Kidney and Pancreas Transplantation in the United States, 1996–2005

Andreoni, Kenneth A.; Brayman, Kenneth L.; Guidinger, Mary K.; Sommers, Cindy; Sung, Randall S.

doi:10.1111/j.1600-6143.2006.01781.x

Cited by 186 publications

(124 citation statements)

References 17 publications

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“…This finding is not surprising because it is widely known that donor age and donor kidney function are closely related to graft survival after SPK transplantation. 5,29 Our study suggests that most AMR episodes in SPK transplant recipients can be diagnosed in a similar way as in isolated kidney transplantation, with the triad of allograft dysfunction, C4d positivity in PTC, and detectable DSA in recipient serum. 9,30,31 Some of the cases reported here with C4d staining and allograft dysfunction are almost undoubtedly AMR episodes, despite the lack of DSA at the time of diagnosis.…”

Section: Discussionmentioning

confidence: 79%

Antibody-Mediated Rejection of the Kidney after Simultaneous Pancreas-Kidney Transplantation

Pascual¹,

Samaniego²,

Torrealba³

et al. 2008

Journal of the American Society of Nephrology

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The prevalence, risk factors, and outcome of antibody-mediated rejection (AMR) of the kidney after simultaneous pancreas-kidney transplantation are unknown. In 136 simultaneous pancreas-kidney recipients who were followed for an average of 3.1 yr, 21 episodes of AMR of the kidney allograft were identified. Eight episodes occurred early (Յ90 d) after transplantation, and 13 occurred later. Histologic evidence of concomitant acute cellular rejection was noted in 12 cases; the other nine had evidence only of humoral rejection. In 13 cases, clinical rejection of the pancreas was diagnosed simultaneously, and two of these were biopsy proven and were positive for C4d immunostaining. Multivariate analysis identified only one significant risk factor: Female patients were three times more likely to experience AMR. Nearly all early episodes resolved with treatment and did not predict graft loss, but multivariate Cox models revealed that late AMR episodes more than tripled the risk for kidney and pancreas graft loss; therefore, new strategies are needed to prevent and to treat late AMR in simultaneous pancreaskidney transplant recipients.

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Section: Discussionmentioning

confidence: 79%

Antibody-Mediated Rejection of the Kidney after Simultaneous Pancreas-Kidney Transplantation

Pascual¹,

Samaniego²,

Torrealba³

et al. 2008

Journal of the American Society of Nephrology

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“…The first is the undeniable improvement in allograft outcomes that has occurred under CNI-based therapy, even as the field has witnessed significant aging of the donor and recipient populations, less MHC similarity between donor and recipient, and, in kidney transplantation, commonplace use of kidneys with preexisting injury (34,35). Although some studies have indeed documented excellent outcomes with CNI-free immunosuppression, CNI-based protocols have been shown over and over again in clinical trials to result in renal function at least as stable as proposed alternatives and graft survival equivalent or superior to those available with any other option, as shown in the Symphony (Efficacy Limiting Toxicity Elimination [ELITE]-Symphony) trial, the CAESAR (Cyclosporine Avoidance Eliminates Serious Adverse Renal toxicity) trial, the ORION (Optimizing Renal Transplant Immunosuppression to Overcome Nephrotoxicity) trial, and numerous single-center studies (36 -39).…”

Section: Alternatives To An Incomplete Paradigmmentioning

confidence: 99%

Chronic Calcineurin Inhibitor Nephrotoxicity

Gaston

2009

Clinical Journal of the American Society of Nephrology

113

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Use of the calcineurin inhibitors (CNI) cyclosporine and tacrolimus has revolutionized solid organ transplantation. For more than 30 yr, the transplant community has dealt with nephrotoxicity attributed to these agents. Acute renal vasoconstriction (as described by many investigators, including John Curtis and colleagues) is the unequivocal consequence of their use; chronic CNI nephropathy, although indistinct in terms of histology and pathophysiology, has become accepted as a major cause of late kidney allograft failure. This article examines clinical, laboratory, and histologic findings that evolved into a paradigm that was never fully consistent with observed outcomes and new evidence that may offer an alternative interpretation for adverse events that are attributed to CNI nephrotoxicity in kidney transplant recipients.

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“…Al fi nal del período de observación 9 pacientes estaban euglicémicos en ayunas, presentaban niveles normales de Péptido C e independencia de insulina o hipoglicemiantes orales, independencia de diálisis en 8 pacientes. En este estudio no se efectuó un análisis prospectivo de la calidad de vida de los receptores, sin embargo, los 9 pacientes con páncreas funcionantes realizan actividades normales, no presentaron eventos cardiovasculares graves ni deterioro mayor de la retinopatía, lo que coincide con la información disponible en diversas publicaciones 4,16 .…”

Section: Discussionunclassified