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Relation Between Calcified Atherosclerosis in the Renal Arteries and Kidney Function (from the Multi-Ethnic Study of
Devesh Vashishtha1, Robyn L McClelland2, Joachim H Ix3
1School of Medicine, University of California, San Diego, La Jolla, CA.
Insights
Renal artery calcium (RAC) is linked to poorer kidney function, including lower estimated glomerular filtration rate (eGFR) and increased odds of chronic kidney disease (CKD). This association highlights RAC as a potential indicator of kidney health decline.
Area of Science:
- Cardiovascular Medicine
- Nephrology
- Radiology
Background:
- Renal artery calcification (RAC) is associated with hypertension.
- The relationship between RAC and overall kidney function requires further investigation.
Purpose of the Study:
- To determine if the presence and extent of RAC are associated with kidney function.
- To analyze the association between RAC and estimated glomerular filtration rate (eGFR), urinary albumin-to-creatinine ratio (UACR), and chronic kidney disease (CKD) stage.
Main Methods:
- Analysis of cross-sectional data from 1,226 participants in the Multi-Ethnic Study of Atherosclerosis (MESA).
- Computed tomography of the abdomen was used to assess RAC.
- Kidney function was measured using eGFR, UACR, and CKD stage, with adjustments for various cardiovascular and demographic factors.
Main Results:
- Participants with RAC (>0) showed a modest association with lower eGFR (β = -2.21, p = 0.06).
- RAC as a continuous variable was associated with increased odds of worse CKD stage (OR = 1.14, p = 0.05).
- No significant association was found between RAC and UACR (β = 0.02, p = 0.79).
Conclusions:
- A modest relationship exists between renal artery calcium and kidney function, particularly when assessed by eGFR and CKD stage.
- Further clinical trials are warranted to explore the impact of managing cardiovascular risk factors in patients with subclinical RAC on preventing or delaying CKD progression.
Abstract:
Renal artery calcium (RAC) has been shown to be associated with higher odds of hypertension (HTN). The purpose of this study was to determine if the presence and extent of RAC is associated with renal function. We analyzed cross-sectional data from the Multi-Ethnic Study of Atherosclerosis (MESA). A subsample of 1,226 participants underwent computed tomography of the abdomen and also had venous blood samples measured for kidney function. RAC was the primary predictor variable and the following measures of kidney function were the outcome variables: estimated glomerular filtration rate (eGFR), urinary albumin-to-creatinine ratio (UACR), and chronic kidney disease (CKD) stage. The analyses were adjusted for age, gender, race, height, visceral fat, dyslipidemia, diabetes, cigarette smoking, hypertension, interleukin-6 and abdominal aortic calcium (AAC). The average age of this cohort was 66.1 years (SD 9.7), 44.8% (549 of 1,226) were men, and nearly 30% had RAC >0. Compared with those with no RAC, those with RAC >0 were significantly older but not different by gender or race. After adjustment for age, gender, and race, those with RAC >0 had significantly higher visceral fat, were more likely to have dyslipidemia, diabetes, and hypertension, had a higher interleukin-6, and a higher prevalence of AAC >0. The mean eGFR and UACR among those without RAC were 80 ml/min/1.73 m2 and 21 mg/g, whereas these values were 78 ml/min/1.73 m2 and 55 mg/g among those with RAC. In fully adjusted multivariable linear regression models, the presence of RAC was associated with a lower eGFR (β = -2.21, p = 0.06) but not with UACR (β = 0.02, p = 0.79). In fully adjusted ordinal logistic regression, RAC as a continuous variable was associated with increased odds of being in a worse CKD category (odds ratio 1.14, p = 0.05). When measured by eGFR and CKD stage, there is a modest relation between RAC and kidney function. Further studies might involve clinical trials to assess the role of intensive cardiovascular disease risk factor management in patients with subclinical RAC to determine if this may prevent or delay the development and progression of CKD.
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