ArticleMedicine2017
Metabolic acidosis of chronic kidney disease and subclinical cardiovascular disease markers: Friend or foe?
Article in Medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Artificial intelligence in chronic kidney diseases: methodology and potential applications.International urology and nephrology · 2025Review
- Dyslipidemia in children with chronic kidney disease-findings from the Cardiovascular Comorbidity in Children with Chronic Kidney Disease (4C) study.Pediatric nephrology (Berlin, Germany) · 2024Article
- Article
- Exhausted Capacity of Bicarbonate Buffer in Renal Failure Diagnosed Using Point of Care Analyzer.Diagnostics (Basel, Switzerland) · 2021Article
- Complications of metabolic acidosis and alkalinizing therapy in chronic kidney disease patients: a clinician-directed organ-specific primer.International urology and nephrology · 2020Review
- Metabolic acidosis is associated with pulse wave velocity in chronic kidney disease: Results from the KNOW-CKD Study.Scientific reports · 2019Article
- Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.