Cardiovascular Autonomic Neuropathy and Risk of Kidney Function Decline in Type 1 and Type 2 Diabetes: Findings From the PERL and ACCORD Cohorts.

IF 6.2 1区医学 Q1 ENDOCRINOLOGY & METABOLISM

Diabetes Pub Date : 2024-05-01 DOI:10.2337/db23-0247

Yaling Tang, Lynn Ang, Mamta Jaiswal, Brendan R Dillon, Nazanene H Esfandiari, Hetal S Shah, Cathie Spino, Cindy Plunkett, Bruce A Perkins, Rodica Pop-Busui, Alessandro Doria

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Abstract

Results of previous studies have suggested that cardiovascular autonomic neuropathy (CAN) may predict rapid kidney function decline among people with diabetes. We analyzed the association between baseline CAN and subsequent glomerular filtration rate (GFR) decline among individuals with type 1 diabetes (T1D) from the Preventing Early Renal Loss in Diabetes (PERL) study (N = 469) and with type 2 diabetes (T2D) from Action to Control Cardiovascular Risk in Diabetes (ACCORD) (N = 7,973). Baseline CAN was ascertained with electrocardiogram-derived heart rate variability indices. Its association with GFR slopes, rapid kidney function decline (GFR loss of ≥5 mL/min/1.73 m2/year), and ≥40% GFR loss was evaluated by linear mixed-effects, logistic, and Cox regression, respectively. Participants with CAN experienced more rapid GFR decline, by an excess 1.15 mL/min/1.73 m2/year (95% CI -1.93 to -0.37; P = 4.0 × 10-3) in PERL and 0.34 mL/min/1.73 m2/year (95% CI -0.49 to -0.19; P = 6.3 × 10-6) in ACCORD. This translated to 2.11 (95% CI 1.23-3.63; P = 6.9 × 10-3) and 1.39 (95% CI 1.20-1.61; P = 1.1 × 10-5) odds ratios of rapid kidney function decline in PERL and ACCORD, respectively. Baseline CAN was also associated with a greater risk of ≥40% GFR loss events during follow-up (hazard ratio 2.60 [95% CI 1.15-5.45], P = 0.02, in PERL and hazard ratio 1.54 [95% CI 1.28-1.84], P = 3.8 × 10-6, in ACCORD). These associations remained significant after adjustment for potential confounders, including baseline GFR and albuminuria. Our findings indicate that CAN is a strong, independent predictor of rapid kidney function decline in both T1D and T2D. Further studies of the link between these two complications may help with development of new therapies to prevent kidney function decline in patients with diabetes.

Article highlights:

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心血管自主神经病变与 1 型和 2 型糖尿病患者肾功能衰退的风险：PERL 和 ACCORD 队列的研究结果。

以往的研究结果表明，心血管自主神经病变（CAN）可能预示着糖尿病患者肾功能的快速下降。我们分析了 "预防糖尿病早期肾功能丧失"（PERL）研究中的 1 型糖尿病（T1D）患者（469 人）和 "控制糖尿病心血管风险行动"（ACCORD）研究中的 2 型糖尿病（T2D）患者（7973 人）基线 CAN 与随后肾小球滤过率（GFR）下降之间的关系。基线 CAN 是通过心电图得出的心率变异性指数确定的。通过线性混合效应、逻辑回归和 Cox 回归分别评估了 CAN 与 GFR 斜率、肾功能快速下降（GFR 下降≥5 mL/min/1.73 m2/年）和 GFR 下降≥40% 的关系。CAN 患者的 GFR 下降速度更快，在 PERL 中超过 1.15 mL/min/1.73 m2/year (95% CI -1.93 to -0.37; P = 4.0 × 10-3)，在 ACCORD 中超过 0.34 mL/min/1.73 m2/year (95% CI -0.49 to -0.19; P = 6.3 × 10-6)。这在 PERL 和 ACCORD 中分别转化为 2.11 (95% CI 1.23-3.63; P = 6.9 × 10-3) 和 1.39 (95% CI 1.20-1.61; P = 1.1 × 10-5) 的肾功能快速下降几率比。基线 CAN 还与随访期间 GFR 下降≥40% 事件的更大风险相关（PERL 的危险比为 2.60 [95% CI 1.15-5.45]，P = 0.02；ACCORD 的危险比为 1.54 [95% CI 1.28-1.84]，P = 3.8 × 10-6）。在对包括基线肾小球滤过率和白蛋白尿在内的潜在混杂因素进行调整后，这些相关性仍然显著。我们的研究结果表明，CAN 是 T1D 和 T2D 肾功能快速下降的一个强有力的独立预测因子。对这两种并发症之间联系的进一步研究可能有助于开发新的疗法，防止糖尿病患者肾功能衰退：

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来源期刊

Diabetes 医学-内分泌学与代谢

CiteScore

12.50

自引率

2.60%

发文量

1968

审稿时长

1 months

期刊介绍： Diabetes is a scientific journal that publishes original research exploring the physiological and pathophysiological aspects of diabetes mellitus. We encourage submissions of manuscripts pertaining to laboratory, animal, or human research, covering a wide range of topics. Our primary focus is on investigative reports investigating various aspects such as the development and progression of diabetes, along with its associated complications. We also welcome studies delving into normal and pathological pancreatic islet function and intermediary metabolism, as well as exploring the mechanisms of drug and hormone action from a pharmacological perspective. Additionally, we encourage submissions that delve into the biochemical and molecular aspects of both normal and abnormal biological processes. However, it is important to note that we do not publish studies relating to diabetes education or the application of accepted therapeutic and diagnostic approaches to patients with diabetes mellitus. Our aim is to provide a platform for research that contributes to advancing our understanding of the underlying mechanisms and processes of diabetes.