How does ckd cause cvd




















Living with a chronic condition can be stressful. Remember to call on your health care team for help and guidance in taking care of your health. Joining a support group external icon is also a great way to connect with others who share your experience.

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What's this? Learn More. If you have heart disease or high blood pressure and CKD, your doctor may prescribe medicines to control your heart disease or high blood pressure. Some of these medicines may cause problems with your kidneys. Talk to your doctor about which medicine could work best for you. Your doctor may also recommend an exercise program or suggest you visit a dietitian to create a kidney- and heart-friendly diet.

The best way to prevent heart disease is to manage the problems that can lead to it. These include conditions such as anemia, high blood pressure, and problems with calcium and phosphorous levels. Some other ways to keep your kidney and heart health on track are to:.

Talk with your doctor about other ways to reduce your chance of getting heart disease if you have CKD. What you eat and how often you exercise are important ways you can help to prevent heart disease. If you have CKD, your doctor may recommend regular physical activity and also refer you to a dietitian who can work with you to create a kidney and heart-friendly diet. What type of exercise you do and how frequently you do it are things you should discuss with your doctor.

Types of physical activity may include:. Your doctor and dietitian will consider what stage of kidney disease you have, how that affects your individual risk for developing heart disease, and create a meal plan that will benefit your health. Generally, a heart-healthy diet is low in fat and salt. But, because you also have CKD, you may need to balance potassium, phosphorous and fluid levels in your body. Your dietitian will consider all of these factors when creating a diet that works for you.

Donate Now. Higher rates of elevated LDL-C levels among those with CKD were observed among older individuals, but differences in treatment and control of elevated LDL-C levels were not evident in age-stratified analyses.

In contrast, differences in the prevalence of diabetes by CKD status were more evident among younger individuals. Among participants without diabetes, dual control of hypertension and elevated LDL-C levels occurred less in participants with Among participants with diabetes, rates of successful triple control of hypertension and LDL-C and hemoglobin A 1c levels were low and did not differ among those with 7. Overall use of cardioprotective medications is shown in Table 1.

A greater proportion of hypertensive participants with CKD were treated with angiotensin-converting enzyme inhibitors than persons without CKD Among participants with prevalent coronary heart disease, there was no difference in aspirin use In general, when we stratified our analysis using an age cutoff of 65 years, older individuals demonstrated more significant differences in hypertension prevalence, treatment, and control.

The prevalence of hypertension was significantly higher among those with compared with those without CKD. Indeed, hypertensive participants with CKD were more likely to be treated with angiotensin-converting enzyme inhibitors and diuretics, which can increase serum creatinine levels.

Hypertension is a well-established independent risk factor for the development of end-stage renal disease 37 , 38 and CKD progression. Three recent studies 40 - 42 of tight vs usual blood pressure control have reported conflicting results regarding outcomes of end-stage renal disease and GFRdecline.

The African-American Study of Kidney Disease and Hypertension 42 and the Ramipril Efficacy in Nephropathy 2 Trial 40 demonstrated no benefit on these outcomes from blood pressure reduction, whereas long-term follow-up of the MDRD Study, 41 which had the longest follow-up period and achieved the largest mean blood pressure difference between treatment groups, showed a benefit in the tight blood pressure control arm among patients with primarily nondiabetic kidney disease.

Therefore, lack of definitive data in this area may contribute to the failure to reach lower blood pressure targets among individuals with CKD. There is evidence that the treatment of hyperlipidemia may reduce the rate of kidney function decline in individuals with stage 3 CKD.

However, a recent randomized clinical trial in patients with diabetes undergoing hemodialysis demonstrated no protective benefit of lipid-lowering medication on CVD end points, 47 although the generalizability of these findings to patients with CKD who are not undergoing hemodialysis is uncertain. Taken together, these data suggest that lipid-lowering therapy among individuals with moderate CKD has beneficial effects on renal and CVD outcomes. Additional clinical trials are necessary to examine the effects of lipid-lowering agents on both CKD progression and CVD risk reduction.

The rates of diabetes control were significantly lower among participants with CKD. This is surprising in light of evidence from the United Kingdom Prospective Diabetes Study 48 and the Diabetes Control and Complications Trial, 49 which demonstrated that tight glycemic control is associated with reduced progression of nephropathy and doubling of serum creatinine levels.

Recent data 50 suggest that tight control of glucose levels among patients with type 1 diabetes reduces long-term CVD risk; however, clinical trial data in those with type 2 diabetes remain inconclusive. Whether subgroups of patients with diabetes and CKD would experience a reduction in CVD outcomes with tight glycemic control requires further research. There are several strengths to our study design. The Framingham Heart Study is a community-based sample not selected for CKD, reducing the risk of referral or selection bias.

We have excellent assessment and documentation of CVD risk factors and treatment. Several limitations exist as well. Our study sample is limited geographically and ethnically because our participants are primarily white individuals.

Nevertheless, the relation between CVD risk factor outcomes observed in the Framingham data set has been validated in 6 ethnically and geographically diverse populations, suggesting that our findings are applicable in other populations. However, given that we did not use GFR as a continuous variable in our analysis, it remains unclear how this would affect the determination of CKD in our sample.

Our definition of CKD as a disease trait falls within the range that has been validated for the MDRD equation, 24 improving the robustness of our results for our dichotomous analysis. Our definition of CKD is limited to a single measurement of serum creatinine level on one occasion, not measured during a period of 3 months or longer as has been defined by the National Kidney Foundation.

To improve the validity and accuracy of the MDRD equation, we indirectly calibrated our creatinine values. We were unable to account for albuminuria, which may have led to an underestimation of CKD in our study.

Although cross-sectional study designs are generally considered to be limiting in that they cannot determine the directionality of our reported relations, our primary aim was to characterize CVD risk factor burden, treatment, and control at a given point in time, therefore making the cross-sectional design the most favorable for this analysis.

Individuals with CKD had higher Framingham risk scores and low rates of optimization of all risk factors. Understanding barriers to effective risk factor modification in CKD is essential. Health care practitioners may not be aware of the relatively low creatinine values that correspond to CKD; among non-Hispanic white individuals aged 60 years, the mean creatinine cut point corresponding to a GFR in the CKD range is only 1.

Given the high prevalence of CVD risk factors and the relatively low levels of risk factor control, there may be a need to more aggressively manage CKD in this specific subgroup of individuals. Chronic kidney disease, with its high burden of vascular disease risk factors and associated risk of adverse CVD outcomes, represents an important public health concern. The identification of an individual with CKD should alert the practitioner to a large underlying burden of potentially modifiable CVD risk factors.

Correspondence: Caroline S. Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy Continue. Figure 1. View Large Download. Table 1. Relation between renal dysfunction and cardiovascular outcomes after myocardial infarction. Level of kidney function as a risk factor for atherosclerotic cardiovascular outcomes in the community. Predictors of new-onset kidney disease in a community-based population.

Influence of smoking and obesity on the development of proteinuria. Atherosclerotic cardiovascular disease risks in chronic hemodialysis patients. Cardiac risk factors and the use of cardioprotective medications in patients with chronic renal insufficiency. Berger AKDuval SKrumholz HM Aspirin, beta-blocker, and angiotensin-converting enzyme inhibitor therapy in patients with end-stage renal disease and an acute myocardial infarction.

Cardiovascular medication use after coronary bypass surgery in patients with renal dysfunction: a National Veterans Administration study.



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