Methods: This longitudinal study enrolled 439 patients The renal

Methods: This longitudinal study enrolled 439 patients. The renal end point was defined as commencement of dialysis

or death. The change in renal function was measured by estimated glomerular filtration rate (eGFR) slope. We measured two ECG P wave parameters corrected by heart rate, i.e. corrected P wave dispersion (PWdisperC) and corrected P wave maximum duration (PWdurMaxC). Results: Kaplan-Meier curves for renal end point-free survival showed PWdisperC tertile 3 (vs. tertile 1, P < 0.001) and VX-770 cost PWdurMaxC tertile 3 (vs. tertile 1, P = 0.001) were associated with progression to renal end poin (Figure 1A and B). Multivariate Cox-regression analysis identified increased PWdisperC (hazard ratio [HR], 1.020; Ceritinib manufacturer P < 0.001) and PWdurMaxC (HR, 1.013; P = 0.012) were independently associated with progression to renal end point (Table 2). Besides, increased

PWdisperC (change in slope, −0.016; P = 0.033) and PWdurMaxC (change in slope, −0.014; P = 0.045) were associated with rapid renal function decline (Table 3). Conclusion: Our study in patients of CKD stage 3–5 demonstrated increased PWdisperC and PWdurMaxC were independently associated with progression to renal end point and faster renal function decline. Screening patients by means of PWdisperC and PWdurMaxC on 12 lead ECG may help identify a high risk group of rapid renal function decline in CKD. “
“Aim:  To clarify whether the level of matrix metalloproteinase-9 (MMP-9), tissue inhibitor matrix metalloproteinase-1 (TIMP-1) or the ratio of MMP-9/TIMP-1 was associated with the renal involvement in Henoch–Schonlein purpura (HSP); and to explore

whether there existed early diagnostic measure for HSP nephritis (HSPN). Methods:  Sixty-six patients with HSPN, 68 patients with HSP and 60 healthy Vorinostat order children (control group) were enrolled into our study. Serum and urine samples before treatment were collected for detection. Results:  Compared with the HSP group and control group, serum MMP-9, TIMP-1 and ratio of MMP-9/TIMP-1 in the HSPN group were significantly higher (P < 0.05 and P < 0.01, respectively). Urine MMP-9, TIMP-1 and ratio of MMP-9/TIMP-1 in the HSPN group were obviously higher than those of the control group (P < 0.05) and the HSP group (P < 0.05). Receiver–operator curve (ROC) analysis was performed to obtain the area under the curve (AUC) and the AUC and its 95% confidence interval (CI) of serum MMP-9 were 0.97 and 0.95–0.99, respectively. The optimal cut-off point (sensitivity; specificity) of serum MMP-9 for diagnosing HSPN was 179.79 mg/L (0.96; 0.88). Conclusion:  Levels of MMP-9, TIMP-1 and ratio of MMP-9/TIMP-1 in serum and urine were remarkably high in the patients with HSPN, but the serum MMP-9 was more sensitive. Serum MMP-9 may be associated with the occurrence and development of renal involvement in HSPN and become an important indicator for early diagnosis of HSPN.

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