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. Author manuscript; available in PMC: 2016 Sep 16.
Published in final edited form as: JCI Insight. 2016 Aug 18;1(13):e87023. doi: 10.1172/jci.insight.87023

Figure 8. Soluble AREG and TNFR1 are significantly increased in the urine of AKI and CKD patients.

Figure 8

The urinary levels of the soluble ADAM17 substrates (AREG [A], TNFR1 [B], HB-EGF [C], TGFα [D], Axl [F], ICAM1 [G], and KIM1 [H]) and of the ADAM10 substrate cMET (E) were measured by ELISA in control, AKI, and CKD patients (n = 10; 50% of CKD patients were diabetics; patient demographics and details in Supplemental Table 1). *P < 0.05; **P < 0.01; ***P < 0.001 as determined by an unpaired 2-tailed Student’s t test. AREG, amphiregulin; TNFR, tumor necrosis factor receptor; AKI, acute kidney injury; CKD, chronic kidney disease; ADAM17, a disintegrin and metalloprotease 17; HB-EGF, heparin binding epidermal growth factor-like growth factor; ICAM1, intercellular adhesion molecule 1; KIM1, kidney injury molecule 1; cMET, met.