Dataset Information

Modeling the impact of obesity on the lifetime risk of chronic kidney disease in the United States using updated estimates of GFR progression from the CRIC study.

ABSTRACT:

Rationale & objective

As the prevalence of obesity continues to rise in the United States, it is important to understand its impact on the lifetime risk of chronic kidney disease (CKD).

Study design

The CKD Health Policy Model was used to simulate the lifetime risk of CKD for those with and without obesity at baseline. Model structure was updated for glomerular filtration rate (GFR) decline to incorporate new longitudinal data from the Chronic Renal Insufficiency Cohort (CRIC) study.

Setting and population

The updated model was populated with a nationally representative cohort from National Health and Nutrition Examination Survey (NHANES).

Outcomes

Lifetime risk of CKD, highest stage and any stage.

Model, perspective, & timeframe

Simulation model following up individuals from current age through death or age 90 years.

Results

Lifetime risk of any CKD stage was 32.5% (95% CI 28.6%-36.3%) for persons with normal weight, 37.6% (95% CI 33.5%-41.7%) for persons who were overweight, and 41.0% (95% CI 36.7%-45.3%) for persons with obesity at baseline. The difference between persons with normal weight and persons with obesity at baseline was statistically significant (p<0.01). Lifetime risk of CKD stages 4 and 5 was higher for persons with obesity at baseline (Stage 4: 2.1%, 95% CI 0.9%-3.3%; stage 5: 0.6%, 95% CI 0.0%-1.1%), but the differences were not statistically significant (stage 4: p = 0.08; stage 5: p = 0.23).

Limitations

Due to limited data, our simulation model estimates are based on assumptions about the causal pathways from obesity to CKD, diabetes, and hypertension.

Conclusions

The results of this study indicate that obesity may have a large impact on the lifetime risk of CKD. This is important information for policymakers seeking to set priorities and targets for CKD prevention and treatment.

SUBMITTER: Yarnoff BO

PROVIDER: S-EPMC6195263 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Modeling the impact of obesity on the lifetime risk of chronic kidney disease in the United States using updated estimates of GFR progression from the CRIC study.

Yarnoff Benjamin O BO Hoerger Thomas J TJ Shrestha Sundar S SS Simpson Siobhan K SK Burrows Nilka R NR Anderson Amanda H AH Xie Dawei D Chen Hsiang-Yu HY Pavkov Meda E ME

PloS one 20181019 10

<h4>Rationale & objective</h4>As the prevalence of obesity continues to rise in the United States, it is important to understand its impact on the lifetime risk of chronic kidney disease (CKD).<h4>Study design</h4>The CKD Health Policy Model was used to simulate the lifetime risk of CKD for those with and without obesity at baseline. Model structure was updated for glomerular filtration rate (GFR) decline to incorporate new longitudinal data from the Chronic Renal Insufficiency Cohort (CRIC) stu ...[more]

PMID: 30339684

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Project description:The US prevalence of reduced estimated glomerular filtration rate (eGFR) based on serum creatinine level increased during the decade ending in 2002. National Health and Nutrition Examination Survey (NHANES) cystatin C measurements recently were calibrated to the international standard, allowing for an independent test of the trend in prevalence of reduced eGFR using cystatin C level.Cross-sectional surveys performed during 2 periods.Nationally representative subsamples of adult participants from NHANES III (1988-1994) and the NHANES 1999-2002 surveys.Survey period.Prevalence of reduced GFR, defined as eGFR <60 mL/min/1.73 m² based on levels of serum creatinine, cystatin C, or both (eGFRcr, eGFRcys, and eGFRcr-cys), using estimating equations developed by the Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI).Serum cystatin C level, measured from stored samples in 2006, calibrated to the international standard in 2012.Between 1988-1994 and 1999-2002, the prevalence of reduced eGFRcr, eGFRcys, and eGFRcr-cys increased from 4.7% (95% CI, 4.1%-5.3%) to 6.5% (95% CI, 5.9%-7.1%) (P < 0.001), from 5.5% (95% CI, 4.6%-6.5%) to 8.7% (95% CI, 7.5%-10.0%) (P < 0.001), and from 4.4% (95% CI, 3.7%-5.2%) to 7.1% (95% CI, 6.2%-8.0%) (P < 0.001), respectively. The higher prevalence of reduced GFR in the later period was observed in all subgroups of age, race, sex, and GFR categories. After adjusting for changes in the US population by age, sex, race, diabetes, hypertension, and body mass index, prevalence ratios of reduced GFR in the later versus earlier survey were 1.24 (95% CI, 1.09-1.45), 1.34 (95% CI, 1.15-1.67), and 1.33 (95% CI, 1.17-1.65) using eGFRcr, eGFRcys, and eGFRcr-cys, respectively.Likely underascertainment of persons with GFR <15 mL/min/1.73 m²; GFR was estimated and not measured; comparability of laboratory assays based on a calibration subsample.The prevalence of reduced eGFRcys in the US civilian noninstitutionalized population increased between 1988-1994 and 1999-2002, confirming the increase observed in the prevalence of reduced eGFRcr.

Project description:Rationale & objectiveEvaluating repeated measures of estimated glomerular filtration rate (eGFR) and urinary protein-creatinine ratio (UPCR) over time may enhance our ability to understand the association between changes in kidney parameters and cardiovascular disease risk.Study designProspective cohort study.Setting & participantsAnnual visit data from 2,438 participants in the Chronic Renal Insufficiency Cohort (CRIC).ExposuresAverage and slope of eGFR and UPCR in time-updated, 1-year exposure windows.OutcomesIncident heart failure, atherosclerotic cardiovascular disease events, death, and a composite of incident heart failure, atherosclerotic cardiovascular disease events, and death.Analytical approachA landmark analysis, a dynamic approach to survival modeling that leverages longitudinal, iterative profiles of laboratory and clinical information to assess the time-updated 3-year risk of adverse cardiovascular outcomes.ResultsAdjusting for baseline and time-updated covariates, every standard deviation lower mean eGFR (19mL/min/1.73m2) and declining slope of eGFR (8mL/min/1.73m2 per year) were independently associated with higher risks of heart failure (hazard ratios [HRs] of 1.82 [95% CI, 1.39-2.44] and 1.28 [95% CI, 1.12-1.45], respectively) and the composite outcome (HRs of 1.32 [95% CI, 1.11-1.54] and 1.11 [95% CI, 1.03-1.20], respectively). Every standard deviation higher mean UPCR (136mg/g) and increasing UPCR (240mg/g per year) were also independently associated with higher risks of heart failure (HRs of 1.58 [95% CI, 1.28-1.97] and 1.20 [95% CI, 1.10-1.29], respectively) and the composite outcome (HRs of 1.33 [95% CI, 1.17-1.50] and 1.12 [95% CI, 1.06-1.18], respectively).LimitationsLimited generalizability of annual eGFR and UPCR assessments; several biomarkers for cardiovascular disease risk were not available annually.ConclusionsUsing the landmark approach to account for time-updated patterns of kidney function, average and slope of eGFR and proteinuria were independently associated with 3-year cardiovascular risk. Short-term changes in kidney function provide information about cardiovascular risk incremental to level of kidney function, representing possible opportunities for more effective management of patients with chronic kidney disease.

Dataset Information

Modeling the impact of obesity on the lifetime risk of chronic kidney disease in the United States using updated estimates of GFR progression from the CRIC study.

Rationale & objective

Study design

Setting and population

Outcomes

Model, perspective, & timeframe

Results

Limitations

Conclusions

Publications

Modeling the impact of obesity on the lifetime risk of chronic kidney disease in the United States using updated estimates of GFR progression from the CRIC study.

Similar Datasets

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