Examining the factors contributing to the association between non-albuminuric CKD and a low rate of kidney function decline in diabetes.

Examining the factors contributing to the association between non-albuminuric CKD and a low rate of kidney function decline in diabetes.
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DOI:
10.1177/20420188221083518
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发表时间:
2022
影响因子:
3.8
通讯作者:
Shaw JE
Shaw JE
中科院分区:
医学3区
文献类型:
--
作者:
Buyadaa O;Salim A;Morton JI;Jandeleit-Dahm K;Magliano DJ;Shaw JE

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研究表明,在糖尿病患者中,非蛋白尿性慢性肾病(CKD)患者的肾功能下降速度比肾功能正常的患者慢。这表明存在保护性因素,确定这些因素可能会开辟干预目标。本研究的目的是确定保护性临床因素和非临床生物标志物,有助于非白蛋白尿CKD和CKD进展率低之间的关联。我们在美国慢性肾功能不全队列(CRIC)研究中的糖尿病和CKD参与者中检测了几个临床因素和33个非临床生物标志物与(1)正常白蛋白尿和(2)CKD进展率低的显著相关性。在线性回归中评估与正常白蛋白尿和低CKD进展率显著相关的因素,以估计其对非白蛋白尿CKD和CKD进展率之间相关性的潜在贡献。收缩压(SBP)、糖化血红蛋白(HbA 1c)、估计肾小球滤过率(eGFR)和6种生物标志物[β-微量蛋白(BTP)、肾损伤分子(KIM-1)、纤维蛋白原、fractalkine、脑利钠肽(BNP)和高敏肌钙蛋白-T(hsTnT)]与正常白蛋白尿和较低的eGFR下降率相关。正常白蛋白尿的单变量β系数为0.93 [95%置信区间(CI):0.82,1.05]。当包括所有相关因素和生物标志物时,回归系数降至0.54(95%CI:0.40,0.67)。非蛋白尿性CKD与eGFR发生率低相关的因素是SBP、HbA 1c、BTP、KIM-1、hsTnT、BNP、纤维蛋白原和fractalkine水平较低。较低水平的SBP和具有促炎和血管调节特征的生物标志物可以解释非白蛋白尿CKD和CKD进展率低之间高达40%的相关性。对这些生物标志物的进一步研究可能会导致治疗干预。
Studies have shown that among people with diabetes, those with non-albuminuric chronic kidney disease (CKD) have a slower rate of reduction in renal function than do those with normal renal function. This suggests the presence of protective factors, the identification of which may open up targets for intervention. The aim of this study was to identify protective clinical factors and nonclinical biomarkers that contribute to the association between non-albuminuric CKD and the low rate of progression of CKD. We tested for significant associations of several clinical factors and 33 nonclinical biomarkers with (1) normoalbuminuria and (2) a low rate of CKD progression among participants with diabetes and CKD enrolled in the Chronic Renal Insufficiency Cohort (CRIC) Study in the United States. Factors significantly associated with both normoalbuminuria and a low rate of CKD progression were assessed in linear regression to estimate their potential contributions to the association between non-albuminuric CKD and rate of CKD progression. Systolic blood pressure (SBP), glycated A1c (HbA1c), estimated glomerular filtration rate (eGFR) and six biomarkers [β-trace protein (BTP), kidney injury molecule (KIM-1), fibrinogen, fractalkine, brain natriuretic peptide (BNP) and high-sensitivity troponin-T (hsTnT)] were associated with both normoalbuminuria and a low rate of eGFR decline. The univariate β-coefficient for normoalbuminuria was 0.93 [95% confidence interval (CI): 0.82, 1.05]. When all associated factors and biomarkers were included, the regression coefficient decreased to 0.54 (95% CI: 0.40, 0.67). The factors that contributed to the association between non-albuminuric CKD and low rate of eGFR were lower levels of SBP, HbA1c, BTP, KIM-1, hsTnT, BNP, fibrinogen and fractalkine. Lower levels of SBP and biomarkers that have pro-inflammatory and vascular modulating features may explain up to 40% of the association between non-albuminuric CKD and low rate of CKD progression. Further investigation of these biomarkers may lead to therapeutic interventions.
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