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William D. Payne

Researcher at University of Minnesota

Publications -  269
Citations -  10254

William D. Payne is an academic researcher from University of Minnesota. The author has contributed to research in topics: Transplantation & Liver transplantation. The author has an hindex of 56, co-authored 268 publications receiving 10026 citations. Previous affiliations of William D. Payne include Mayo Clinic & Kyushu University.

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Risk factors for chronic rejection in renal allograft recipients.

TL;DR: In this article, the authors found that acute rejection, CsA dosage < 5 mg/kg/day at 1 year, and infection are the major risk factors for the development of chronic rejection.
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The impact of an acute rejection episode on long-term renal allograft survival (t1/2).

TL;DR: It is concluded that a single rejection episode shortens t1/2, the time it takes for 1/2 of the grafts functioning at 1 year to fail, and those with ≥1 rejection, the first episode after the first year, are at high risk for late graft loss.
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Early versus late acute renal allograft rejection: impact on chronic rejection.

TL;DR: It is concluded that acute rejection is strongly related to the development of biopsy-proven chronic rejection and subsequent graft loss and patients undergoing their first acute rejection episode > 60 days have an increased incidence of chronic rejection.
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Are wound complications after a kidney transplant more common with modern immunosuppression

TL;DR: Despite immunosuppression including chronic steroids, the incidence of wound infections, incisional hernias, and fascial dehiscence is low in kidney recipients, and the main risk factors are obesity, reoperation, and increased age.
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Heme protein-induced chronic renal inflammation: suppressive effect of induced heme oxygenase-1.

TL;DR: It is concluded that up-regulation of HO-1 occurs in the kidney in humans and rats repetitively exposed to heme proteins, which represents an anti-inflammatory response since the genetic deficiency ofHO-1 markedly increases activation of NF-kappaB, MCP-1 expression, and tubulointerstitial cellular inflammation.