Biopsied tissues were evalueted by light microscopy & indirect im

Biopsied tissues were evalueted by light microscopy & indirect immunofluresence study. Reports were demanded within 24 hours time. The initial reports were validated by subsequent clinical course &/or re-biopsy. Results: Amongst 623 renal transplants performed during the study period (jan 2010 to jan 2013), 72 patients had primary graft dysfunction & were biopsied. Biopsy results on day 1 were as shown

in table no.1. Conclusion: Per-operative graft biopsy of non-functioning kidney is a safe procedure with high diagnostic yield & considerable specificity. AN JUNG NAM1, HWANG JIN HO1, JEON HEE JUNG2, JUNG IN MOK1, PARK SU-KIL3, KIM YON SU2, KIM YOUNG HOON3, OH YUN KYU1, LIM CHUN SOO1, LEE JUNG PYO1 1Seoul National University Boramae Medical Center; 2Seoul National University College see more of Medicine; 3Asan Medical Center and University of Ulsan College of Medicine Introduction: Cardiovascular

disease is a leading cause of mortality in patients with end-stage renal disease, even undergoing PXD101 in vivo transplantation. Left ventricular hypertrophy (LVH) is the most common feature and an independent risk factor for cardiac complications in kidney transplant recipients. The aim of this study was to identify cardiac alteration after kidney transplantation and analyze predictors of the post-transplant LVH. Methods: Among 2957 kidney transplant recipients in a multicenter cohort from 1997 to 2012, a total of 206 patients who conducted echocardiography before and one year after transplantation were enrolled in this study. Echocardiographic findings and clinical

parameters were evaluated. Results: Kidney transplantation Tideglusib significantly reduced mean left ventricular mass index (LVMI) from 128.8 ± 47.2 g/m2 to 106.4 ± 33.0 g/m2 (p < 0.001) [Figure 1]. The ejection fraction was improved (59.4 ± 8.0% vs. 62.1 ± 6.7%, p < 0.001). The prevalence of LVH by echocardiography significantly decreased (62.6% vs. 46.1%, p = 0.001). The prevalence of diastolic dysfunction, mitral and tricuspid regurgitation, and pulmonary hypertension also decreased. Pre-transplant lower hemoglobin level (OR 0.74, 95% CI 0.56–0.96, p = 0.026) and pre-transplant higher LVMI (OR 1.02, 95% CI 1.01–1.02, p < 0.001) were independently associated with persistent LVH after kidney transplantation. On the other hand, ejection fraction, diastolic dysfunction, underlying renal disease, albumin or cholesterol level, blood pressure, rejection, and allograft function were not correlated with post-transplant LVH. Conclusions: Cardiac morphology and function were significantly improved by kidney transplantation. Treatment of anemia might be crucial in regression and prevention of persistent LVH in kidney transplant recipients.

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