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. 2017 May 3;313(2):F487–F494. doi: 10.1152/ajprenal.00074.2017

Table 3.

Association of creatinine-adjusted urine concentration or activity of each RAS pathway component with DKD in people with type 1 diabetes

n
No DKD DKD OR (95% CI) P Value
No DKD DKD
Angiotensinogen/Cr, μg/g 76 37 15 (8, 24) 170 (18, 597) 2.2 (1.6, 3.3) 9.6 × 10−10
Cathepsin D/Cr, μg/g 73 37 31 (22, 46) 147 (85, 219) 6.5 (3.5, 14.6) 2.3 × 10−14
ACE/Cr, μg/g 73 37 0.8 (0.4, 1.4) 1.4 (0.9, 2.5) 2.2 (1.4, 3.9) 3.8 × 10−4
ACE activity/Cr, 109 RFU/g 81 37 1.6 (1.0, 2.1) 1.0 (0.8, 1.2) 0.3 (0.1, 0.6) 4.6 × 10−4
ACE2/Cr, μg/g 73 37 2.7 (1.7, 4.2) 4.1 (1.6, 5.7) 1.1 (0.8, 1.7) 0.54
ACE2 activity/Cr, 106 RFU/h/g 81 37 0.3 (0.1, 0.9) 0.4 (0.2, 0.9) 1.2 (1.0, 1.4) 0.03
APA activity/Cr, 106 RFU/h/g 81 37 22 (4, 89) 40 (11, 210) 1.2 (1.0, 1.3) 0.05

Values are medians (IQR). People with no DKD had eGFR ≥90 ml/min/1.73m2 and ACR <300 mg/g after ≥30 yr of type 1 diabetes. Those with DKD had either an ACR ≥300 mg/g or both eGFR <60 ml/min/1.73m2 and ACR ≥30 mg/g. Odds ratios (OR) were obtained from logistic regression models with case-control status as outcome and urine concentration or activity of a single RAS component as exposure. Models were adjusted for age, sex, race, and diabetes duration.

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