Hobeika Liliane, Hunt Kelly J, Neely Benjamin A, Arthur John M
Department of Internal Medicine, Division of Nephrology (LH), Department of Internal Medicine, University of Louisville, Louisville, Kentucky; Department of Public Health Sciences (KJH), Medical University of South Carolina, Charleston, South Carolina; Ralph H Johnson VA Medical Center (KJH), Charleston, South Carolina; Division of Nephrology (BAN), Department of Internal Medicine, Medical University of South Carolina, Charleston, South Carolina; Division of Nephrology (JMA), Department of Internal Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas; and Central Arkansas Veterans Healthcare System (JMA), Little Rock, AR.
Am J Med Sci. 2015 Dec;350(6):447-52. doi: 10.1097/MAJ.0000000000000583.
Patients with diabetes and chronic kidney disease (CKD) without proteinuria are often believed to have a cause of CKD other than diabetes. It was hypothesized that if this is true, the rate of renal function decline should be similar among nonproteinuric patients with and without diabetes.
Patients seen in the nephrology, endocrinology and general internal medicine clinics at the Medical University of South Carolina (MUSC) between 2008 and 2012 with hypertension and diabetes were identified by ICD9 diagnosis codes. Patients with less than 2 measures of serum creatinine, without urine studies over the study period and with proteinuria were excluded. Four hundred seventy-two patients met the inclusion and exclusion criteria and had an initial estimated glomerular filtration rate (eGFR) between 35 and 80 mL/min per 1.73 m2. The annual rate of decline in eGFR was estimated for each patient from the lowest eGFR in each year by fitting a regression model with random intercept and slope.
In unadjusted analyses, the rate of eGFR decline was greater in patients with diabetes than without diabetes (-0.71 versus -0.30 mL · min(-1) · yr(-1), P = 0.03). After adjusting for age, race, sex, baseline eGFR and use of renin-angiotensin-aldosterone system blockade, the rate of decline was still greater among patients with diabetes than among those without diabetes (-0.68 versus -0.36 mL · min(-1) · yr(-1), P = 0.03).
Patients with diabetes had more rapid decline in kidney function compared with individuals without diabetes, despite the absence of proteinuria. These results suggest that even in the absence of proteinuria, diabetes may be associated with CKD.
糖尿病合并无蛋白尿的慢性肾脏病(CKD)患者常被认为患有非糖尿病所致的CKD。据推测,如果情况属实,那么有无糖尿病的非蛋白尿患者的肾功能下降速率应相似。
通过ICD9诊断编码识别2008年至2012年间在南卡罗来纳医科大学(MUSC)肾脏病科、内分泌科和普通内科门诊就诊的高血压合并糖尿病患者。排除血清肌酐测量次数少于2次、研究期间未进行尿液检查以及有蛋白尿的患者。472例患者符合纳入和排除标准,初始估计肾小球滤过率(eGFR)在35至80 mL/(min·1.73 m²)之间。通过拟合具有随机截距和斜率的回归模型,根据每年的最低eGFR估计每位患者的eGFR年下降率。
在未校正分析中,糖尿病患者的eGFR下降速率高于非糖尿病患者(-0.71对-0.30 mL·min⁻¹·yr⁻¹,P = 0.03)。在校正年龄、种族、性别、基线eGFR和肾素-血管紧张素-醛固酮系统阻滞剂的使用后,糖尿病患者的下降速率仍高于非糖尿病患者(-0.68对-0.36 mL·min⁻¹·yr⁻¹,P = 0.03)。
尽管无蛋白尿,但糖尿病患者的肾功能下降比非糖尿病个体更快。这些结果表明,即使没有蛋白尿,糖尿病也可能与CKD有关。