Sirolimus Use and De Novo Minimal Change Nephropathy Following Renal Transplantation

Mainra, Rahul; Mulay, Atul; Bell, Robert; Karpinski, Jolanta; Hoar, Stephanie; Knoll, Greg; Robertson, Susan J.; Don, Wang

doi:10.1097/01.tp.0000181385.68835.a0

Cited by 12 publications

(7 citation statements)

References 4 publications

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“…If a causal relationship does exist, the exact mechanism by which SRL may induce proteinuria remains speculative. Some studies implicate the induction of a specific glomerulopathy by SRL (19,21,22). However the majority of biopsied patients in our SRL group with proteinuria did not have a specific glomerular diagnosis.…”

Section: Discussionmentioning

confidence: 73%

Differences in Proteinuria and Graft Function in De Novo Sirolimus-Based vs. Calcineurin Inhibitor-Based Immunosuppression in Live Donor Kidney Transplantation

et al. 2006

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Section: Discussionmentioning

confidence: 73%

Differences in Proteinuria and Graft Function in De Novo Sirolimus-Based vs. Calcineurin Inhibitor-Based Immunosuppression in Live Donor Kidney Transplantation

et al. 2006

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“…A variety of glomerular findings associated with proteinuria have been attributed to sirolimus in the kidney transplantation setting, including MCD, FSGS, MN, MPGN, and IgA nephropathy. [96][97][98] Urinary protein loss presumably results from reduced tubular protein reabsorption. 99 A specific Glomerulus displaying changes of acute thrombotic microangiopathy with red blood cell congestion, intracapillary fibrin thrombi, and mesangiolysis.…”

Section: Calcineurin and Mammalian Target Of Rapamycin Inhibitorsmentioning

confidence: 99%

Glomerular diseases seen with cancer and chemotherapy: a narrative review

Jhaveri

Shah

Calderon

et al. 2013

Kidney International

123

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Glomerular lesions have been recognized in a number of malignant diseases. Membranous nephropathy is the most common glomerular pathology associated with solid tumors. In Hodgkin's disease, the most common lesion is minimal change disease, reflecting possibly an anomaly of T-cell function. On the other hand, in patients with chronic lymphocytic leukemia, a large proportion of glomerular lesions fall into the category of membranoproliferative glomerulonephritis. Membranous nephropathy is also the most common glomerular disease seen following stem cell transplantation, suggesting a possible immune-mediated mechanism. Chemotherapy agents such as interferon, anti-vascular endothelial growth factor agents, tyrosine kinase inhibitors, and bisphosphonates have also been associated with various glomerular diseases and thrombotic microangiopathy. Failure to recognize certain paraneoplastic glomerular diseases can lead to potentially unnecessary therapies. This review describes the association of glomerular diseases with solid tumors, hematological malignancies, stem cell transplantation, and chemotherapeutic agents. We also describe the pitfalls in diagnosis and the dilemma in treating these entities.

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“…The patient had been diagnosed with type I diabetes at the age of 43 and started hemodialysis for end-stage renal failure at the age of 54 without past history of nephrotic syndrome. The donor blood type was incompatible with that of the recipient (type AB to type B), and there were four mismatches in human leukocyte antigen (HLA)-A, -B, -DR typing (donor: A 24, B 7, 52, DR 1, 15 to recipient: A 11,24,B 46,60,DR 9). At first, the patient received immunosuppressive therapy consisting of cyclosporine A, mycophenolate mofetil, methylprednisolone, rituximab and basiliximab.…”

Section: Case Reportmentioning

confidence: 99%

De novo minimal change disease after ABO‐incompatible kidney transplantation

Mochizuki

Iwata

Nishikido

et al. 2012

Clinical Transplantation

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De novo minimal change disease after ABO-incompatible kidney transplantation Mochizuki Y, Iwata T, Nishikido M, Uramatsu T, Sakai H, Taguchi T. De novo minimal change disease after ABO-incompatible kidney transplantation.Abstract: We report the clinical and pathological findings of a case of de novo minimal change disease (MCD) after ABO-incompatible living kidney transplantation. A 62-yr-old man with end-stage renal disease associated with type I diabetes received ABO-incompatible kidney transplantation from his 58-yr-old wife. Although allograft function was excellent immediately after surgery, massive proteinuria (35 g/d) appeared on post-transplantation day 5. After the allograft biopsy taken on post-transplantation day 6, he was treated with 12 cycles of plasma exchange, but the nephrotic-range proteinuria showed no remission. The biopsy specimen showed no significant pathological findings on light microscopy, but electron microscopy showed diffuse effacement of podocyte foot processes. Based on the diagnosis of de novo MCD, the patient received intravenous methylprednisolone pulse therapy, followed by high-dose steroid maintenance therapy. The steroid therapy induced complete remission of nephrotic syndrome and stable allograft function immediately, which was also maintained at one yr after the transplantation.

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Sirolimus Use and De Novo Minimal Change Nephropathy Following Renal Transplantation

Cited by 12 publications

References 4 publications

Differences in Proteinuria and Graft Function in De Novo Sirolimus-Based vs. Calcineurin Inhibitor-Based Immunosuppression in Live Donor Kidney Transplantation

Differences in Proteinuria and Graft Function in De Novo Sirolimus-Based vs. Calcineurin Inhibitor-Based Immunosuppression in Live Donor Kidney Transplantation

Glomerular diseases seen with cancer and chemotherapy: a narrative review

De novo minimal change disease after ABO‐incompatible kidney transplantation

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