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Original article
The reciprocal interaction between LV remodelling and allograft outcomes in kidney transplant recipients
  1. Jung Nam An1,2,
  2. Young Hoon Kim3,
  3. Jun-Bean Park4,
  4. Jin Ho Hwang5,
  5. Kyung Don Yoo2,
  6. Jae Yoon Park2,
  7. Clara Tammy Kim6,
  8. Hack-Lyoung Kim7,
  9. Yong-Jin Kim4,
  10. Duck-Jong Han3,
  11. Chun Soo Lim1,2,
  12. Yon Su Kim2,
  13. Jung Pyo Lee1,2
  1. 1Division of Nephrology, Department of Internal Medicine, Seoul National University Boramae Medical Center, Seoul, Korea
  2. 2Division of Nephrology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea
  3. 3Department of Surgery, Asan Medical Center and University of Ulsan College of Medicine, Seoul, Korea
  4. 4Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea
  5. 5Division of Nephrology, Department of Internal Medicine, Chung-Ang University Hospital, Seoul, Korea
  6. 6Graduate School of Public Health, Seoul National University, Seoul, Korea
  7. 7Division of Cardiology, Department of Internal Medicine, Seoul National University Boramae Medical Center, Seoul, Korea
  1. Correspondence to Professor Jung Pyo Lee, Department of Internal Medicine, Seoul National University Boramae Medical Center, 20 Boramae-ro 5-gil, Dongjak-gu, Seoul 156-707, Republic of Korea; nephrolee{at}gmail.com

Abstract

Objective This study aimed to investigate the incidence and related clinical factors of LV hypertrophy (LVH) regression after kidney transplantation and its effect on graft outcome.

Methods Among the 3373 kidney transplant recipients who were enrolled in a multicentre cohort from 1997 to 2012, a total of 767 patients who underwent echocardiography before and after transplantation were included in this study followed for a median of 7.5 years.

Results LVH regression steadily increased from 7.4% at 1 year to 35.4% at 5 years over the 5-year post-transplantation period. The probability of LVH regression decreased in the patients who received a kidney transplant due to end-stage renal disease of unknown aetiology (p=0.041) or who underwent pretransplant haemodialysis (p=0.020). The probability of LVH regression also decreased as the pretransplant LV mass index (p<0.001) and post-transplant systolic blood pressure increased (p=0.005). Conversely, LVH regression was significantly associated with the highest tertile of the pretransplant haemoglobin level (p=0.029). Furthermore, in the 5th year after transplantation, persistent LVH was independently associated with allograft failure (HR 1.95; 95% CI 1.14 to 3.33; p=0.015) and the LV mass index reliably predicted graft outcome.

Conclusions LVH consistently regressed after kidney transplantation in most patients. Persistent LVH, low haemoglobin levels and elevated blood pressure were associated with an increased risk of allograft failure in kidney transplant recipients.

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