Figure 1.
PsuPAR levels correlate with stages of CKD in patients with SCD. (A) PsuPAR levels for patients with SCD without CKD (n = 44) and patients without SCD as healthy control participants (n = 8). Results for each patient and means for groups are shown. (B) PLAUR expression determined by RNA-seq in activated PBMCs collected from patients with SCD (n = 9) and non-SCD healthy control participants (n = 9). (C) PLAUR expression determined by RNA-seq in THP-1–derived macrophages treated with either sickle (HbS) or healthy (HbA) human hemoglobin for 24 hours (n = 2). (D) Quantification of immunofluorescent (IF) staining of uPAR in THP-1–derived macrophages treated with mutated HbS or normal hemoglobin (HbA) for 72 hours. 4′, 6-diamidino-2-phenylindole (DAPI) is used for nuclear staining. Results are normalized for DAPI (n = 3). (E) GPLD1 expression determined by RNA-seq in PBMCs collected from patients with SCD (n = 6) and patients without SCD as healthy control participants (n = 6). (F) Plasma uPA activity determined by enzyme-linked immunosorbent assays in patients with SCD (n = 13) and healthy control participants (n = 10). (G) Pearson correlation analysis of plasma log2 (PsuPAR) with log2 (eGFR) in patients with SCD (n = 77). (H) Pearson correlation analysis of urine log2 (UsuPAR/CRE) with log2 (eGFR) in patients with SCD (n = 44). (I) Pearson correlation analysis of plasma log2 (PsuPAR) with CKD stages in patients with SCD (n = 77). (J) Pearson correlation analysis of urine log2 (UsuPAR/CRE) with CKD stages in patients with SCD (n = 44). (K) Receiver operating characteristic analysis of PsuPAR shown for patients with SCD with stages 1 (n = 18) vs stages 2 to 4 (n = 10). Correlation and receiver operating characteristic were performed using GraphPad Prism 6. Results are shown as mean ± standard deviation. P < .05 was considered statistically significant. AUC, area under the curve; CRE, creatinine; MFI, mean fluorescence intensity; PsuPAR, plasma suPAR; UsuPAR, urine suPAR.

PsuPAR levels correlate with stages of CKD in patients with SCD. (A) PsuPAR levels for patients with SCD without CKD (n = 44) and patients without SCD as healthy control participants (n = 8). Results for each patient and means for groups are shown. (B) PLAUR expression determined by RNA-seq in activated PBMCs collected from patients with SCD (n = 9) and non-SCD healthy control participants (n = 9). (C) PLAUR expression determined by RNA-seq in THP-1–derived macrophages treated with either sickle (HbS) or healthy (HbA) human hemoglobin for 24 hours (n = 2). (D) Quantification of immunofluorescent (IF) staining of uPAR in THP-1–derived macrophages treated with mutated HbS or normal hemoglobin (HbA) for 72 hours. 4′, 6-diamidino-2-phenylindole (DAPI) is used for nuclear staining. Results are normalized for DAPI (n = 3). (E) GPLD1 expression determined by RNA-seq in PBMCs collected from patients with SCD (n = 6) and patients without SCD as healthy control participants (n = 6). (F) Plasma uPA activity determined by enzyme-linked immunosorbent assays in patients with SCD (n = 13) and healthy control participants (n = 10). (G) Pearson correlation analysis of plasma log2 (PsuPAR) with log2 (eGFR) in patients with SCD (n = 77). (H) Pearson correlation analysis of urine log2 (UsuPAR/CRE) with log2 (eGFR) in patients with SCD (n = 44). (I) Pearson correlation analysis of plasma log2 (PsuPAR) with CKD stages in patients with SCD (n = 77). (J) Pearson correlation analysis of urine log2 (UsuPAR/CRE) with CKD stages in patients with SCD (n = 44). (K) Receiver operating characteristic analysis of PsuPAR shown for patients with SCD with stages 1 (n = 18) vs stages 2 to 4 (n = 10). Correlation and receiver operating characteristic were performed using GraphPad Prism 6. Results are shown as mean ± standard deviation. P < .05 was considered statistically significant. AUC, area under the curve; CRE, creatinine; MFI, mean fluorescence intensity; PsuPAR, plasma suPAR; UsuPAR, urine suPAR.

Close Modal

or Create an Account

Close Modal
Close Modal