Wednesday, June 10, 2015

Recurrent Membranoproliferative Glomerulonephritis Type I After Kidney Transplantation: A 17-Year Single-Center Experience

Transplantation - Current Issue Recurrent Membranoproliferative Glomerulonephritis Type I After Kidney Transplantation: A 17-Year Single-Center Experience

imageBackground: Most previously published studies of patients with membranoproliferative glomerulonephritis type I are small or have short follow-up period. We report the outcome of a fairly large cohort of patients followed up for nearly 10 years. Methods: Retrospective cohort study. Graft survival, recurrence rate and risk factors for recurrence were analyzed for 43 patients transplanted between the years 1995 and 2012. Results: At a mean overall follow-up of 118±61 months (median, 127.8; range, 4.9–217), 12 patients lost their graft (28%). Death-censored actuarial 15-year graft survival rate was 56%. Membranoproliferative glomerulonephritis recurred in eight patients (19%) at a median time of 15.4 months (range, 4.4–70 months). Recurrence led to graft loss in seven patients (88%) within a median of 11.6 months (range, 1.3–54 months) from diagnosis. Median graft survival was 30.5 months for recurrence (range, 7–86). Actuarial 15-year graft survival was 71% for nonrecurrent. The risk for recurrence was higher for patients with human leukocyte antigen (HLA) B49 (odds ratio, 16.9; 95% confidence interval, 1.1–246; P=0.038) and HLA DR4 (odds ratio, 15.9; 95% confidence interval, 1.07–237; P=0.044) alleles. A trend toward increased risk was found with shorter duration of dialysis before transplantation. Four of 16 (25%) living-related versus none of the living-unrelated donors' recipients recurred. The HLA B49, acute tubular necrosis after transplantation, previous transplantations, and Arab origin were all associated with decreased graft and patient survival. Conclusion: Patients without recurrence in the first years should expect an excellent graft survival. Nonrelated living donors should be preferred. The HLA B49 and DR4 alleles may increase the risk for recurrence.


http://journals.lww.com/transplantjournal/Fulltext/2015/06000/Recurrent_Membranoproliferative_Glomerulonephritis.15.aspx

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Alberto Reino Buelvas

Rates and Determinants of Progression to Graft Failure in Kidney Allograft Recipients With De Novo Donor-Specific Antibody

AJT - Early Rates and Determinants of Progression to Graft Failure in Kidney Allograft Recipients With De Novo Donor-Specific Antibody

Understanding rates and determinants of clinical pathologic progression for recipients with de novo donor-specific antibody (dnDSA), especially subclinical dnDSA, may identify surrogate endpoints and inform clinical trial design. A consecutive cohort of 508 renal transplant recipients (n = 64 with dnDSA) was studied. Recipients (n = 388) without dnDSA or dysfunction had an eGFR decline of −0.65 mL/min/1.73 m2/year. In recipients with dnDSA, the rate eGFR decline was significantly increased prior to dnDSA onset (−2.89 vs. −0.65 mL/min/1.73 m2/year, p < 0.0001) and accelerated post-dnDSA (−3.63 vs. −2.89 mL/min/1.73 m2/year, p < 0.0001), suggesting that dnDSA is both a marker and contributor to ongoing alloimmunity. Time to 50% post-dnDSA graft loss was longer in recipients with subclinical versus a clinical dnDSA phenotype (8.3 vs. 3.3 years, p < 0.0001). Analysis of 1091 allograft biopsies found that dnDSA and time independently predicted chronic glomerulopathy (cg), but not interstitial fibrosis and tubular atrophy (IFTA). Early T cell–mediated rejection, nonadherence, and time were multivariate predictors of IFTA. Independent risk factors for post-dnDSA graft survival available prior to, or at the time of, dnDSA detection were delayed graft function, nonadherence, dnDSA mean fluorescence intensity sum score, tubulitis, and cg. Ultimately, dnDSA is part of a continuum of mixed alloimmune-mediated injury, which requires solutions targeting T and B cells.




http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fajt.13347

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Alberto Reino Buelvas