Kidney Transplant Rejection¶
Background¶
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Rejection is divided into acute vs chronic and T-cell mediated or antibody mediated
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Pathologists can determine the type of rejection and the chronicity by observing the structures that are acutely involved (e.g. tubulitis, glomerulitis, arteritis, and capillaritis) as well as the time course of involvement (e.g. presence of fibrosis)
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Structures exhibiting fibrosis represent chronic rejection that is unlikely to respond to treatment, whereas acute inflammation may be amenable to acute therapies
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This section will focus on acute rejection since this is the clinical entity we will most likely manage while on the wards
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Acute Rejection¶
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Acute T cell mediated rejection
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Infiltration of the graft by lymphocytes and inflammatory cells characterized by tubulitis, interstitial inflammation, and arteritis (on occasion)
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Treatment:
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High dose glucocorticoids (methyl prednisolone) is first line (~ 5 days)
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Thymoglobulin (polyclonal Ig anti-T cell)
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Use depends on severity of rejection
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Indicated if Cr fails to improve after steroids
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T cell subsets are measured during treatment until depleted
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Tacro target levels are reset to ~8-10 if treated for acute T cell mediated rejection
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Acute antibody mediated rejection (ABMR)
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Donor specific antibody mediated rejection characterized by glomerulitis, peri-tubular capillaritis (microcirculation inflammation), complement deposition (C4d staining), and presence of DSA
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Treatment = B-cell depletion therapy
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IV methyl prednisone 500 mg IV x 3-5 days
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Plasmapheresis (If with high titers of DSA)
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IVIG 2 g/kg (max 140 g)
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Rituximab 375 mg/m2
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