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慢性肾脏病的代谢性酸中毒与亚临床心血管疾病标志物:朋友还是敌人?

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

作者信息

Căpuşă Cristina, Ştefan Gabriel, Stancu Simona, Lipan Mariana, Tsur Lilach Daniel, Mircescu Gabriel

机构信息

Nephrology Department, "Carol Davila" University of Medicine and Pharmacy "Dr Carol Davila" Teaching Hospital of Nephrology "Carol Davila" University of Medicine and Pharmacy Romanian Renal Registry, Bucharest, Romania.

出版信息

Medicine (Baltimore). 2017 Nov;96(47):e8802. doi: 10.1097/MD.0000000000008802.

DOI:10.1097/MD.0000000000008802
PMID:29381982
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5708981/
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.

摘要

慢性代谢性酸中毒(MA)在慢性肾脏病(CKD)背景下对心血管疾病(CVD)的影响在很大程度上尚不清楚。因此,我们旨在研究非透析CKD患者中的这种关系。

这项横断面、单中心研究前瞻性纳入了95例临床稳定的CKD患者(中位年龄61(58,65)岁,60%为男性,中位估算肾小球滤过率(eGFR)27(22,32)mL/min)。获取了CKD病因、CVD病史、CVD传统和非传统危险因素的数据。此外,还评估了亚临床CVD的标志物:内膜中层厚度(IMT)、腹主动脉钙化(考皮拉评分 - AACs)、心踝血管指数(CAVI)、踝臂指数(ABI)、射血分数和室间隔厚度。使用血清碳酸氢盐临界值22 mEq/L,对MA组(<22 mEq/L;43例患者)和非MA组(≥22 mEq/L;52例患者)进行了比较。

血管性(40%)、肾小管间质(24%)和肾小球(22%)肾病是CKD的主要病因。23%的患者患有糖尿病,但只有5%被认为患有糖尿病肾病。慢性MA患者的eGFR较低(P <.01),全段甲状旁腺激素(iPTH)较高(P =.01),血清磷酸盐较高(P <.01),血清胆固醇(P =.04)和甘油三酯(P =.01)升高。

慢性MA患者的ABI较高(P =.04),IMT较低(P =.03),CAVI较低(P =.05),AACs较低(P =.03)。

分别以ABI(临界值0.9)、CAVI(临界值9)、IMT(临界值0.1 cm)和AACs(临界值1)作为因变量进行二项逻辑回归模型分析。将MA作为自变量,并对iPTH、血清磷酸盐、eGFR、蛋白尿、胆固醇、甘油三酯、CVD评分进行调整。仅对于AACs的存在,MA的缺乏被保留为独立预测因子。

总之,本研究表明MA对透析前CKD患者的血管钙化具有潜在的有利影响。因此,对于有血管钙化高风险的CKD患者,放宽血清碳酸氢盐目标的指南可能被证明是有益的。然而,人们应始终考虑MA的负面影响。因此,在做出任何明确的临床推荐之前,有必要进行更多的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52ed/5708981/2cd8198f2642/medi-96-e8802-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52ed/5708981/0dcfff26926f/medi-96-e8802-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52ed/5708981/2cd8198f2642/medi-96-e8802-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52ed/5708981/0dcfff26926f/medi-96-e8802-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/52ed/5708981/2cd8198f2642/medi-96-e8802-g003.jpg

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