Martine Neau-Cransac

Renal failure after liver transplantation: outcome after calcineurin inhibitor withdrawal

Neau‐Cransac M, Morel D, Bernard P‐H, Merville P, Revel P, Potaux L, Saric J. Renal failure after liver transplantation. Outcome after calcineurin inhibitor withdrawal. Clin Transplant 2002: 16: 368–373.

Gamma‐delta T cell expansion is closely associated with cytomegalovirus infection in all solid organ transplant recipients

We read with interest the manuscript published by Puig-Pey et al. entitled ‘‘Characterisation of gammadelta T cells in organ transplantation’’ [1]. For a better reading of this paper, we would like to add several comments on the basis of our experience in cd T cell immunomonitoring in kidney transplant recipients (KTR), to enlighten their role in the context of cytomegalovirus (CMV) infection. Indeed, in KTR, we demonstrated, 10 years ago, that CMV infection is the sole parameter independently associated with a persistent

Evolution of donor-specific antibodies (DSA) and incidence of de novo DSA in solid organ transplant recipients after switch to everolimus alone or associated with low dose of calcineurin inhibitors.

Everolimus (EVR) is used in organ transplantation to minimize calcineurin inhibitors (CNI). Some studies pointed out an increase in rejection and de novo donor‐specific antibodies (DSA) incidence in kidney transplant patients after switch to EVR and CNI withdrawal. The aims of our study were to determine the evolution of anti‐HLA antibodies and the incidence of de novo DSA in transplant recipients after conversion to EVR.

Decrease in sirolimus-induced proteinuria after switch to everolimus in a liver transplant recipient with diabetic nephropathy

Mammalian Target of rapamycine (mTOR) inhibitors are effective in preventing acute rejection in renal as also cardiac transplantations, causing less nephrotoxicity than calcineurin inhibitors (CNI) and benefit in prevention of post-transplant malignancies [1,2]. However, proteinuria and worsening of renal function have been reported after switchover from CNI to sirolimus in renal transplantation [3]. There are few data on renal function evaluation with everolimus. We report a case of decrease in proteinuria after switching over from sirolimus to everolimus in a liver transplant recipient with diabetic nephropathy. A 63-year-old male with type 2 diabetes underwent a liver transplantation (LT) for alcoholic cirrhosis in 1996. Immunosuppressive treatment combined initially tacrolimus and corticosteroids. Steroids were stopped 3 years post-LT. Because of diabetes, proteinuria was monitored annually. Until December 2005, there was a mild renal dysfunction and microalbuminuria (Fig. 1). In 2000, a spinocellular carcinoma of the scalp in this patient was treated by surgical resection. Spinocellular carcinoma recurrences were then observed, requiring surgical treatments, external radiotherapy and autologous cutaneous graft. Sirolimus was introduced in June 2006 and tacrolimus was stopped. At sirolimus initiation, creatininemia was 127 lmol/l, Cockcroft-Gault-calculated creatininemia clearance 51 ml/min/1.73 m, and microalbuminuria 0.15 g/day. Liver function, hepatic and renal echographies were normal. In February 2007, edema of the face and of the legs appeared. Laboratory data showed anemia, proteinuria over 3 g/day without hypoprotidemia [62 g/l (normal values 60–75 g/l)] or hypoalbuminemia [36 g/l (normal values 32–52 g/l)], and mild increase of creatininemia to 150 lmol/l. Sirolimus trough levels were between 3.8 and 8 ng/ml. Sirolimus dosage was then decreased. The other treatments consisted of insulin, pravastatin, allopurinol, nicardipine and candesartan cilexetil, unchanged for more than 1 year. One month later, edema disappeared without biologic improvement. A renal biopsy was performed, revealing diabetic nephropathy without sign of sirolimus toxicity. However, sirolimus

Evolution of serum and intra-graft donor-specific anti-HLA antibodies in a patient with two consecutive liver transplantations

The current literature suggests that anti-HLA donor-specific antibodies (DSA) may have deleterious effects on liver grafts but there is no proof that they are directly involved in the graft lesions. We report the case of a donor HLA-sensitized patient who needed a second graft 6 months after the first transplantation owing to a progressive cholestatic disease that we could finally attribute to antibody-mediated rejection (AMR). We describe the longitudinal evolution of graft function, tissue histology, serum DSA and, for the first time, intra-graft DSA after elution from biopsies.

γδLymphocytosis Associated with Granulomatous Disease in a Patient with Common Variable Immunodeficiency

: Common variable immunodeficiency (CVID) is a heterogeneous group of immunodeficiency syndromes that involves defective production of specific antibodies and decreased serum concentrations of > or =1 immunoglobulin isotype. We describe a patient with an atypical case of CVID who had extensive granulomatous lesions that were partially attributable to mycobacterial infection. In the peripheral blood, there was a massive increase in the number of double-negative CD3+ T cells that expressed the gammadelta T cell receptor.

Uncommon Localization of Calcinosis Cutis after Liver Transplantation

Calcinosis cutis is a general term for the cutaneous deposition of calcium salts. Three groups of calcinosis cutis have been described: (i) calcinosis with abnormalities of the calcium-phosphorus metabolism, (ii) dystrophic calcinosis associated with underlying tissular alterations, normal serum calcium and phosphorus levels, (iii) idiopathic calcinosis if there is no other associated abnormality [1, 2] . After liver transplantation, soft tissue calcium deposits are observed, but calcinosis cutis was rarely described [3–7] . We report the case of a liver graft recipient who developed an uncommon clinical picture of calcinosis cutis, which was associated with intrahepatic calcifi cations and successfully treated with disodium etidronate. A 23-year-old Caucasian man received a liver graft on November 30, 1998, for fulminant hepatitis of unknown etiology. During surgery, 3 red blood cell units and 23 plasma units were transfused. The immunosuppressive regimen consisted of tacrolimus and corticosteroids. Six months after transplantation, the total bilirubin level rose to 215 mol/l (normal ! 20 mol/l), -glutamyltransferase ( -GT) to 375 IU/l (normal ! 45 IU/l), and cytolysis appeared (aspartate aminotransferase, ASAT, 478 IU/l and alanine aminotransferase, ALAT, 668 IU/l, normal ! 45 IU/l). The results of viral and immunological investigations were negative. Arteriography showed hepatic arterial stenosis, and angioplasty was performed; however, liver function failed to improve, and mycophenolate mofetil was introduced. Fifteen months after transplantation, liver biopsy showed ductopenic and arteriopathic chronic rejection. In October 2000, the patient had severe portal hypertension and developed hepatorenal syndrome (serum creatinine was 369 mol/l, normal ! 120 mol/l, and blood urea was 29.3 mmol/l, normal