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  • 1.
    Ejerblad, E.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fored, C. M.
    Karolinska Institutet, Clinical Epidemiology Unit, Department of Medicine, Karolinska University Hospital, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Fryzek, J.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Dickman, P. W.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Elinder, C. G.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Renal Medicine, Huddinge University Hospital, Huddinge, Sweden.
    McLaughlin, J. K.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Nyren, O.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Association between smoking and chronic renal failure in a nationwide population-based case-control study2004Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 15, nr 8, s. 2178-2185Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    For determining whether smoking is associated with an increased risk for chronic renal failure (CRF) overall and by type of renal disease, smoking data were analyzed from a nationwide population-based case-control study. Eligible as cases were native 18- to 74-yr-old Swedes whose serum creatinine for the first time and permanently exceeded 3.4 mg/dl (men) or 2.8 mg/dl (women). A total of 926 cases (78% of all eligible) and 998 control subjects (75% of 1330 randomly selected subjects from the source population), frequency matched to the cases by gender and age within 10 yr, were included. A face-to-face interview and a self-administered questionnaire provided information about smoking habits and other lifestyle factors. Logistic regression models estimated odds ratios (OR) as measures of relative risk for disease-specific types of CRF among smokers compared with never-smokers. Despite a modest and nonsignificant overall association, the risk increased with high daily doses (OR among smokers of >20 cigarettes/d, 1.51; 95% confidence interval [CI], 1.06 to 2.15), long duration (OR among smokers for >40 yr, 1.45; 95% CI, 1.00 to 2.09), and a high cumulative dose (OR among smokers with >30 pack-years, 1.52; 95% CI, 1.08 to 2.14). Smoking increased risk most strongly for CRF classified as nephrosclerosis (OR among smokers with >20 pack-years, 2.2; 95% CI, 1.3 to 3.8), but significant positive associations were also noted with glomerulonephritis. This study thus suggests that heavy cigarette smoking increases the risk of CRF for both men and women, at least CRF classified as nephrosclerosis and glomerulonephritis.

  • 2.
    Ejerblad, E.
    et al.
    Department of Medical Epidemiology and Biostatistic Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
    Fored, C. M.
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden.
    Lindblad, Per
    Department of Medical Epidemiology and Biostatistics, Karolinska Institute and Karolinsak University Hospital, Stockholm, Sweden; Department of Urology, Sundsvall Hospital, Sundsvall, Sweden.
    Fryzek, J.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    McLaughlin, J. K.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Nyren, O.
    Department of Medical Epidemiology and Biostatistic Karolinska Institutet and Karolinska University Hospital, Stockholm, Sweden; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Obesity and risk for chronic renal failure2006Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 17, nr 6, s. 1695-1702Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Few large-scale epidemiologic studies have quantified the possible link between obesity and chronic renal failure (CRF). This study analyzed anthropometric data from a nationwide, population-based, case-control study of incident, moderately severe CRF. Eligible as cases were all native Swedes who were aged 18 to 74 yr and had CRF and whose serum creatinine for the first time and permanently exceeded 3.4 mg/dl (men) or 2.8 mg/dl (women) during the study period. A total of 926 case patients and 998 control subjects, randomly drawn from the study base, were enrolled. Face-to-face interviews, supplemented with self-administered questionnaires, provided information about anthropometric measures and other lifestyle factors. Logistic regression models with adjustments for several co-factors estimated the relative risk for CRF in relation to body mass index (BMI). Overweight (BMI>or=25 kg/m2) at age 20 was associated with a significant three-fold excess risk for CRF, relative to BMI<25. Obesity (BMI>or=30) among men and morbid obesity (BMI>or=35) among women anytime during lifetime was linked to three- to four-fold increases in risk. The strongest association was with diabetic nephropathy, but two- to three-fold risk elevations were observed for all major subtypes of CRF. Analyses that were confined to strata without hypertension or diabetes revealed a three-fold increased risk among patients who were overweight at age 20, whereas the two-fold observed risk elevation among those who had a highest lifetime BMI of >35 was statistically nonsignificant. Obesity seems to be an important-and potentially preventable-risk factor for CRF. Although hypertension and type 2 diabetes are important mediators, additional pathways also may exist.

  • 3.
    Fored, C. M.
    et al.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Renal Medicine, Huddinge University Hospital, Stockholm, Sweden.
    Nise, G.
    Division of Occupational Department of Renal Medicine, Huddinge University Hospital, Stockholm, Sweden.
    Ejerblad, E.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Fryzek, J. P.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Lindblad, Per
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    McLaughlin, J. K.
    The International Epidemiology Institute, Rockville, Maryland, USA; Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
    Elinder, C. G.
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden; Department of Renal Medicine, Huddinge University Hospital, Stockholm, Sweden.
    Nyren, O.
    Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden.
    Absence of association between organic solvent exposure and risk of chronic renal failure: a nationwide population-based case-control study2004Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 15, nr 1, s. 180-186Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Exposure to organic solvents has been suggested to cause or exacerbate renal disease, but methodologic concerns regarding previous studies preclude firm conclusions. We examined the role of organic solvents in a population-based case-control study of early-stage chronic renal failure (CRF). All native Swedish residents aged 18 to 74 yr, living in Sweden between May 1996 and May 1998, formed the source population. Incident cases of CRF in a pre-uremic stage (n = 926) and control subjects (n = 998), randomly selected from the study base, underwent personal interviews that included a detailed occupational history. Expert rating by a certified occupational hygienist was used to assess organic solvent exposure intensity and duration. Relative risks were estimated by odds ratios (OR) in logistic regression models, with adjustment for potentially important covariates. The overall risk for CRF among subjects ever exposed to organic solvents was virtually identical to that among never-exposed (OR, 1.01; 95% confidence interval [CI], 0.81 to 1.25). No dose-response relationships were observed for lifetime cumulative solvent exposure, average dose, or exposure frequency or duration. The absence of association pertained to all subgroups of CRF: glomerulonephritis (OR, 0.96; 95% CI, 0.68 to 1.34), diabetic nephropathy (OR, 1.02; 95% CI, 0.74 to 1.41), renal vascular disease (OR, 1.16; 95% CI, 0.76 to 1.75), and other renal CRF (OR, 0.92; 95% CI, 0.66 to 1.27). The results from a nationwide, population-based study do not support the hypothesis of an adverse effect of organic solvents on CRF development, in general. Detrimental effects from subclasses of solvents or on specific renal diseases cannot be ruled out.

  • 4.
    Jarrick, Simon
    et al.
    Örebro universitet, Institutionen för medicinska vetenskaper. Department of Pediatrics, Örebro University Hospital, Örebro, Sweden.
    Lundberg, Sigrid
    Department of Nephrology, Danderyd University Hospital, Stockholm, Sweden; Department of Clinical Sciences, Danderyd Hospital, Stockholm, Sweden.
    Welander, Adina
    Clinical Epidemiology Unit, Department of Medicine, Karolinska Institutet, stockholm, Sweden.
    Carrero, Juan-Jesus
    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden.
    Höijer, Jonas
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Bottai, Matteo
    Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
    Ludvigsson, Jonas F.
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. Department of Pediatrics, Örebro University Hospital, Örebro, Sweden; Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden; Division of Epidemiology and Public Health, School of Medicine, University of Nottingham, Nottingham, UK; Department of Medicine, Columbia University College of Physicians and Surgeons, New York, New York, USA.
    Mortality in IgA Nephropathy: A Nationwide Population-Based Cohort Study.2019Ingår i: Journal of the American Society of Nephrology, ISSN 1046-6673, E-ISSN 1533-3450, Vol. 30, nr 5, s. 866-876Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    BACKGROUND: The clinical course of IgA nephropathy (IgAN) varies from asymptomatic nonprogressive to aggressive disease, with up to one in four patients manifesting ESRD within 20 years of diagnosis. Although some studies have suggested that mortality appears to be increased in IgAN, such studies lacked matched controls and did not report absolute risk.

    METHODS: We conducted a population-based cohort study in Sweden, involving patients with biopsy-verified IgAN diagnosed in 1974-2011; main outcome measures were death and ESRD. Using data from three national registers, we linked 3622 patients with IgAN with 18,041 matched controls; we also conducted a sibling analysis using 2773 patients with IgAN with 6210 siblings and a spousal analysis that included 2234 pairs.

    RESULTS: During a median follow-up of 13.6 years, 577 (1.1%) patients with IgAN died (10.67 per 1000 person-years) compared with 2066 deaths (0.7%) in the reference population during a median follow-up of 14.1 years (7.45 per 1000 person-years). This corresponded to a 1.53-fold increased risk and an absolute excess mortality of 3.23 per 1000 person-years (equaling one extra death per 310 person-years) and a 6-year reduction in median life expectancy. Similar increases in risk were seen in comparisons with siblings and spouses. IgAN was associated with one extra case of ESRD per 54 person-years. Mortality preceding ESRD was not significantly increased compared with controls, spouses, or siblings. Overall mortality did not differ significantly between patients with IgAN-associated ESRD and patients with ESRD from other causes.

    CONCLUSIONS: Patients with IgAN have an increased mortality compared with matched controls, with one extra death per 310 person-years and a 6-year reduction in life expectancy.

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