Evolución del compromiso cardiovascular de pacientes insuficientes renales, en hemodiálisis, sin bloqueo del eje renina-angiotensina
Background: Diabetes mellitus is an important risk factor for cardiovascular complications among patients on hemodialysis. However, the incidence of these complications among non diabetic patients on hemodialysis is not well known. Aim: To assess the incidence of cardiovascular complications in non...
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Sociedad Médica de Santiago
2009
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oai:scielo:S0034-988720090003000052009-06-15Evolución del compromiso cardiovascular de pacientes insuficientes renales, en hemodiálisis, sin bloqueo del eje renina-angiotensinaKunstmann,SoniaVukusich,AntonioMichea,LuisVarela,CristianAllende,IreneBravo,SebastiánGainza,DanielaSepúlveda,DanielaMarusic,ElisaFigueroa,Fernando Cytokines Heartfailure Kidney failure chronic Background: Diabetes mellitus is an important risk factor for cardiovascular complications among patients on hemodialysis. However, the incidence of these complications among non diabetic patients on hemodialysis is not well known. Aim: To assess the incidence of cardiovascular complications in non diabetic patients on hemodialysis. Patients and methods: Seventy five non diabetic patients aged 55.6 ± 17 years (48 males), receiving hemodialysis three times a week were evaluated with laboratory tests, echocardiogram anda carotid ultrasound. In 26 patients, interleukin 6, tumor necrosis factor alpha, and intercellular adhesión molecule (ICAM-1) were also measured. Patients were followed during two years. Results: The mean lapse of dialysis therapy was 6.5 ±5 years. The main cause of renal failure was hypertension. Sixty two percent had systolic hypertension, 86% had concentric left ventricular hypertrophy, 43% had atrial dilatation and 60% had calcifications in the thoracic aorta. Compared with normal controls, patients had higher levels of interleukin 6, tumor necrosis factor alpha and ICAM-1. Carotid media thickness was also higher and increased in the two years of follow up. No correlations were found between ventricular hypertrophy and dialysis lapse, packed red cell volume, calcium phosphorus product, parathormone levels or median arterial pressure. No cardiovascular events were recorded during the follow up period. Conclusions: Non diabetic patients on chronic hemodialysis have a high frequency of ventricular hypertrophy, carotid media thickening, aortic calcifications and an increase in proinflammatory cytokines.info:eu-repo/semantics/openAccessSociedad Médica de SantiagoRevista médica de Chile v.137 n.3 20092009-03-01text/htmlhttp://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872009000300005es10.4067/S0034-98872009000300005 |
institution |
Scielo Chile |
collection |
Scielo Chile |
language |
Spanish / Castilian |
topic |
Cytokines Heartfailure Kidney failure chronic |
spellingShingle |
Cytokines Heartfailure Kidney failure chronic Kunstmann,Sonia Vukusich,Antonio Michea,Luis Varela,Cristian Allende,Irene Bravo,Sebastián Gainza,Daniela Sepúlveda,Daniela Marusic,Elisa Figueroa,Fernando Evolución del compromiso cardiovascular de pacientes insuficientes renales, en hemodiálisis, sin bloqueo del eje renina-angiotensina |
description |
Background: Diabetes mellitus is an important risk factor for cardiovascular complications among patients on hemodialysis. However, the incidence of these complications among non diabetic patients on hemodialysis is not well known. Aim: To assess the incidence of cardiovascular complications in non diabetic patients on hemodialysis. Patients and methods: Seventy five non diabetic patients aged 55.6 ± 17 years (48 males), receiving hemodialysis three times a week were evaluated with laboratory tests, echocardiogram anda carotid ultrasound. In 26 patients, interleukin 6, tumor necrosis factor alpha, and intercellular adhesión molecule (ICAM-1) were also measured. Patients were followed during two years. Results: The mean lapse of dialysis therapy was 6.5 ±5 years. The main cause of renal failure was hypertension. Sixty two percent had systolic hypertension, 86% had concentric left ventricular hypertrophy, 43% had atrial dilatation and 60% had calcifications in the thoracic aorta. Compared with normal controls, patients had higher levels of interleukin 6, tumor necrosis factor alpha and ICAM-1. Carotid media thickness was also higher and increased in the two years of follow up. No correlations were found between ventricular hypertrophy and dialysis lapse, packed red cell volume, calcium phosphorus product, parathormone levels or median arterial pressure. No cardiovascular events were recorded during the follow up period. Conclusions: Non diabetic patients on chronic hemodialysis have a high frequency of ventricular hypertrophy, carotid media thickening, aortic calcifications and an increase in proinflammatory cytokines. |
author |
Kunstmann,Sonia Vukusich,Antonio Michea,Luis Varela,Cristian Allende,Irene Bravo,Sebastián Gainza,Daniela Sepúlveda,Daniela Marusic,Elisa Figueroa,Fernando |
author_facet |
Kunstmann,Sonia Vukusich,Antonio Michea,Luis Varela,Cristian Allende,Irene Bravo,Sebastián Gainza,Daniela Sepúlveda,Daniela Marusic,Elisa Figueroa,Fernando |
author_sort |
Kunstmann,Sonia |
title |
Evolución del compromiso cardiovascular de pacientes insuficientes renales, en hemodiálisis, sin bloqueo del eje renina-angiotensina |
title_short |
Evolución del compromiso cardiovascular de pacientes insuficientes renales, en hemodiálisis, sin bloqueo del eje renina-angiotensina |
title_full |
Evolución del compromiso cardiovascular de pacientes insuficientes renales, en hemodiálisis, sin bloqueo del eje renina-angiotensina |
title_fullStr |
Evolución del compromiso cardiovascular de pacientes insuficientes renales, en hemodiálisis, sin bloqueo del eje renina-angiotensina |
title_full_unstemmed |
Evolución del compromiso cardiovascular de pacientes insuficientes renales, en hemodiálisis, sin bloqueo del eje renina-angiotensina |
title_sort |
evolución del compromiso cardiovascular de pacientes insuficientes renales, en hemodiálisis, sin bloqueo del eje renina-angiotensina |
publisher |
Sociedad Médica de Santiago |
publishDate |
2009 |
url |
http://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872009000300005 |
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