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Metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: Friend or foe?

The effect of chronic metabolic acidosis (MA) on cardiovascular disease (CVD) in the setting of chronic kidney disease (CKD) is largely unknown. Therefore, we aimed to study this relationship in nondialysis CKD patients. This cross-sectional, single-center study prospectively enrolled 95 clinically...

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Autores principales: Căpuşă, Cristina, Ştefan, Gabriel, Stancu, Simona, Lipan, Mariana, Tsur, Lilach Daniel, Mircescu, Gabriel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5708981/
https://www.ncbi.nlm.nih.gov/pubmed/29381982
http://dx.doi.org/10.1097/MD.0000000000008802
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author Căpuşă, Cristina
Ştefan, Gabriel
Stancu, Simona
Lipan, Mariana
Tsur, Lilach Daniel
Mircescu, Gabriel
author_facet Căpuşă, Cristina
Ştefan, Gabriel
Stancu, Simona
Lipan, Mariana
Tsur, Lilach Daniel
Mircescu, Gabriel
author_sort Căpuşă, Cristina
collection PubMed
description The effect of chronic metabolic acidosis (MA) on cardiovascular disease (CVD) in the setting of chronic kidney disease (CKD) is largely unknown. Therefore, we aimed to study this relationship in nondialysis CKD patients. This cross-sectional, single-center study prospectively enrolled 95 clinically stable CKD patients (median age 61 (58, 65) years, 60% male, median eGFR 27 (22, 32) mL/min). Data on CKD etiology, CVD history, CVD traditional, and nontraditional risk factors were obtained. Also, markers of subclinical CVD were assessed: intima-media thickness (IMT), abdominal aortic calcifications (Kauppila score—AACs), cardio-ankle vascular index (CAVI), ankle-brachial index (ABI), ejection fraction, and interventricular septum thickness. Using the serum bicarbonate cutoff value of 22 mEq/L, comparisons between MA (<22 mEq/L; 43 patients) and non-MA (≥22 mEq/L; 52 patients) groups were performed. Vascular (40%), tubulointerstitial (24%), and glomerular (22%) nephropathies were the main causes of CKD. Twenty-three percent of patients had diabetes mellitus, but only 5% were considered to have diabetic nephropathy. Patients with chronic MA had lower eGFR (P < .01), higher iPTH (P = .01), higher serum phosphate (P < .01), and increased serum cholesterol (P = .04) and triglycerides (P = .01). Higher ABI (P = .04), lower IMT (P = .03), CAVI (P = .05), and AACs (P = .03) were found in patients with chronic MA. Separate binomial logistic regression models were performed using ABI (cutoff 0.9), CAVI (cutoff 9), IMT (cutoff 0.1 cm), and AACs (cutoff 1) as dependent variables. MA was used as independent variable and adjustments were made for iPTH, serum phosphate, eGFR, proteinuria, cholesterol, triglycerides, CVD score. The absence of MA was retained as an independent predictor only for the presence of AACs. In conclusion, the present study shows a potential advantageous effect of MA on vascular calcifications in predialysis CKD patients. Thus, a guideline relaxation of the serum bicarbonate target might prove to be beneficial in CKD patients at high risk of vascular calcifications. However, one should always consider the negative effects of MA. Therefore, additional research is warranted before any clear clinical recommendation.
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spelling pubmed-57089812017-12-07 Metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: Friend or foe? Căpuşă, Cristina Ştefan, Gabriel Stancu, Simona Lipan, Mariana Tsur, Lilach Daniel Mircescu, Gabriel Medicine (Baltimore) 5200 The effect of chronic metabolic acidosis (MA) on cardiovascular disease (CVD) in the setting of chronic kidney disease (CKD) is largely unknown. Therefore, we aimed to study this relationship in nondialysis CKD patients. This cross-sectional, single-center study prospectively enrolled 95 clinically stable CKD patients (median age 61 (58, 65) years, 60% male, median eGFR 27 (22, 32) mL/min). Data on CKD etiology, CVD history, CVD traditional, and nontraditional risk factors were obtained. Also, markers of subclinical CVD were assessed: intima-media thickness (IMT), abdominal aortic calcifications (Kauppila score—AACs), cardio-ankle vascular index (CAVI), ankle-brachial index (ABI), ejection fraction, and interventricular septum thickness. Using the serum bicarbonate cutoff value of 22 mEq/L, comparisons between MA (<22 mEq/L; 43 patients) and non-MA (≥22 mEq/L; 52 patients) groups were performed. Vascular (40%), tubulointerstitial (24%), and glomerular (22%) nephropathies were the main causes of CKD. Twenty-three percent of patients had diabetes mellitus, but only 5% were considered to have diabetic nephropathy. Patients with chronic MA had lower eGFR (P < .01), higher iPTH (P = .01), higher serum phosphate (P < .01), and increased serum cholesterol (P = .04) and triglycerides (P = .01). Higher ABI (P = .04), lower IMT (P = .03), CAVI (P = .05), and AACs (P = .03) were found in patients with chronic MA. Separate binomial logistic regression models were performed using ABI (cutoff 0.9), CAVI (cutoff 9), IMT (cutoff 0.1 cm), and AACs (cutoff 1) as dependent variables. MA was used as independent variable and adjustments were made for iPTH, serum phosphate, eGFR, proteinuria, cholesterol, triglycerides, CVD score. The absence of MA was retained as an independent predictor only for the presence of AACs. In conclusion, the present study shows a potential advantageous effect of MA on vascular calcifications in predialysis CKD patients. Thus, a guideline relaxation of the serum bicarbonate target might prove to be beneficial in CKD patients at high risk of vascular calcifications. However, one should always consider the negative effects of MA. Therefore, additional research is warranted before any clear clinical recommendation. Wolters Kluwer Health 2017-11-27 /pmc/articles/PMC5708981/ /pubmed/29381982 http://dx.doi.org/10.1097/MD.0000000000008802 Text en Copyright © 2017 the Author(s). Published by Wolters Kluwer Health, Inc. http://creativecommons.org/licenses/by/4.0 This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0
spellingShingle 5200
Căpuşă, Cristina
Ştefan, Gabriel
Stancu, Simona
Lipan, Mariana
Tsur, Lilach Daniel
Mircescu, Gabriel
Metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: Friend or foe?
title Metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: Friend or foe?
title_full Metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: Friend or foe?
title_fullStr Metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: Friend or foe?
title_full_unstemmed Metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: Friend or foe?
title_short Metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: Friend or foe?
title_sort metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: friend or foe?
topic 5200
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5708981/
https://www.ncbi.nlm.nih.gov/pubmed/29381982
http://dx.doi.org/10.1097/MD.0000000000008802
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