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Abstract Number: 92

Kidney Function and Alcohol Intake and The Risk Of Incident Gout In a Population-Based Cohort Of Adults: Atherosclerosis Risk In Communities Study

Mara McAdams DeMarco1, Anna Kottgen2, Andrew Law3, Janet W. Maynard4, Morgan Grams5, Josef Coresh1 and Alan N. Baer6, 1Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD, 2Renal Division, University Hospital Freiburg, Freiburg, Germany, 3Epidemiology, Johns Hopkins, Baltimore, MD, 4Rheum/Mason F Lord Bldg/CtrTow, Johns Hopkins University School of Medicine, Division of Rheumatology, Baltimore, MD, 5Nephrology, Johns Hopkins, Baltimore, MD, 6Division of Rheumatology, Johns Hopkins University School of Medicine, Baltimore, MD

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Alcohol use and gout

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Session Information

Session Title: Epidemiology and Health Services I

Session Type: Abstract Submissions (ACR)

Background/Purpose: Reduced kidney function is associated with higher urate levels as well as an increased risk of gout. Additionally, alcohol intake is known to increase serum urate levels and is associated with both kidney function and the development of gout. The interaction of modifiable risk factors for gout and kidney function on the development of gout is understudied. We estimated the risk of developing gout over a range of estimated glomerular filtration rate (eGFR) values and stratified by alcohol intake in participants enrolled in the Atherosclerosis Risk in Communities (ARIC) cohort study.

Methods: ARIC is a prospective population-based cohort recruited in 1987-1989 from 4 US communities, consisting of 4 visits over 9 years. Participants were included in this analysis if they answered the gout query and were free of gout at baseline. Incident gout was defined as self-reported onset between baseline and visit 4 (9 years after baseline). Serum creatinine was estimated using a modified kinetic JaffŽ reaction. Glomerular filtration rate (eGFR) was estimated using the CKD-Epi equation and alcohol intake was ascertained using a food frequency questionnaire. Using a Cox Proportional Hazards model (age as time scale), we estimated the hazard ratio (HR) and 95% confidence intervals (CI) of incident gout by baseline eGFR (modeled as a linear function and a spline), adjusted for confounders (sex, race, and center) and clinical factors (diuretic use, diabetes, hypertension, and obesity) and stratified by alcohol intake.

Results: A total of 10,858 ARIC participants were included in the analysis. The study population was 43% male, 21% African American and the mean age at cohort entry was 54 years (SD=5.7). The mean eGFR was 92 (SD=14.9) ml/min/1.73 m2. At baseline, 2% participants were classified as having eGFR<60 ml/min/1.73 m2; 41% with an eGFR between 60 and 90 ml/min/1.73 m2; and 57% with an eGFR >90 ml/min/1.73 m2. The mean alcohol intake was 40.2 grams/week. There were 274 incident gout cases. There was slight evidence that the risk of gout by kidney function was higher in those who drank ³50 g/week of alcohol (Table; P for interaction=0.08). For those with alcohol intake³50 g/week and an eGFR<60, there was 1.65-times (95% CI: 1.10-2.48, P=0.02) the risk of gout for every 10 ml/min/1.73 m2 decrease in eGFR. The risk of gout by eGFR was similar for those with alcohol intake <50 g/week.

Conclusion: There is slight evidence, potentially due to limited power, that the impact of reduced kidney function is greater for adults with alcohol intake ³50 g/week than for those with lower alcohol intake.

Risk of Gout by eGFR stratified by alcohol intake

Binary alcohol intake

(>=50 g per week)

Binary alcohol intake

(<50 g per week)

HR (95% CI)

p-value

HR (95% CI)

p-value

N=2,542

N=8,316

eGFR*

1.18 (1.03, 1.34)

0.01

1.12 (1.02, 1.23)

0.02

eGFR³90*

0.92 (0.68, 1.25)

0.61

1.05 (0.85, 1.29)

0.64

60²eGFR<90*

1.25 (0.96, 1.61)

0.09

1.17 (0.97, 1.41)

0.11

eGFR <60*

1.65 (1.10, 2.48)

0.02

1.16 (0.66, 2.07)

0.6

Adjusted for sex, race, center, diuretic use, hypertension, diabetes, and obesity.

* for each 10 unit decrease in eGFR.


Disclosure:

M. McAdams DeMarco,
None;

A. Kottgen,
None;

A. Law,
None;

J. W. Maynard,
None;

M. Grams,
None;

J. Coresh,
None;

A. N. Baer,
None.

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