Alberto Reino Buelvas
Monday, January 25, 2016
Thursday, January 14, 2016
Recurrent Membranous Nephropathy After Kidney Transplantation: Treatment and Long-Term Implications.
Background: Membranous nephropathy (MN) can recur in kidney allografts leading to graft dysfunction and failure. The aims of these analyses were to assess MN recurrence, clinical and histologic progression, and response to anti-CD20 therapy. Methods: Included were 63 kidney allograft recipients with biopsy proven primary MN followed up for 77.0 (39-113) months (median, interquartile range). Disease recurrence was diagnosed by biopsy (protocol or clinical), and follow-up was monitored by laboratory parameters and protocol biopsies. Results: Thirty of 63 patients (48%) had histologic recurrence often during the first year. In 53% of the cases, recurrence was diagnosed by protocol biopsy. Recurrence risk was higher in patients with higher proteinuria pretransplant [hazard ratio = 1.869 (95% confidence interval, 1.164-3.001) per gram, P = 0.010] and those with anti-phospholipase A2 receptor antibodies [hazard ratio = 3.761 (1.635-8.652), P = 0.002]. Thirteen patients with recurrence had no clinical progression, and in 2, MN resolved histologically. Seventeen of 63 patients (27%) had progressive proteinuria and were treated with anti-CD20 antibodies, resulting in complete response in 9 (53%), partial response in 5 (29%), and no response in 3 (18%). Posttreatment biopsies were obtained in 15 patients and showed histologic resolution in 6 (40%). Disease recurrence did not correlate with graft survival. However, 5 of 11 (45.4%) graft losses were due to recurrent MN. Death-censored graft survival in MN did not differ from that of 273 control recipients with autosomal dominant polycystic kidney disease. Conclusions: Membranous nephropathy recurs in 48% of cases threatening the allograft. Treatment of early but progressive recurrence with anti-CD20 antibodies is quite effective achieving clinical remission and histologic resolution of MN. Copyright (C) 2015 Wolters Kluwer Health, Inc. All rights reserved.
http://pdfs.journals.lww.com/transplantjournal/9000/00000/Recurrent_Membranous_Nephropathy_After_Kidney.97556.pdf
http://pdfs.journals.lww.com/transplantjournal/9000/00000/Recurrent_Membranous_Nephropathy_After_Kidney.97556.pdf
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Alberto Reino Buelvas
Effect of twice-yearly denosumab on prevention of bone mineral density loss in de novo kidney transplant recipients: a randomized controlled trial
Abstract
We conducted an open-label, prospective, randomized trial to assess the efficacy and safety of RANKL inhibition with denosumab to prevent the loss of BMD in the first year after kidney transplantation. Ninety kidney transplant recipients were randomized 1:1 two weeks after surgery to receive denosumab (60 mg at baseline and 6 months) or no treatment. After 12 months, total lumbar spine aBMD increased by 4.6% (95% CI 3.3-5.9%) in 46 patients in the denosumab group and decreased by -0.5% (95% CI -1.8-0.9%) in 44 patients in the control group (between-group difference 5.1% (95% CI 3.1-7.0%), P<0.0001). Denosumab also increased aBMD at the total hip by 1.9% (95% CI, 0.1 to 3.7%; P=0.035) over that in the control group at 12 months. HR-pQCT in a subgroup of 24 patients showed that denosumab increased vBMD at the distal tibia and radius (all P<0.05). Biomarkers of bone turnover (β-CTX, P1NP) markedly decreased with denosumab (all P<0.0001). Episodes of cystitis and asymptomatic hypocalcemia occurred more often with denosumab, whereas graft function, rate of rejections and incidence of opportunistic infections were similar. In conclusion, denosumab increased BMD in the first year after kidney transplantation but was associated with more frequent episodes of urinary tract infection.
This article is protected by copyright. All rights reserved.
http://onlinelibrary.wiley.com/resolve/doi?DOI=10.1111%2Fajt.13692
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Alberto Reino Buelvas
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