Department of Medicine, Division of Nephrology, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada.
Department of Medicine, Division of Nephrology, Toronto General Hospital, University of Toronto, Toronto, Ontario, Canada; Division of Nephrology, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
J Diabetes Complications. 2022 Nov;36(11):108320. doi: 10.1016/j.jdiacomp.2022.108320. Epub 2022 Sep 28.
To determine the relationship between renal hemodynamic function and neuropathy in adults with ≥50-years of type 1 diabetes (T1D) compared to nondiabetic controls.
Glomerular filtration rate (GFR, inulin), effective renal plasma flow (ERPF, p-aminohippurate), modified Toronto Clinical Neuropathy Score (mTCNS), corneal confocal microscopy, nerve conduction, and heart rate variability (autonomic function) were measured; afferent (R) and efferent (R) arteriolar resistances were estimated using the Gomez equations in 74 participants with T1D and in 75 controls. Diabetic kidney disease (DKD) non-resistors were defined by eGFR < 60 ml/min/1.73 m or 24-h urine albumin excretion >30 mg/day. Linear regression was applied to examine the relationships between renal function (dependent variable) and neuropathy measures (independent variable), adjusted for age, sex, HbA1c, systolic blood pressure, low density lipoprotein cholesterol, and 24-h urine albumin to creatinine ratio.
Higher mTCNS associated with lower renal blood flow (β ± SE:-9.29 ± 4.20, p = 0.03) and greater R (β ± SE:32.97 ± 15.43, p = 0.04) in participants with T1D, but not in controls. DKD non-resistors had a higher mTCNS and worse measures of corneal nerve morphology compared to those without DKD. Renal hemodynamic parameters did not associate with autonomic nerve function.
Although neurological dysfunction in the presence of diabetes may contribute to impaired renal blood flow resulting in ischemic injury in patients with T1D, early autonomic dysfunction does not appear to be associated with kidney function changes.
与非糖尿病对照相比，确定≥50 岁的 1 型糖尿病（T1D）成人的肾脏血流动力学功能与神经病变之间的关系。
测量肾小球滤过率（GFR，菊粉）、有效肾血浆流量（ERPF，对氨基马尿酸）、改良的多伦多临床神经病变评分（mTCNS）、角膜共焦显微镜、神经传导和心率变异性（自主神经功能）；使用 Gomez 方程在 74 名 T1D 患者和 75 名对照者中估计了传入（R）和传出（R）小动脉阻力。将 eGFR<60ml/min/1.73m 或 24 小时尿白蛋白排泄量>30mg/天定义为糖尿病肾病（DKD）非抵抗者。线性回归用于检查肾功能（因变量）与神经病变测量值（自变量）之间的关系，调整年龄、性别、HbA1c、收缩压、低密度脂蛋白胆固醇和 24 小时尿白蛋白与肌酐比值。
在 T1D 患者中，较高的 mTCNS 与较低的肾血流量（β±SE：-9.29±4.20，p=0.03）和较大的 R（β±SE：32.97±15.43，p=0.04）相关，但在对照组中没有。与无 DKD 相比，DKD 非抵抗者的 mTCNS 更高，角膜神经形态学测量值更差。肾脏血流动力学参数与自主神经功能无关。
尽管糖尿病存在的神经功能障碍可能导致 T1D 患者的肾血流受损，导致缺血性损伤，但早期自主神经功能障碍似乎与肾功能变化无关。
