Capillary/myocyte mismatch in the heart in renal failure—a role for erythropoietin?

Amann, Kerstin; Buzello, Moriz; Simonaviciene, Aurelia; Miltenberger-Miltényi, Gábriel; Koch, Andreas; Nabokov, Alexander; Groß, Marie-Luise; Gless, Bernhard; Mall, Gerhard; Ritz, Eberhard

doi:10.1093/ndt/15.7.964

Cited by 56 publications

(43 citation statements)

References 30 publications

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“…A similar study by Koivuviita et al, which included 31 individuals (21 with CKD) without cardiovascular disease who underwent myocardial positron emission tomography, also did not show a significant association between nuclear flow reserve and CKD (26). In the context of these prior investigations, our findings raise new questions about animal models that have consistently demonstrated microvascular dropout in the myocardium of uremic animals (17,(27)(28)(29).…”

Section: Discussionsupporting

confidence: 67%

CKD and Coronary Collateral Supply in Individuals Undergoing Coronary Angiography after Myocardial Infarction

Charytan

Stern

Mauri

2012

Clinical Journal of the American Society of Nephrology

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SummaryBackground and objectives CKD patients have high mortality risk after myocardial infarction (MI). An adequate supply of coronary collaterals to the culprit vessel responsible for MI is associated with reduced risks of death and complications. Whether a diminished supply of collaterals contributes to the high risk in CKD patients is uncertain.Design, setting, participants, & measurements Quantitative coronary angiography was performed in a consecutive series of individuals with (n=58) and without (n=165) CKD (estimated GFR ,60 ml/min per 1.73 m 2 ) who underwent coronary angiography at the time of MI. Collateral supply was analyzed and candidate predictors were assessed in patient-level and individual artery-level models using logistic regression and ordered categorical regression, respectively.Results There were no significant differences in collateral supply among 58 CKD patients and 165 individuals with preserved renal function. Culprit artery collaterals were present in 25.0% of CKD patients compared with 27.2% of individuals with preserved renal function (P=0.76). The odds of having an adequate supply of culprit vessel collaterals were also not significantly different in individuals with and without CKD, respectively. CKD patients were 2.22-fold more likely to have visible collaterals to the nonculprit vessels in unadjusted analyses. The difference was not significant after correction for percent stenosis and comorbid factors.Conclusions Our results do not support an independent association between CKD and diminished collateral supply to either the culprit or nonculprit vessels in MI. Additional studies are warranted to better define associations between myocardial capillary supply, collateral supply, and the full range of human CKD.

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Section: Discussionsupporting

confidence: 67%

CKD and Coronary Collateral Supply in Individuals Undergoing Coronary Angiography after Myocardial Infarction

Charytan

Stern

Mauri

2012

Clinical Journal of the American Society of Nephrology

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“…In this case, the effect of ACE inhibitors could be dissociated from accumulation of bradykinin. In contrast, nonspecific antihypertensive treatment (dihydralazine and furosemide), sympatholytic agents, or correction of anemia with rhEPO did not prevent intramyocardial microarteriopathy (68).…”

Section: Cardiac Consequences Of Disturbed Renal Functionmentioning

confidence: 72%

Cross-Talk between the Kidney and the Cardiovascular System

Amann¹,

Wanner²,

Ritz³

2006

Journal of the American Society of Nephrology

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137

114

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In recent years, increasing evidence has been provided that even minor renal dysfunction is a powerful cardiovascular risk factor that induces typical cardiovascular alterations and thus predisposes to coronary heart disease as well as to noncoronary cardiovascular problems. This first had been noted in patients with diabetes but now has been confirmed amply in patients without diabetes as well. Numerous heterogeneous abnormalities have been described in patients with early renal dysfunction (e.g., microalbuminuria, reduced estimated GFR). One final common pathway seems to be endothelial cell dysfunction. The link between albuminuria and generalized endothelial cell dysfunction (as indicated by diminished flow-mediated vasodilation, markers of endothelial cell dysfunction, sloughed off endothelial cells, and high transcapillary albumin escape rate) is unclear. In patients with early renal dysfunction, a long list of classical and nonclassical cardiovascular risk factors have been identified: Elevated asymmetric dimethyl-L-arginine concentrations, markers of microinflammation, oxidative stress, features of metabolic syndrome, abnormal adipokine concentrations, dyslipidemia, inappropriate activation of the renin-angiotensin system, and sympathetic overactivity. The mechanisms that link dysfunction of the kidney and the cardiovascular system are being sought. The most interesting unifying concept, however, is deranged fetal programming linking nephron underdosing to the increased cardiovascular risk.

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“…EPO treatment has been shown to improve cardiac function and to induce neovascularisation in rats with heart failure after myocardial infarction [5]. In a rat model for left ventricular hypertrophy associated with chronic renal failure, EPO treatment seemed to increase cardiac capillary density [42]. This increased vascular growth after EPO treatment has been correlated with the number of circulating EPCs [43].…”

Section: Discussionmentioning

confidence: 99%

Effects of erythropoietin on advanced pulmonary vascular remodelling

Albada

Sarvaas²,

Koster³

et al. 2007

Eur Respir J

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Erythropoietin (EPO) mobilises endothelial progenitor cells and promotes neovascularisation in heart failure. The present authors studied the effects of EPO on pulmonary vascular and cardiac remodelling in a model for flow-associated pulmonary arterial hypertension (PAH).PAH was induced in adult male Wistar rats by the injection of monocrotaline combined with an abdominal aortocaval shunt 1 week later (PAH or experimental group). Immediately afterwards, rats were randomised into those who received treatment with EPO (PAH+EPO group) and controls. Pulmonary and systemic haemodynamics, and right ventricular and pulmonary vascular remodelling were evaluated 3 weeks later.Vascular occlusion of the intra-acinar pulmonary vessels (13.4¡0.7 versus 16.7¡1.3% in PAH+EPO and PAH, respectively) and medial wall thickness of the pre-acinar arteries (wall-tolumen ratio 0.13¡0.01 versus 0.17¡0.01 in PAH+EPO and PAH, respectively) decreased after treatment with EPO. Moreover, right ventricular capillary density was increased by therapy (2,322¡61 versus 2,100¡63 capillaries?mm -2 in PAH+EPO and PAH, respectively). Increased mean pulmonary arterial pressure and decreased right ventricular contractility in the model were not altered by EPO treatment. In this rat model of flow-associated pulmonary arterial hypertension, erythropoietin treatment beneficially affected pulmonary vascular and cardiac remodelling. These histopathological effects were not accompanied by significantly improved haemodynamics.

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Capillary/myocyte mismatch in the heart in renal failure—a role for erythropoietin?

Cited by 56 publications

References 30 publications

CKD and Coronary Collateral Supply in Individuals Undergoing Coronary Angiography after Myocardial Infarction

CKD and Coronary Collateral Supply in Individuals Undergoing Coronary Angiography after Myocardial Infarction

Cross-Talk between the Kidney and the Cardiovascular System

Effects of erythropoietin on advanced pulmonary vascular remodelling

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