中文摘要

心-肾-代谢综合征及其组分对全因及心血管死亡影响研究

心血管病（Cardiovascular Disease, CVD）、慢性肾脏病（Chronic Kidney Disease, CKD）与代谢异常密切相关，并相互作用，形成一个高度交织的疾病谱。为全面认识这一复杂关系，美国心脏协会（American Heart Association, AHA）于2023年提出“心-肾-代谢综合征”（Cardiovascular-Kidney-Metabolic Syndrome, CKM）的新概念，强调在全生命周期内对心血管、肾脏和代谢三大系统的协同管理，以实现精准预防和干预。CKM综合征被分为0至4期，涵盖了从代谢异常的早期阶段到临床CVD的全程过程。然而，当前关于CKM综合征在人群中的分布特征、各组分对死亡的独立作用及其交互效应仍缺乏系统研究，尤其在中国人群中更显不足。

本研究基于国家级公共卫生项目：心血管病高危人群早期筛查与综合干预项目（China Health Evaluation and Risk Reduction through Nationwide Teamwork, ChinaHEART），由国家财政部和国家卫生健康委支持、国家心血管病中心牵头实施。项目自2014年启动，覆盖全国31个省级行政区、285个地市、353个调查区，涵盖城乡不同人群，具有良好的全国代表性。截至2023年，ChinaHEART项目已建立覆盖时间长达10年的大规模前瞻性人群队列，提供了开展CKM综合征及其相关研究的宝贵数据资源与现实基础。

 

第一部分 “临床正常范围”尿白蛋白与肌酐比值与全因及心血管死亡的关联

背景：白蛋白尿是CKD早期敏感性指标，与CVD的发生及预后密切相关，其中尿白蛋白与肌酐比值（Urine Albumin to Creatinine Ratio, UACR）是评估白蛋白尿严重程度最常用的指标。根据肾脏疾病：改善全球预后（Kidney Disease: Improving Global Outcomes, KDIGO）组织指南，白蛋白尿可分为三个阶段：（1）UACR < 30 mg/g（A1期），尿白蛋白正常或轻度升高；（2）UACR 30-300 mg/g（A2期），尿白蛋白中度升高；（3）UACR > 300 mg/g（A3期），尿白蛋白重度升高。既往研究已证实，A2、A3期白蛋白尿显著增加终末期肾病（End Stage Kidney Disease, ESKD）的发病及不良预后风险。因此，我国临床实践通常以UACR 30mg/g作为白蛋白尿的临界值，高于该水平即被视为异常。近期研究表明，白蛋白尿是CVD发病与死亡的独立危险因素，并且在特定高危人群（如糖尿病、高血压患者及心血管病高危个体）中，即使UACR处于0-30 mg/g的“正常”范围内，其升高仍可能与死亡风险增加相关。然而，目前关于微量白蛋白尿在中国普通人群中的分布情况仍缺乏系统研究，UACR的安全范围尚不明确。此外，UACR在“正常”范围内的波动与全因死亡及特定死因之间的关联，尤其是在不同人群亚组中的具体影响，仍有待进一步探索。

 

目的：探讨白蛋白尿不同阶段在中国人群中的分布特征，分析UACR与全因死亡、CVD死亡及具体死因（包括缺血性心脏病、缺血性脑卒中及出血性脑卒中死亡）的关联。此外，进一步评估UACR导致死亡风险增加的阈值，并探讨其在不同人群亚组中的差异。

 

方法：基于ChinaHEART项目，在2014年11月至2021年12月，该项目在全国31个省筛查的35-75岁居民中，纳入包含完整尿微量白蛋白、尿肌酐数据的人群，计算UACR及其分布情况。将UACR分为A1、A2、A3期，A1期每5 mg/g为一组，分为6组。结局为全因死亡、总CVD死亡以及缺血性心脏病、缺血性脑卒中、出血性脑卒中死亡。分别使用COX风险比例回归模型和竞争风险模型分析探索不同UACR水平对全因死亡与具体死因的影响。

根据年龄（＜65和≥65岁）、性别、身体质量指数（body mass index, BMI）（＜28和≥28 kg/m²）、糖尿病、高血压、血脂异常、世界卫生组织（World Health Organization, WHO）/国际高血压学会（International Society of Hypertension, ISH）10年CVD风险评分（≥20%，10% ~ 20%，＜10%）进行亚组分析。

 

结果：在纳入分析的人287537中，经过年龄和性别标化的微量白蛋白尿发生率为8.4%。经过中位随访时间为5.7（四分位距：4.0 ~ 6.7）年的随访，共发生8604例死亡。UACR水平与全因死亡及CVD死亡风险正相关，竞争风险模型提示在所有UACR水平，CVD死亡风险比（Hazard Ratios, HRs）均高于全因死亡。即使UACR水平低至5-10 mg/g，全因死亡和CVD死亡风险仍显著增加。在调整了多因素的模型中，与UACR＜5 mg/g相比，UACR 5-10 mg/g时全因死亡、CVD死亡、缺血性心脏病死亡、缺血性脑卒中死亡、出血性脑卒中死亡的HRs及95%置信区间（Confidence Intervals, CIs）分别为1.18 (1.10-1.26) (P < 0.001)，1.36 (1.23-1.51) (P < 0.001)，1.36 (1.15-1.61) (P < 0.001)，1.37 (1.03-1.83) (P = 0.03)，1.40 (1.12-1.74) (P < 0.001)。UACR为0-30 mg/g时，糖尿病对UACR水平升高全因死亡风险增加有修饰作用（交互作用P = 0.01）。0-30 mg/g范围内UACR升高全因死亡和CVD死亡的风险越高的趋势在年龄、性别、BMI水平、10年CVD风险水平、和是否合并高血压、高脂血症的亚组中是一致的。

 

结论：

（1）UACR即使在5-10 mg/g范围内，也与全因死亡和CVD死亡风险增加相关；

（2）该关联在不同性别、年龄 <65岁、BMI <28 kg/m²、无糖尿病、无高血压、无血脂异常及低CVD风险（<10%）人群中均存在；

（3）本研究说明将UACR早期筛查纳入CVD风险评估以及早期降尿蛋白治疗的重要性。

 

第二部分 心血管病高危人群中代谢危险因素及生活方式对慢性肾脏病风险分层及预后的影响

背景：CKD是指肾脏结构或功能异常持续时间大于等于3个月，以肾小球滤过率（Glomerular Filtration Rate, GFR）小于60 ml/min/1.73m²或UACR大于等于30 mg/g为主要诊断标准。CKD已成为全球重要的公共卫生问题，中国患病率约10%。根据KDIGO指南，CKD可按照GFR和UACR水平进行风险分层，风险越高，预后越差。

CKD与CVD关系密切，CKD可增加CVD发病和死亡的风险，CKD、CVD二者相互作用，形成恶性循环，其中高血压、糖尿病、血脂异常是共同危险因素，氧化应激、水钠潴留、尿毒症毒素、炎症及肾素-血管紧张素-醛固酮系统过度激活等机制加速CVD进展。

CVD高危人群（包括既往CVD事件、糖尿病、代谢综合征、根据公式预测的CVD风险为高危人群）是CKD进展的重点关注对象。然而，当前对于CVD高危者CKD进展风险的认识不足：

（1）缺乏CVD高危人群CKD发生率及分布特征的数据，影响精准防控策略的制定；

（2）代谢危险因素对CKD进展的影响及生活方式改善的作用仍待明确；

（3）CKD与死亡风险的研究多为单次测量，缺乏对CKD进展及风险分层变化的动态观察；

（4）现有研究集中于代谢指标对CVD预防的作用，尚需探索其对CKD进展的影响及最佳控制目标。

 

目的：基于ChinaHEART项目，探索中国CVD高危人群中CKD的患病率及其风险分层分布特点。评估血糖、血压、血脂、饮食、运动、吸烟、饮酒与CKD进展的关系，分析不同代谢指标包括血糖、糖化血红蛋白、血压、血脂对CKD进展的影响。探索CKD风险分层的动态变化对全因死亡和CVD死亡、癌症死亡的影响。

 

方法：本研究基于ChinaHEART队列，在2020年1月至2021年12月该项目在全国31个省筛查的具有完整变量信息的35-75岁居民中，纳入包含完整尿蛋白、血肌酐数据的人群，计算UACR和估算肾小球滤过率（estimated glomerular filtration rate, eGFR）。基于UACR和eGFR，根据KDIGO指南将进行CKD风险分层，分为低危（无CKD）、中危、高危、极高危CKD。描述CVD高危人群中CKD风险分层特点。主要结局为CKD风险分层的变化，采用多因素COX比例风险回归模型分析代谢危险因素、生活方式与CKD风险分层进展的关联。在COX比例风险回归模型的基础上，采用限制立方样条对上述代谢指标进行建模，拟合其与CKD进展风险的非线性关系。次要结局为死亡，采用多因素COX比例风险回归模型以及竞争风险模型探索CKD风险分层的变化与全因死亡、心血管死亡、癌症死亡的关联。

 

结果：在符合条件的185034名CVD高危患者中，9.6%合并不同程度的CKD，经过877天（四分位距：818-926）的随访后，5.6% CVD高危患者发生CKD风险分层进展，糖尿病（HR 1.96, 95% CI 1.89-2.04）是影响CKD进展最显著的因素，其次为高血压（HR 1.81, 95% CI 1.66-1.98），肥胖（HR 1.13, 95% CI 1.08-1.18）。在血脂方面，高甘油三酯血症（HR 1.21, 95% CI 1.15-1.26），总胆固醇（total cholesterol, TC）升高（HR 1.11, 95% CI 1.04-1.19）以及高密度脂蛋白胆固醇（high-density lipoprotein cholesterol, HDL-C）减低（HR 1.10, 95% CI 1.04-1.15）均为危险因素。在生活方式方面，饮酒（HR 0.90, 95%CI 0.84-0.97）、摄入充足新鲜蔬菜（HR 0.81, 95%CI 0.78-0.85）、肉类（HR 0.87, 95%CI 0.82-0.91）使CKD进展风险减低，而摄入充足豆制品（HR 1.10, 95%CI 1.04-1.16）使CKD进展风险显著增加。收缩压、舒张压与CKD风险进展呈U型关系，而BMI、腰围、血糖、糖化血红蛋白与CKD风险进展正相关。血脂方面，TC与CKD风险分层进展呈U型关系，HDL-C与CKD风险分层进展呈负相关，甘油三酯与CKD风险分层进展呈正相关。与CKD风险分层不变相比，CKD风险分层进展显著增加全因死亡（HR 1.63, 95% CI 1.22-2.16）与癌症死亡（HR 2.17, 95% CI 1.16-4.04）风险，CVD死亡风险边界显著（HR 1.41, 95% CI 0.95-2.10, P ＜ 0.1）。

 

结论：

（1）CVD高危人群CKD风险分成进展风险较高，糖尿病、高血压、肥胖、血脂异常是CKD进展的主要风险因素；

（2）生活方式对CKD风险分层进展有显著影响，主要包括饮酒以及蔬菜、肉类与豆制品的摄入。

（3）CKD进展显著增加全因死亡和癌症死亡风险，并可能增加CVD死亡风险；

（4）应重视CVD高危人群CKD早筛、精准风险分层及综合管理，以降低CKD进展及相关死亡风险。

 

第三部分 心-肾-代谢综合征与死亡的关联及其各组分与死亡风险的异质性

背景：随着对心血管疾病，慢性肾脏病，代谢综合征之间相互关系的认识加深，AHA在2023年提出了CKM综合征的概念。CKM综合征与CKD、CVD和肾脏不良结局的风险密切相关。且大部分CKM综合征患者的死亡是由于CVD。目前对CKM与死亡的研究存在以下不足：

尽管CKM综合征的流行病学特征已得到一定程度的揭示，但现有研究样本量有限，并且集中于特定人群，缺乏对一般人群的代表性，且缺乏死因别死亡的差异研究，CKM综合征对健康结局的影响仍未得到充分探索。

CKM综合征涉及多个组成部分，在CKM框架中其各组分对死亡影响的异质性需要进一步探索。主要体现在：首先，CKD在CKM框架中对死亡的风险需要进一步评估；其次，CKM 2期涵盖了所有的代谢危险因素及CKD，但目前尚不清楚在CKM 2期中各组分对死亡的作用。因此，明确不同代谢危险因素、CKD危险分层以及其相互作用对死亡风险的影响，有助于进一步完善CKM分期体系。

 

目的：探讨CKM综合征在中国CVD高危人群中的发生率及分布特点。探索CKM分期对全因死亡，CVD死亡以及CVD具体死因（包括缺血性心脏病、缺血性脑卒中、出血性脑卒中）的影响，以及CKM的组分，尤其是CKD以及CKM2期中不同代谢危险因素与死亡的关联的异质性。

 

方法：本研究基于ChinaHEART队列，2014年11月到2023年12月之间，有完整血肌酐和尿蛋白数据的参与者。排除年龄、性别、纳入时间缺失的人群。描述CKM综合征各个分期的比例和不同人群中的特征。采用COX回归模型分析CKM综合征分期，以及CKM综合征的组分（主要是代谢危险因素和CKD）与全因死亡的关联；采用竞争风险模型分析CKM综合征分期，以及CKM综合征的组分与CVD死亡及CVD具体死因的关联。

 

结果：共纳入764856名研究对象，平均年龄为61.2±9.4岁，其中57.3%为女性。CKM综合征的发生率为98.4%，其中3.8%合并CKM 1期；61.1%合并CKM 2期；14.4%合并CKM 3期，即CVD高危；19.1%合并CKM 4期，即临床CVD期。经过中位时间为926天（四分位距：588-1087）的随访，共发生16694例死亡，其中8393例死因为CVD。CKM 0期与1期之间全因死亡和CVD死亡无显著差异（P＞0.05），因此我们将CKM 0-1期作为对照组。与CKM 0-1期相比，CKM分期越高，全因死亡和CVD死亡风险越大，即使CKM 2期全因死亡（HR 1.47, 95% CI 1.31-1.64）和CVD死亡风险也显著增加（HR 2.62, 95% CI 2.10-3.27）。

CKM综合征的各个组分对全因和CVD死亡的影响存在异质性：CKM 2、3、4期合并CKD者全因死亡风险比同期无CKD者增加90%、129%、167%，CVD死亡风险增加180%、254%、372%，即使中危CKD也会显著增加全因和CVD死亡的风险。对于CKM 2期而言，CKD对全因及CVD死亡的影响最大，其次为糖尿病合并高血压，而对于全因死亡而言，其次为糖尿病，而后为高血压，对于CVD死亡而言其次为高血压，而后为糖尿病。空腹血糖升高、腰围增加、甘油三酯升高和高密度脂蛋白胆固醇减低对全因死亡和CVD死亡无显著影响。

 

结论：

（1）在中国CVD高危人群中CKM综合征普遍存在，大部分个体处于CKM 2期；

（2）CKM分期与全因死亡及CVD死亡风险呈正相关；

（3）CKD，即使是中危CKD在各期中均显著增加死亡风险，提示在CKM分期可能需要进一步根据是否合并CKD或CKD风险分层进行优化，以及早期关注肾小球结构和功能的保护、维持低水平白蛋白尿和正常GFR的重要性，以降低远期死亡风险；

（4）不同代谢异常对全因死亡和CVD死亡的影响存在差异，提示未来需进一步细化CKM分期，以优化个体化筛查和预防策略。

 

 

Abstract

The Impact of Cardiovascular-Kidney-Metabolic Syndrome and Its Components on All-Cause and Cardiovascular Mortality

Cardiovascular disease (CVD), chronic kidney disease (CKD), and metabolic disorders are interrelated and mutually reinforcing. To address this complex interplay, the American Heart Association (AHA) introduced the concept of Cardiovascular-Kidney-Metabolic (CKM) Syndrome in 2023, highlighting the need for integrated, life-course management of cardiovascular, renal, and metabolic health. CKM syndrome spans five stages (0–4), from early metabolic abnormalities to clinical CVD. However, evidence on the distribution of CKM syndrome and the contribution of its components to mortality—particularly in Chinese populations—remains limited.

This study is based on the China Health Evaluation and Risk Reduction through Nationwide Teamwork (ChinaHEART) project, a national public health initiative supported by the Ministry of Finance and the National Health Commission, and led by the National Center for Cardiovascular Diseases. Since 2014, ChinaHEART has covered 31 provinces, 285 cities, and 353 survey sites, with broad urban-rural representation. By 2023, it had established a large-scale, prospective cohort with up to 10 years of follow-up, offering a robust foundation for CKM-related research.

 

Part I: Association Between Clinically "Normal Range" Urine Albumin-to-Creatinine Ratio and Risk of All-Cause and Cardiovascular Mortality

Background: Albuminuria is an early and sensitive marker of CKD, closely linked to the onset and prognosis of CVD. The urine albumin-to-creatinine ratio (UACR) is the most widely used measure to quantify albuminuria severity. According to the Kidney Disease: Improving Global Outcomes (KDIGO) guidelines, UACR is categorized into three stages: A1 (<30 mg/g), A2 (30-300 mg/g), and A3 (>300 mg/g). While UACR ≥30 mg/g is considered abnormal in clinical practice and associated with adverse kidney outcomes, emerging evidence suggests that even UACR within the "normal" range (<30 mg/g) may increase the risk of CVD and mortality, particularly in high-risk populations. However, the distribution and prognostic significance of low-grade albuminuria in the general Chinese population remain understudied.

Objective: To assess the distribution of UACR stages in the Chinese population and investigate associations between UACR and all-cause mortality, CVD mortality, and cause-specific mortality (including ischemic heart disease, ischemic stroke, and hemorrhagic stroke). Risk thresholds and subgroup differences were also evaluated.

Methods: We analyzed data from the ChinaHEART project, including adults aged 35-75 years with available urinary albumin and creatinine data across 31 provinces between November 2014 and December 2021. UACR was categorized into A1-A3 stages, with A1 further divided into six 5 mg/g subgroups. Outcomes included all-cause death and cause-specific deaths. COX regression and competing risk models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs), with subgroup analyses by age, sex, body mass index (BMI), diabetes, hypertension, dyslipidemia, and World Health Organization/International Society of Hypertension (WHO/ISH) 10-year CVD risk levels.

Results: The age- and sex-standardized prevalence of microalbuminuria was 8.4%. During a median follow-up of 5.7 years [interquartile range (IQR): 4.0-6.7], a total of 8604 deaths were recorded. The UACR level was positively associated with both all-cause and CVD mortality. In competing risk models, the HRs for CVD mortality exceeded those for all-cause mortality across all UACR categories. Notably, even within the 5-10 mg/g UACR range significantly elevated risks of all-cause and CVD mortality were observed. After adjustment for multiple confounders, compared to UACR <5 mg/g, the HRs (95% CIs) for UACR 5-10 mg/g were: 1.18 (1.10-1.26) for all-cause mortality, 1.36 (1.23-1.51) for CVD mortality, 1.36 (1.15-1.61) for ischemic heart disease mortality, 1.37 (1.03-1.83) for ischemic stroke mortality, and 1.40 (1.12-1.74) for hemorrhagic stroke mortality. Within the UACR range of 0-30 mg/g, diabetes significantly modified the association with all-cause mortality (P for interaction = 0.01). The positive associations between UACR and both all-cause and CVD mortality were consistent across subgroups defined by age, sex, BMI, 10-year CVD risk, and the presence of hypertension or dyslipidemia.

Conclusion: Elevated UACR, even at 5-10 mg/g, was linked to higher all-cause and CVD mortality. This association was observed across subgroups, including individuals of different genders, those under 65, with BMI < 28 kg/m², without diabetes, hypertension, or dyslipidemia, and those with low CVD risk (< 10%). Within the 0-30 mg/g UACR range, the mortality increase due to elevated UACR was mainly attributable to CVD mortality. Early UACR screening should be integrated into CVD risk assessment to facilitate timely albumin-lowering interventions and reduce mortality risk.

 

Part II: Influence of Metabolic Risk Factors and Lifestyle on Chronic Kidney Disease Progression and Prognosis in High-Risk Cardiovascular Populations

Background: CKD, defined as kidney structural or functional abnormalities persisting for ≥3 months, is commonly diagnosed by estimated glomerular filtration rate (eGFR) <60 ml/min/1.73m² or urine albumin-to-creatinine ratio (UACR) ≥30 mg/g. In China, CKD affects approximately 10% of the population. According to KDIGO guidelines, CKD can be stratified into risk categories based on GFR and UACR, with higher risk levels predicting poorer outcomes. CKD and CVD are closely interrelated, sharing common risk factors such as hypertension, diabetes, and dyslipidemia, and promoting each other through mechanisms including oxidative stress, inflammation, and RAAS overactivation. However, in high-CVD-risk populations, CKD progression remains underexplored, particularly regarding its prevalence, metabolic contributors, and lifestyle influences.

Objective: To evaluate CKD prevalence and risk stratification distribution in Chinese adults at high risk of CVD; to investigate the influence of metabolic factors (e.g., glycemic, blood pressure, lipid profiles) and lifestyle behaviors on CKD risk progression; and to assess the association between CKD progression and mortality outcomes.

Methods: Using data from the ChinaHEART project (2020-2021), we included 185034 adults aged 35-75 years with complete biomarker data. CKD risk was categorized into low, moderate, high, and very high according to KDIGO guidelines. COX proportional hazards models and restricted cubic splines were used to assess the associations of metabolic factors and lifestyle behaviors with CKD progression. Mortality outcomes were assessed using COX and competing risk models.

Results: Among high-CVD-risk individuals, 9.6% had CKD at baseline. During a median follow-up of 877 days (IQR: 818-926), 5.6% experienced CKD risk progression. Diabetes, hypertension, and obesity were key contributors. Lipid profiles showed heterogeneity: hypertriglyceridemia, elevated total cholesterol (TC), and reduced high-density lipoprotein cholesterol (HDL-C) were both risk factors. Protective lifestyle factors included alcohol intake, sufficient fresh vegetable and meat consumption; excessive soy product intake increased risk. Systolic and diastolic blood pressure showed U-shaped associations, while BMI, waist circumference, blood glucose, and glycosylated hemoglobin (HbA1c) were positively associated with CKD progression. Advanced CKD risk was associated with higher risks of all-cause death and cancer death, and borderline increased CVD mortality (P <0.1).

Conclusion: Nearly 10% of individuals at high CVD risk have CKD, and 5.6% experience CKD progression within 2 years. Diabetes, hypertension, obesity, and dyslipidemia are major risk factors. Certain lifestyle behaviors are protective (vegetables, meat, moderate alcohol), while excess soy may increase risk. CKD progression significantly raises all-cause and cancer mortality. Early screening and precision management of CKD in high-CVD-risk populations are critical to reducing disease burden.

 

Part III: Association of Cardiovascular-Kidney-Metabolic Syndrome with Mortality and the Heterogeneity of Its Components in Mortality Risk.

Background: As understanding of the interrelationship between cardiovascular disease, chronic kidney disease, and metabolic syndrome deepens, the AHA introduced the concept of CKM syndrome in 2023. CKM syndrome is strongly linked to the risk of chronic kidney disease, cardiovascular disease, and adverse renal outcomes. Furthermore, most deaths in CKM syndrome patients are attributed to CVD. However, significant gaps remain in understanding the association between CKM syndrome and mortality risk, the heterogeneity of mortality risk across its components, and the mortality risk of CKM syndrome in different populations.

Methods: The study was based on the ChinaHEART project, which included participants with available data on serum creatinine and urinary protein between November 2014 and December 2023. Participants with missing data on age, sex, date of birth, or inclusion time were excluded. The study described the distribution of CKM syndrome stages and characteristics across different populations. COX regression was used to analyze the relationship between CKM syndrome stages and its components (mainly metabolic components and CKD) with all-cause mortality. A competing risk model was applied to assess the association between CKM stage, components, and CVD mortality. Participants were grouped by age, gender, smoking, drinking, diet, and exercise to explore the effects of CKM syndrome stages and components on all-cause and CVD mortality within each subgroup.

Results: A significant positive correlation was established between CKM stages and mortality risk, particularly pronounced for cardiovascular mortality, with adjusted HRs and 95% CIs of 2.62 (2.10-3.27), 4.04 (3.22-5.07), and 5.64 (4.51-7.05) for stages 2, 3, and 4, respectively. When comparing to those without CKD at each CKM stage, the presence of CKD was associated with an increased risk of all-cause mortality by 90%, 129%, and 167%, and an increased risk of cardiovascular mortality by 180%, 254%, and 372% for CKM stages 2, 3, and 4, respectively. Notably, even moderate-risk CKD was linked to an increased mortality risk. Among the various components at CKM stage 2, CKD emerged as the most significant risk factor of mortality, followed by diabetes and hypertension.

Conclusions: The risk of mortality, primarily by CVD, increases with advancing stages of CKM. Sub-staging CKM syndrome by prioritizing the presence of CKD or CKD risk stratification, and metabolic risk factors can improve the accuracy of mortality risk evaluations. Consistent monitoring and early interventions aimed at maintaining renal function may significantly reduce the risk of mortality.