P-157

Kidney graft dysfunction in SPK transplant recipients after pancreas loss

D. Viglietti, T. Serrato, I. Abboud, C. Antoine, M.N. Peraldi
Hôpital Saint-Louis, Paris, France

Objective: Kidney graft survival in SPK recipients is known to be inferior in patients who early experience pancreas graft failure compared to patients with a functioning pancreas. We assess kidney graft function and histopathologic findings between these two groups of SPK recipients.

Patients and methods: Medical files of 63 consecutive patients who received SPK transplantation were retrospectively reviewed. Kidney graft function estimated by the MDRD formula and proteinuria were evaluated at 3 months after the transplantation and at last follow-up. Histopathologic findings of protocol biopsies performed 3 months after transplantation were analysed.

Results: 12 of 63 patients had lost the pancreas graft. Donors characteristics were similar in the two groups. At 32 months of median follow-up, eGFR after pancreas failure was 69.5 (range 37.1-125.5) mL/min/1.73m? versus 56.3 (range 30.3-112.0) mL/min/1.73m? (p = 0.01) in patients with a functioning pancreas graft. Patients who had lost pancreas had a median proteinuria of 0.28 g per 24 hours versus 0.13 g per 24 hours (p = 0.02). Analysis of histopathologic findings of 3-months protocol biopsies revealed more frequent and intense glomerulitis lesions in after pancreas failure without peritubular capillaritis nor C4d deposition. 30% of patients who had lost the pancreas had glomerulitis graded 2 or 3 according to the Banff score versus 0% in the patients with functioning graft (p = 0.0001). There were no evidences for diabetic nephropathy recurrence. No DSA were detectable in these patients.

Conclusion: SPK recipients develop an early kidney graft dysfunction after pancreas failure without diabetic nephropathy recurrence. Histopathologic findings revealed frequent and intense glomerulitis without other antibody mediated rejection evidence we currently explore.

P-157

Kidney graft dysfunction in SPK transplant recipients after pancreas loss

D. Viglietti, T. Serrato, I. Abboud, C. Antoine, M.N. Peraldi
Hôpital Saint-Louis, Paris, France

Objective: Kidney graft survival in SPK recipients is known to be inferior in patients who early experience pancreas graft failure compared to patients with a functioning pancreas. We assess kidney graft function and histopathologic findings between these two groups of SPK recipients.

Patients and methods: Medical files of 63 consecutive patients who received SPK transplantation were retrospectively reviewed. Kidney graft function estimated by the MDRD formula and proteinuria were evaluated at 3 months after the transplantation and at last follow-up. Histopathologic findings of protocol biopsies performed 3 months after transplantation were analysed.

Results: 12 of 63 patients had lost the pancreas graft. Donors characteristics were similar in the two groups. At 32 months of median follow-up, eGFR after pancreas failure was 69.5 (range 37.1-125.5) mL/min/1.73m? versus 56.3 (range 30.3-112.0) mL/min/1.73m? (p = 0.01) in patients with a functioning pancreas graft. Patients who had lost pancreas had a median proteinuria of 0.28 g per 24 hours versus 0.13 g per 24 hours (p = 0.02). Analysis of histopathologic findings of 3-months protocol biopsies revealed more frequent and intense glomerulitis lesions in after pancreas failure without peritubular capillaritis nor C4d deposition. 30% of patients who had lost the pancreas had glomerulitis graded 2 or 3 according to the Banff score versus 0% in the patients with functioning graft (p = 0.0001). There were no evidences for diabetic nephropathy recurrence. No DSA were detectable in these patients.

Conclusion: SPK recipients develop an early kidney graft dysfunction after pancreas failure without diabetic nephropathy recurrence. Histopathologic findings revealed frequent and intense glomerulitis without other antibody mediated rejection evidence we currently explore.