Perticone, Francesco aut Enthalten in Internal and emergency medicine Milan : Springer Milan, 2006 18(2022), 1 vom: 18. Okt., Seite 105-112 (DE-627)538216425 (DE-600)2378342-4 1970-9366 nnns volume:18 year:2022 number:1 day:18 month:10 pages:105-112 https://dx.doi.org/10.1007/s11739-022-03123-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 18 2022 1 18 10 105-112 |
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10.1007/s11739-022-03123-5 doi (DE-627)SPR049166271 (SPR)s11739-022-03123-5-e DE-627 ger DE-627 rakwb eng Perticone, Maria verfasserin aut Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions. COPD (dpeaa)DE-He213 Renal function (dpeaa)DE-He213 e-GFR (dpeaa)DE-He213 Arterial hypertension (dpeaa)DE-He213 Maio, Raffaele aut Tripepi, Giovanni aut Abelardo, Domenico aut Andreucci, Michele aut Imbalzano, Egidio aut Toscani, Alfredo Francesco aut Sciacqua, Angela aut Andreozzi, Francesco aut Sesti, Giorgio aut Perticone, Francesco aut Enthalten in Internal and emergency medicine Milan : Springer Milan, 2006 18(2022), 1 vom: 18. Okt., Seite 105-112 (DE-627)538216425 (DE-600)2378342-4 1970-9366 nnns volume:18 year:2022 number:1 day:18 month:10 pages:105-112 https://dx.doi.org/10.1007/s11739-022-03123-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 18 2022 1 18 10 105-112 |
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10.1007/s11739-022-03123-5 doi (DE-627)SPR049166271 (SPR)s11739-022-03123-5-e DE-627 ger DE-627 rakwb eng Perticone, Maria verfasserin aut Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions. COPD (dpeaa)DE-He213 Renal function (dpeaa)DE-He213 e-GFR (dpeaa)DE-He213 Arterial hypertension (dpeaa)DE-He213 Maio, Raffaele aut Tripepi, Giovanni aut Abelardo, Domenico aut Andreucci, Michele aut Imbalzano, Egidio aut Toscani, Alfredo Francesco aut Sciacqua, Angela aut Andreozzi, Francesco aut Sesti, Giorgio aut Perticone, Francesco aut Enthalten in Internal and emergency medicine Milan : Springer Milan, 2006 18(2022), 1 vom: 18. Okt., Seite 105-112 (DE-627)538216425 (DE-600)2378342-4 1970-9366 nnns volume:18 year:2022 number:1 day:18 month:10 pages:105-112 https://dx.doi.org/10.1007/s11739-022-03123-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 18 2022 1 18 10 105-112 |
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10.1007/s11739-022-03123-5 doi (DE-627)SPR049166271 (SPR)s11739-022-03123-5-e DE-627 ger DE-627 rakwb eng Perticone, Maria verfasserin aut Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions. COPD (dpeaa)DE-He213 Renal function (dpeaa)DE-He213 e-GFR (dpeaa)DE-He213 Arterial hypertension (dpeaa)DE-He213 Maio, Raffaele aut Tripepi, Giovanni aut Abelardo, Domenico aut Andreucci, Michele aut Imbalzano, Egidio aut Toscani, Alfredo Francesco aut Sciacqua, Angela aut Andreozzi, Francesco aut Sesti, Giorgio aut Perticone, Francesco aut Enthalten in Internal and emergency medicine Milan : Springer Milan, 2006 18(2022), 1 vom: 18. Okt., Seite 105-112 (DE-627)538216425 (DE-600)2378342-4 1970-9366 nnns volume:18 year:2022 number:1 day:18 month:10 pages:105-112 https://dx.doi.org/10.1007/s11739-022-03123-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 18 2022 1 18 10 105-112 |
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10.1007/s11739-022-03123-5 doi (DE-627)SPR049166271 (SPR)s11739-022-03123-5-e DE-627 ger DE-627 rakwb eng Perticone, Maria verfasserin aut Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions. COPD (dpeaa)DE-He213 Renal function (dpeaa)DE-He213 e-GFR (dpeaa)DE-He213 Arterial hypertension (dpeaa)DE-He213 Maio, Raffaele aut Tripepi, Giovanni aut Abelardo, Domenico aut Andreucci, Michele aut Imbalzano, Egidio aut Toscani, Alfredo Francesco aut Sciacqua, Angela aut Andreozzi, Francesco aut Sesti, Giorgio aut Perticone, Francesco aut Enthalten in Internal and emergency medicine Milan : Springer Milan, 2006 18(2022), 1 vom: 18. Okt., Seite 105-112 (DE-627)538216425 (DE-600)2378342-4 1970-9366 nnns volume:18 year:2022 number:1 day:18 month:10 pages:105-112 https://dx.doi.org/10.1007/s11739-022-03123-5 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 18 2022 1 18 10 105-112 |
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English |
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Enthalten in Internal and emergency medicine 18(2022), 1 vom: 18. Okt., Seite 105-112 volume:18 year:2022 number:1 day:18 month:10 pages:105-112 |
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Enthalten in Internal and emergency medicine 18(2022), 1 vom: 18. Okt., Seite 105-112 volume:18 year:2022 number:1 day:18 month:10 pages:105-112 |
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COPD Renal function e-GFR Arterial hypertension |
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Perticone, Maria @@aut@@ Maio, Raffaele @@aut@@ Tripepi, Giovanni @@aut@@ Abelardo, Domenico @@aut@@ Andreucci, Michele @@aut@@ Imbalzano, Egidio @@aut@@ Toscani, Alfredo Francesco @@aut@@ Sciacqua, Angela @@aut@@ Andreozzi, Francesco @@aut@@ Sesti, Giorgio @@aut@@ Perticone, Francesco @@aut@@ |
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Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. 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Perticone, Maria |
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Perticone, Maria misc COPD misc Renal function misc e-GFR misc Arterial hypertension Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients |
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Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients COPD (dpeaa)DE-He213 Renal function (dpeaa)DE-He213 e-GFR (dpeaa)DE-He213 Arterial hypertension (dpeaa)DE-He213 |
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misc COPD misc Renal function misc e-GFR misc Arterial hypertension |
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Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients |
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Perticone, Maria Maio, Raffaele Tripepi, Giovanni Abelardo, Domenico Andreucci, Michele Imbalzano, Egidio Toscani, Alfredo Francesco Sciacqua, Angela Andreozzi, Francesco Sesti, Giorgio Perticone, Francesco |
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competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients |
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Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients |
abstract |
Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions. © The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
abstractGer |
Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions. © The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
abstract_unstemmed |
Abstract Chronic kidney disease is a risk factor for cardiovascular events. Smoking and chronic obstructive pulmonary disease (COPD) are risk factors for renal impairment. The aim of this study was to test the combined effect of smoking and COPD on renal function decline in hypertensives. We enrolled 1728 hypertensives stratified by smoking status and presence/absence of COPD. To test the mutual effect modification by both smoking and COPD and e-GFR, we performed crude and adjusted linear regression analyses, these latter taking into account potential confounders. Smokers displayed significantly lower e-GFR values than non-smokers (90 ± 24 vs. 121 ± 35 ml/min/1.73 $ m^{2} $); this difference was confirmed when comparing e-GFR values between patients with/without COPD (81 ± 17 vs. 109 ± 32 ml/min/1.73 $ m^{2} $). Smoking and COPD were directly and significantly interrelated (Cramer’s V coefficient = 0.200; P = < 0.001). At interaction analyses, smoking significantly modified the effect of COPD on e-GFR and COPD significantly modified the effect of smoking on e-GFR, indicating a competitive interaction between smoking and COPD in the appearance of renal damage. e-GFR was 35 ml/min/1.73 $ m^{2} $ lower in patients with COPD than in those without; this reduction was of higher magnitude than that found between COPD and COPD-free patients among smokers (19 ml/min/1.73 $ m^{2} $). Smoking and COPD competitively interact in the appearance of renal function decline. These results suggest to screen for kidney damageboth smokers and COPD patients, especially those with both conditions. © The Author(s), under exclusive licence to Società Italiana di Medicina Interna (SIMI) 2022. Springer Nature or its licensor holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. |
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container_issue |
1 |
title_short |
Competitive interaction between smoking and chronic obstructive pulmonary disease for explaining renal function reduction in hypertensive patients |
url |
https://dx.doi.org/10.1007/s11739-022-03123-5 |
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author2 |
Maio, Raffaele Tripepi, Giovanni Abelardo, Domenico Andreucci, Michele Imbalzano, Egidio Toscani, Alfredo Francesco Sciacqua, Angela Andreozzi, Francesco Sesti, Giorgio Perticone, Francesco |
author2Str |
Maio, Raffaele Tripepi, Giovanni Abelardo, Domenico Andreucci, Michele Imbalzano, Egidio Toscani, Alfredo Francesco Sciacqua, Angela Andreozzi, Francesco Sesti, Giorgio Perticone, Francesco |
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doi_str |
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up_date |
2024-07-03T23:38:19.008Z |
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score |
7.40236 |