Outcome in patients with end‐stage renal disease following heart or heart–lung transplantation receiving peritoneal dialysis

Jayasena, Shyama D.; Ahmad, Rasheed; Lewis, Catherine E.; Neild, Guy H.; Thompson, F. D.; Woolfson, Robin G.

doi:10.1093/ndt/16.8.1681

Cited by 35 publications

(32 citation statements)

References 7 publications

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“…[2][3][4][5][6][7][8][9] Van Gelder et al 11 noted that endstage renal disease occurred in 8% of heart transplant recipients treated with cyclosporine. Goldstein et al 12 observed that 6.5% of patients developed end-stage renal failure.…”

Section: Discussionmentioning

confidence: 99%

“…1 A number of clinical studies [2][3][4][5][6][7][8][9] suggest that one of the common clinical complications after heart transplantation is chronic cyclosporine-induced nephrotoxicity, which generally leads to progressive renal failure. 10 Van Gelder et al 11 demonstrated that a significant rise in serum creatinine was found in cases compared with controls as early as 3 months after transplantation.…”

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confidence: 99%

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Anti–Transforming Growth Factor Antibody at Low but Not High Doses Limits Cyclosporine-Mediated Nephrotoxicity Without Altering Rat Cardiac Allograft Survival

et al. 2004

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Background-Long-term treatment of cardiac transplant recipients with cyclosporine results in a progressive decline in kidney function in a large number of patients. This complication is one of the most important prognostic parameters that determine the outcome of cardiac transplantation. Transforming growth factor-␤ (TGF-␤) is one of the most potent mediators of the fibrogenic effects of cyclosporine. Methods and Results-With the use of an experimental rodent model, heterotopic heart transplantation was performed, creating histocompatibility-disparate allografts. Because TGF-␤ in part mediates both the immunosuppressive and nephrotoxic effects of cyclosporine, recipients were treated with cyclosporine with and without anti-TGF-␤ antibody to determine whether anti-TGF-␤ antibody could reduce the nephrotoxic effects of cyclosporine. Intrarenal expression of TGF-␤, collagen, fibronectin, matrix metalloproteinase-2, and tissue inhibitor of metalloproteinase-2 was studied with the use of reverse transcription-polymerase chain reaction. Intrarenal expression of TGF-␤ protein was studied by immunohistochemistry and with the use of ELISA to quantify circulating levels of TGF-␤ protein in plasma. Cyclosporine-induced graft survival (immunosuppressive effect) was abrogated with a higher concentration (2.5 mg/kg) of anti-TGF-␤ antibody, whereas a lower concentration (1 mg/kg) inhibited both cyclosporine-induced expression of fibrogenic molecules and renal toxicity. Conclusions-These results provide credence to the pivotal role of TGF-␤ in immunosuppression-associated renal toxicity in recipients of cardiac transplantation. Furthermore, these findings support a potentially significant therapeutic use of optimal concentration of anti-TGF-␤ antibody to ameliorate cyclosporine-associated nephrotoxicity in cardiac transplant recipients.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Anti–Transforming Growth Factor Antibody at Low but Not High Doses Limits Cyclosporine-Mediated Nephrotoxicity Without Altering Rat Cardiac Allograft Survival

et al. 2004

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“…Renal failure in these patients has been found to be a major risk factor for patient survival, mainly after heart and lung transplantation (4,6,7,14,(20)(21)(22)(23). Calcineurin- (24)(25)(26)(27).…”

Section: Transplanted Kidneys Fail After Years For Various Poorly Defmentioning

confidence: 99%

Biopsy‐Diagnosed Renal Disease in Patients After Transplantation of Other Organs and Tissues

Schwarz¹,

Haller²,

Schmitt³

et al. 2010

American Journal of Transplantation

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Renal function deteriorates in about half of patients undergoing other transplants. We report the results of 105 renal biopsies from 101 nonrenal transplant recipients (bone marrow 14, liver 41, lung 30, heart 20). Biopsy indications were protracted acute renal failure (9%), creatinine increases (83%), heavy proteinuria (22%), or renal insufficiency before re-transplantation (9%). Histological findings other than nonspecific chronic changes, hypertension-related damage, and signs of chronic CNI toxicity included primary glomerular disease (17%), mostly after liver transplantation (21%) or after bone marrow transplantation (29%), and thrombotic microangiopathy (TMA) namely (10%). TMA had the most serious impact on the clinical course. Besides severe hypertension, one TMA patient died of cerebral hemorrhage, 5 had hemolyticuremic syndrome, and 6 rapidly developed end-stage renal failure. TMA patients had the shortest kidney survival post-biopsy and, together with patients with acute tubular injury, the shortest kidney and patient survival since transplantation. Nine TMA patients had received CNI, 3 of them concomitantly received an mTOR-inhibitor. CNI toxicity is implicated in most patients with renal failure after transplant of other organs and may play a role in the development of TMA, the most serious complication. However, decreased renal function should not be routinely ascribed to CNI.

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“…Most organ recipients who need renal replacement therapy undergo hemodialysis (HD), although small series of transplant recipients undergoing peritoneal dialysis (PD) have been reported. Jayasena et al 96 performed a study of 17 heart and heart-lung transplant recipients who underwent PD. An increased frequency of peritonitis was observed in these patients compared with a control group who were immunosuppressed because of either autoimmune disease or recent transplant failure.…”

Section: Dialysis and Sequential Kidney Transplantationmentioning

confidence: 99%

Chronic Kidney Disease after Nonrenal Solid-Organ Transplantation

Bloom

Reese

2007

Journal of the American Society of Nephrology

160

138

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Outcome in patients with end‐stage renal disease following heart or heart–lung transplantation receiving peritoneal dialysis

Abstract: Increased risk of PD peritonitis and reduced PD survival is reported in this cohort of 17 heart and heart--lung recipients with ESRD. Nevertheless, for patients with severely impaired cardiac function, PD may still offer therapeutic advantage.

Cited by 35 publications

References 7 publications

Anti–Transforming Growth Factor Antibody at Low but Not High Doses Limits Cyclosporine-Mediated Nephrotoxicity Without Altering Rat Cardiac Allograft Survival

Anti–Transforming Growth Factor Antibody at Low but Not High Doses Limits Cyclosporine-Mediated Nephrotoxicity Without Altering Rat Cardiac Allograft Survival

Biopsy‐Diagnosed Renal Disease in Patients After Transplantation of Other Organs and Tissues

Chronic Kidney Disease after Nonrenal Solid-Organ Transplantation

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