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J Renal Inj Prev. 2015 Nov 30;4(4):135-8. doi: 10.12861/jrip.2015.28. eCollection 2015.

De novo post-transplant thrombotic microangiopathy localized only to the graft in autosomal dominant polycystic kidney disease with thrombophilia.

Journal of renal injury prevention

Davide Rolla, Iris Fontana, Jean Louis Ravetti, Luigina Marsano, Diego Bellino, Laura Panaro, Francesca Ansaldo, Lisa Mathiasen, Giulia Storace, Matteo Trezzi

Affiliations

  1. Divisione di Nefrologia - Dialisi -Trapianto, Ospedale Sant'Andrea, La Spezia, Italy.
  2. Divisione di Chirurgia Vascolare e Trapianto di rene, Azienda Ospedaliera Universitaria San Martino, Genova, Italy.
  3. Servizio di Anatomia Patologica, Azienda Ospedaliera Universitaria San Martino, Genova, Italy.
  4. Clinica Nefrologica, Azienda Ospedaliera Universitaria San Martino, Genova, Italy.
  5. Estor Spa, Pero, Milan, Italy.

PMID: 26693501 PMCID: PMC4685984 DOI: 10.12861/jrip.2015.28

Abstract

INTRODUCTION: Thrombotic microangiopathy (TMA) is a serious complication of renal transplantation and is mostly related to the prothrombotic effect of calcineurin inhibitors (CNIs). A subset of TMA (29%-38%) is localized only to the graft. Case 1: A young woman suffering from autosomal dominant polycystic kidney disease (ADPKD) underwent kidney transplant. After 2 months, she showed slow renal deterioration (serum creatinine from 1.9 to 3.1 mg/dl), without hematological signs of hemolytic-uremic syndrome (HUS); only LDH enzyme transient increase was detected. Renal biopsy showed TMA: temporary withdraw of tacrolimus and plasmapheresis was performed. The renal function recovered (serum creatinine 1.9 mg/dl). From screening for thrombophilia, we found a mutation of the Leiden factor V gene. Case 2: A man affected by ADPKD underwent kidney transplantation, with delay graft function; first biopsy showed acute tubular necrosis, but a second biopsy revealed TMA, while no altered hematological parameters of HUS was detected. We observed only a slight increase of lactate dehydrogenase (LDH) levels. The tacrolimus was halved and plasmapheresis was performed: LDH levels normalized within 10 days and renal function improved (serum creatinine from 9 to 2.9 mg/dl). We found a mutation of the prothrombin gene. Only a renal biopsy clarifies the diagnosis of TMA, but it is necessary to pay attention to light increasing level of LDH.

CONCLUSION: Prothrombotic effect of CNIs and mTOR inhibitor, mutation of genes encoding factor H or I, anticardiolipin antibodies, vascular rejection, cytomegalovirus infection are proposed to trigger TMA; we detected mutations of factor II and Leiden factor V, as facilitating conditions for TMA in patients affected by ADPKD.

Keywords: Kidney transplantation; Leiden factor V; Protrombin gene; Thrombotic miocroangiopathy

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