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2000
Volume 14, Issue 5
  • ISSN: 1570-1611
  • E-ISSN: 1875-6212

Abstract

Background: Chronic kidney disease (CKD) accounts for a significant proportion of the morbidity and mortality in the United States. CKD is defined as glomerular filtration rate (GFR) <60ml/min/1.73m2 or clear evidence of renal damage from biopsy. All-cause cardiovascular risk increases with decreasing GFR. Clinically, detection of CKD is through changes in creatinine clearance which estimates GFR, an indicator of kidney function. We reviewed conventional and nonconventional cardiovascular risk factors associated with CKD. Clinically, we reviewed the status of statins as a treatment option for CKD-induced dyslipidemia. Objective: CKD has dramatic consequences on cardiovascular risk profile due to a complex pathophysiologic response to declining kidney function. In this review, we explored new, more accurate methods of detecting decreasing kidney function, discerned risk factors for the development of cardiovascular events, and examined the controversial use of statins for renoprotection. Results: Detection of declining renal function by monitoring creatinine has been the clinical gold standard, but it substantially fluctuates with muscle mass, sex, and ethnicity. Newer methods using cystatin C have been at the forefront as the next substance that will be used for detection of CKD. Traditional and non-traditional risk factors contribute to the cardiovascular risk profile of patients with declining renal function. Statins, along with angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB)s, have been used for renoprotection, but evidence shows only modest benefits in non-dialysis patients. Conclusion: Cardio-renal interaction involves multiple risk factors that contribute significantly to the CKD-induced development of accelerated atherosclerosis, an inflammatory state that causes cardiovascular events.

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/content/journals/cvp/10.2174/1570161114999160719104512
2016-09-01
2025-10-13
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