Progression of interstitial fibrosis during the first year after deceased donor kidney transplantation among patients with and without delayed graft function

Raymond L. Heilman, Maxwell L. Smith, Byron H. Smith, Ibrahim Qaqish, Hasan Khamash, Andrew L. Singer, Bruce Kaplan, Kunam Sudhakar Reddy

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Background and objectives Delayed graft function is a form of AKI resulting from ischemia-reperfusion injury. Our aim was to study the effect of delayed graft function on the progression of interstitial fibrosis after deceased donor kidney transplantation. Design, setting, participants, & measurements Our study is a retrospective study of all patients transplanted at our center between July of 2003 and September of 2014 using a kidney from a deceased donor. The primary outcome was the progression of interstitial fibrosis on serial protocol biopsies done during the first year posttransplant. We analyzed the distribution of the change in the Banff interstitial fibrosis (ci) score between the delayed graft function and nondelayed graft function groups for all of the paired biopsies done at time 0 and 12 months post-transplant (Δfibrosis). We also performed a linear mixed model analyzing the difference in the slopes for the progression ofmean Banff ci score for all of the biopsies done at time 0 and 1, 4, and 12months posttransplant. Results Therewere 343 (36.7%) in the delayed graft function group and 591 in the control group. The biopsy rates for the delayed graft function and nondelayed graft function groups at time 0 were 65.3% (n=224) and 67.0% (n=396), respectively, and at 12 months, theywere 64.4% (n=221) and 68.4%(n=404), respectively. Paired biopsies were available for 155 in the delayed graft function group and 283 in the control group. In a risk-adjustedmodel, Banff ci score >0 on the time 0 biopsy had a higher odds of delayed graft function (odds ratio, 1.70; 95% confidence interval, 1.03 to 2.82). The distribution of the Δfibrosis between 0 and 12monthswas similar in delayed graft function and control groups (P=0.91). The slopes representing the progression of fibrosis were also similar between the groups (P=0.66). Conclusions Donor-derived fibrosis may increase the odds of delayed graft function; however, delayed graft function does not seem to increase the progression of fibrosis during the first year after transplantation.

Original languageEnglish (US)
Pages (from-to)2225-2232
Number of pages8
JournalClinical Journal of the American Society of Nephrology
Volume11
Issue number12
DOIs
StatePublished - 2016

Fingerprint

Delayed Graft Function
Kidney Transplantation
Fibrosis
Tissue Donors
Biopsy
Transplants
Control Groups
Reperfusion Injury
Linear Models
Retrospective Studies
Transplantation
Odds Ratio
Confidence Intervals

Keywords

  • Acute kidney injury
  • Biopsy
  • Control Groups
  • Delayed graft function
  • Delayed graft function after kidney transplant
  • Fibrosis
  • Humans
  • Interstitial fibrosis
  • Ischemia reperfusion injury and kidney transplant
  • Kidney
  • Kidney transplantation
  • Reperfusion Injury
  • Retrospective Studies
  • Tissue Donors

ASJC Scopus subject areas

  • Epidemiology
  • Critical Care and Intensive Care Medicine
  • Nephrology
  • Transplantation

Cite this

Progression of interstitial fibrosis during the first year after deceased donor kidney transplantation among patients with and without delayed graft function. / Heilman, Raymond L.; Smith, Maxwell L.; Smith, Byron H.; Qaqish, Ibrahim; Khamash, Hasan; Singer, Andrew L.; Kaplan, Bruce; Reddy, Kunam Sudhakar.

In: Clinical Journal of the American Society of Nephrology, Vol. 11, No. 12, 2016, p. 2225-2232.

Research output: Contribution to journalArticle

Heilman, Raymond L. ; Smith, Maxwell L. ; Smith, Byron H. ; Qaqish, Ibrahim ; Khamash, Hasan ; Singer, Andrew L. ; Kaplan, Bruce ; Reddy, Kunam Sudhakar. / Progression of interstitial fibrosis during the first year after deceased donor kidney transplantation among patients with and without delayed graft function. In: Clinical Journal of the American Society of Nephrology. 2016 ; Vol. 11, No. 12. pp. 2225-2232.
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abstract = "Background and objectives Delayed graft function is a form of AKI resulting from ischemia-reperfusion injury. Our aim was to study the effect of delayed graft function on the progression of interstitial fibrosis after deceased donor kidney transplantation. Design, setting, participants, & measurements Our study is a retrospective study of all patients transplanted at our center between July of 2003 and September of 2014 using a kidney from a deceased donor. The primary outcome was the progression of interstitial fibrosis on serial protocol biopsies done during the first year posttransplant. We analyzed the distribution of the change in the Banff interstitial fibrosis (ci) score between the delayed graft function and nondelayed graft function groups for all of the paired biopsies done at time 0 and 12 months post-transplant (Δfibrosis). We also performed a linear mixed model analyzing the difference in the slopes for the progression ofmean Banff ci score for all of the biopsies done at time 0 and 1, 4, and 12months posttransplant. Results Therewere 343 (36.7{\%}) in the delayed graft function group and 591 in the control group. The biopsy rates for the delayed graft function and nondelayed graft function groups at time 0 were 65.3{\%} (n=224) and 67.0{\%} (n=396), respectively, and at 12 months, theywere 64.4{\%} (n=221) and 68.4{\%}(n=404), respectively. Paired biopsies were available for 155 in the delayed graft function group and 283 in the control group. In a risk-adjustedmodel, Banff ci score >0 on the time 0 biopsy had a higher odds of delayed graft function (odds ratio, 1.70; 95{\%} confidence interval, 1.03 to 2.82). The distribution of the Δfibrosis between 0 and 12monthswas similar in delayed graft function and control groups (P=0.91). The slopes representing the progression of fibrosis were also similar between the groups (P=0.66). Conclusions Donor-derived fibrosis may increase the odds of delayed graft function; however, delayed graft function does not seem to increase the progression of fibrosis during the first year after transplantation.",
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T1 - Progression of interstitial fibrosis during the first year after deceased donor kidney transplantation among patients with and without delayed graft function

AU - Heilman, Raymond L.

AU - Smith, Maxwell L.

AU - Smith, Byron H.

AU - Qaqish, Ibrahim

AU - Khamash, Hasan

AU - Singer, Andrew L.

AU - Kaplan, Bruce

AU - Reddy, Kunam Sudhakar

PY - 2016

Y1 - 2016

N2 - Background and objectives Delayed graft function is a form of AKI resulting from ischemia-reperfusion injury. Our aim was to study the effect of delayed graft function on the progression of interstitial fibrosis after deceased donor kidney transplantation. Design, setting, participants, & measurements Our study is a retrospective study of all patients transplanted at our center between July of 2003 and September of 2014 using a kidney from a deceased donor. The primary outcome was the progression of interstitial fibrosis on serial protocol biopsies done during the first year posttransplant. We analyzed the distribution of the change in the Banff interstitial fibrosis (ci) score between the delayed graft function and nondelayed graft function groups for all of the paired biopsies done at time 0 and 12 months post-transplant (Δfibrosis). We also performed a linear mixed model analyzing the difference in the slopes for the progression ofmean Banff ci score for all of the biopsies done at time 0 and 1, 4, and 12months posttransplant. Results Therewere 343 (36.7%) in the delayed graft function group and 591 in the control group. The biopsy rates for the delayed graft function and nondelayed graft function groups at time 0 were 65.3% (n=224) and 67.0% (n=396), respectively, and at 12 months, theywere 64.4% (n=221) and 68.4%(n=404), respectively. Paired biopsies were available for 155 in the delayed graft function group and 283 in the control group. In a risk-adjustedmodel, Banff ci score >0 on the time 0 biopsy had a higher odds of delayed graft function (odds ratio, 1.70; 95% confidence interval, 1.03 to 2.82). The distribution of the Δfibrosis between 0 and 12monthswas similar in delayed graft function and control groups (P=0.91). The slopes representing the progression of fibrosis were also similar between the groups (P=0.66). Conclusions Donor-derived fibrosis may increase the odds of delayed graft function; however, delayed graft function does not seem to increase the progression of fibrosis during the first year after transplantation.

AB - Background and objectives Delayed graft function is a form of AKI resulting from ischemia-reperfusion injury. Our aim was to study the effect of delayed graft function on the progression of interstitial fibrosis after deceased donor kidney transplantation. Design, setting, participants, & measurements Our study is a retrospective study of all patients transplanted at our center between July of 2003 and September of 2014 using a kidney from a deceased donor. The primary outcome was the progression of interstitial fibrosis on serial protocol biopsies done during the first year posttransplant. We analyzed the distribution of the change in the Banff interstitial fibrosis (ci) score between the delayed graft function and nondelayed graft function groups for all of the paired biopsies done at time 0 and 12 months post-transplant (Δfibrosis). We also performed a linear mixed model analyzing the difference in the slopes for the progression ofmean Banff ci score for all of the biopsies done at time 0 and 1, 4, and 12months posttransplant. Results Therewere 343 (36.7%) in the delayed graft function group and 591 in the control group. The biopsy rates for the delayed graft function and nondelayed graft function groups at time 0 were 65.3% (n=224) and 67.0% (n=396), respectively, and at 12 months, theywere 64.4% (n=221) and 68.4%(n=404), respectively. Paired biopsies were available for 155 in the delayed graft function group and 283 in the control group. In a risk-adjustedmodel, Banff ci score >0 on the time 0 biopsy had a higher odds of delayed graft function (odds ratio, 1.70; 95% confidence interval, 1.03 to 2.82). The distribution of the Δfibrosis between 0 and 12monthswas similar in delayed graft function and control groups (P=0.91). The slopes representing the progression of fibrosis were also similar between the groups (P=0.66). Conclusions Donor-derived fibrosis may increase the odds of delayed graft function; however, delayed graft function does not seem to increase the progression of fibrosis during the first year after transplantation.

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KW - Delayed graft function after kidney transplant

KW - Fibrosis

KW - Humans

KW - Interstitial fibrosis

KW - Ischemia reperfusion injury and kidney transplant

KW - Kidney

KW - Kidney transplantation

KW - Reperfusion Injury

KW - Retrospective Studies

KW - Tissue Donors

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