Parameters derived by ultrasonic myocardial characterization in dialysis patients are associated with mortality

Pizzarelli, Francesco; Dattolo, Pietro; Ferdeghini, E.M.; Morales, Maria Aurora

doi:10.1111/j.1523-1755.2005.00530.x

Cited by 9 publications

(3 citation statements)

References 25 publications

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“…In other words, the effect of a fixed increase in TIMP-1 on the myocardium was amplified by the presence of the risk genotype (192). Thus insulin resistance seems to be involved not only in the pathogenesis of LVH but also in myocardial fibrosis, an alteration of primary importance in the high death risk of patients with kidney failure (161).…”

Section: Insulin Resistance and Cardiovascular And Renal Risk In Ckdmentioning

confidence: 99%

Insulin resistance in chronic kidney disease: a systematic review

Spoto

Pisano

Zoccali

2016

American Journal of Physiology-Renal Physiology

311

230

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Insulin resistance (IR) is an early metabolic alteration in chronic kidney disease (CKD) patients, being apparent when the glomerular filtration rate is still within the normal range and becoming almost universal in those who reach the end stage of kidney failure. The skeletal muscle represents the primary site of IR in CKD, and alterations at sites beyond the insulin receptor are recognized as the main defect underlying IR in this condition. Estimates of IR based on fasting insulin concentration are easier and faster but may not be adequate in patients with CKD because renal insufficiency reduces insulin catabolism. The hyperinsulinemic euglycemic clamp is the gold standard for the assessment of insulin sensitivity because this technique allows a direct measure of skeletal muscle sensitivity to insulin. The etiology of IR in CKD is multifactorial in nature and may be secondary to disturbances that are prominent in renal diseases, including physical inactivity, chronic inflammation, oxidative stress, vitamin D deficiency, metabolic acidosis, anemia, adipokine derangement, and altered gut microbiome. IR contributes to the progression of renal disease by worsening renal hemodynamics by various mechanisms, including activation of the sympathetic nervous system, sodium retention, and downregulation of the natriuretic peptide system. IR has been solidly associated with intermediate mechanisms leading to cardiovascular (CV) disease in CKD including left ventricular hypertrophy, vascular dysfunction, and atherosclerosis. However, it remains unclear whether IR is an independent predictor of mortality and CV complications in CKD. Because IR is a modifiable risk factor and its reduction may lower CV morbidity and mortality, unveiling the molecular mechanisms responsible for the pathogenesis of CKD-related insulin resistance is of importance for the identification of novel therapeutic targets aimed at reducing the high CV risk of this condition.

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Section: Insulin Resistance and Cardiovascular And Renal Risk In Ckdmentioning

confidence: 99%

Insulin resistance in chronic kidney disease: a systematic review

Spoto

Pisano

Zoccali

2016

American Journal of Physiology-Renal Physiology

311

230

View full text Add to dashboard Cite

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“…Beyond exhibiting a cluster of traditional Framingham risk factors (9), patients with CKD are subject to anemia, volume overload, left ventricular hypertrophy, poor vascular compliance, and excess oxidative stress coronary calcification, among others that have yet to be fully characterized (10). This pathologic transformation that eventually promotes myocardial fibrosis is most evident in end-stage renal disease and is associated with excessive mortality (12)(13)(14)(15). In nondiabetic pre-dialysis CKD patients, we recently demonstrated a significant inverse correlation between myocardial glucose use in mol/min/100 g and eGFR employing quantitative F18-fluorodeoxyglucse positron emission tomography as a means to measure myocardial metabolic changes (11).…”

mentioning

confidence: 99%

Chronic Kidney Disease as a Potent Risk Modifier for CAD in Diabetics

Fink

2010

JACC: Cardiovascular Imaging

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With the demographic shift in the U.S. to an older and heavier population, there has been a welldocumented increase in the incidence of diabetes mellitus (1). Paralleling this rise in diabetes has been a growth in the number of Americans with chronic kidney disease (CKD). Estimates of the number of adults with CKD and reduced kidney See page 734 function are reported to be over 16 million (2). In fact, there is a substantial overlap of the 2 diseases, with a majority of patients with CKD also having diabetes, and both diabetes and CKD are strong risk factors for coronary heart disease (CHD) (3). Although end-stage renal disease is often expected as the disease outcome of CKD, a majority of patients with CKD are likely to die of CHD before reaching end-stage renal disease (4 -6).The timely and accurate diagnosis of CHD is a challenge in those patients who have a preponderance of traditional cardiac risk factors along with diabetes and CKD. Such individuals might present with silent ischemia or atypical coronary syndromes or are not ideal candidates for invasive diagnostic testing (7). It is in this population that effective noninvasive strategies are needed to assist in CHD risk-stratification and guide cardiac medical management. However, when assessing patients for their likelihood of CHD and their prognosis when CHD is present, it is important to determine how much high-risk comorbidities such as diabetes and CKD affect the initial assessment of risk for CHD and then to consider how the use of a diagnostic test modifies that baseline risk and improves the predictive power for that disease.In this issue of iJACC, Hakeem et al. (8) retrospectively examined the impact of CKD and diabetes in relation to myocardial perfusion defects and both cardiac and all-cause mortality over a mean of 2 years. The patient cohort consisted of 1,747 patients with "known or suspected" CHD who underwent noninvasive cardiac testing with myocardial perfusion single-photon emission computed tomography (MPS) for evaluation of ischemia. CKD (defined as an estimated glomerular filtration rate [eGFR] of Ͻ60 ml/min/1.73 m 2 ) was present in 20% of the subjects, with approximately the same proportion having diabetes alone and 16% suffering from both CKD and diabetes. The authors showed that presence of CKD alone, with and without diabetes, conferred a several-fold higher risk of cardiac death for the various strata of MPS perfusion defects. The incidence of death was higher with increasing severity of stress perfusion defects in all disease sub-categories, but with the relationship most pronounced in the group with both CKD and diabetes. A normal MPS conferred a lower risk in CKD patients with and without diabetes. In multivariate analysis, the presence of both CKD and diabetes were highly predictive of cardiovascular death. Likewise, perfusion defects on stress imaging and depressed ejection fraction were also significant predictors of cardiovascular death. The investigators concluded that both eGFR and myocardial perfusion defects were impo...

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“…The shift from a predominance of aerobic (fatty acid) to anaerobic (glucose) metabolism may account for a significant portion of the excessive cardiovascular morbidity and mortality observed in kidney disease [15]. This pathologic transformation that eventually promotes myocardial fibrosis is most evident in end-stage renal disease and is associated with excessive mortality; however, it is likely to develop in early stages of impaired renal function [16,17,18]. …”

Section: Introductionmentioning

confidence: 99%

Pre-Clinical Myocardial Metabolic Alterations in Chronic Kidney Disease

Fink

Lodge²,

Smith

et al. 2010

Cardiology

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The risk for cardiovascular events conferred by decreased renal function is curvilinear with exponentially greater increases in risk as estimated glomerular filtration rate (eGFR) declines. In 13 non-diabetic pre-dialysis chronic kidney disease (CKD) patients, we employed quantitative F-18 fluorodeoxyglucose (FDG) positron emission tomography (PET) as a means to measure myocardial metabolic changes. Methods: Dynamic cardiac FDG PET images were acquired after 6 h fasting and glucose loading. Corrections for attenuation, scatter, randoms, dead time and decay were applied to the PET data and myocardial glucose utilization (MGU) was calculated using the Patlak method in conjunction with standardized myocardial regions of interest and an image-derived input function (left atrium). MGU was compared with eGFR based on a serum creatinine drawn within 2 weeks of the study date. Results: MGU was relatively uniform between the myocardial sectors (coefficient of variation = 16.2 ± 6.8%) within each patient. Between patients, whole myocardium MGU varied considerably with a range of 37.3–156.2 µmol/min/100 g and a mean of 68.9 ± 38.3 µmol/min/ 100 g. eGFR ranged from 11–89 ml/min/1.73 m² with a mean of 42.8 ± 26.9 ml/min/1.73 m². There was an inverse correlation between whole myocardium MGU and eGFR (Spearman’s rho correlation = –0.615, p = 0.025). In multivariate analysis, the relationship between MGU and eGFR was sustained with adjustment for age, race and gender (adjusted β = –1.56 ± 0.48, p = 0.01). There was no correlation between cardiac workload and eGFR (p = NS). Conclusions: A significant inverse correlation between MGU and eGFR is supportive of the hypothesis that CKD is associated with myocardial metabolic changes, which could not be attributed to demographic factors or cardiac workload. Dynamic FDG PET could provide a sensitive, non-invasive, quantitative tool for investigating pre-clinical myocardial abnormalities in patients with CKD.

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Parameters derived by ultrasonic myocardial characterization in dialysis patients are associated with mortality

Cited by 9 publications

References 25 publications

Insulin resistance in chronic kidney disease: a systematic review

Insulin resistance in chronic kidney disease: a systematic review

Chronic Kidney Disease as a Potent Risk Modifier for CAD in Diabetics

Pre-Clinical Myocardial Metabolic Alterations in Chronic Kidney Disease

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