Marion Mehrenberger

Centre Hospitalier Universitaire de Toulouse, Tolosa de Llenguadoc, Midi-Pyrénées, France

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Publications (15)20.88 Total impact

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    ABSTRACT: The aims of the present study were to assess the incidence of cytomegalovirus (CMV) reactivation, and to determine the predictive factors for CMV reactivation in CMV seropositive kidney-transplant patients. One hundred ninety CMV seropositive kidney-transplant patients were included in this study; of these, 39 patients had received CMV prophylaxis. CMV DNAemia was assessed by real-timepolymerase chain reaction assay every 2 weeks until day 120, then every 3-4 weeks until day 180, and then every month until day 365. One hundred seven patients (56.3%) had at least one positive CMV DNAemia within the first year. The time between renal transplantation and the first positive CMV DNAemia was 59 +/- 5 days. The number of positive CMV DNAemia/patient was 3.28 +/- 0.22. CMV viral load at first positive CMV DNAemia was 704 (10-742,000) copies/ml. The donor CMV seropositivity, the absence of CMV prophylaxis, and the occurrence of acute rejection before CMV reactivation were independent factors associated with CMV reactivation within the first year after kidney transplantation. Hence, CMV reactivation is frequent after kidney transplantation. CMV prophylaxis in CMV seropositive kidney-transplant patients should be offered to avoid CMV-related side-effects.
    Journal of Medical Virology 07/2008; 80(6):1012-7. · 2.37 Impact Factor
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    ABSTRACT: Membranous glomerulopathy (MG) is a rare cause of chronic kidney disease. However, after kidney transplantation (KT), despite immunosuppression, it often relapses on the allograft. Herein, we report on a male kidney-transplant patient, aged 27 years, who developed overt nephrotic syndrome 11 months after KT. This was related to relapsing MG, as evidenced by the allograft biopsy, which, in addition, showed CD3 (+) and CD20 (+) interstitial lymphocyte infiltration. The patient was treated with rituximab: 375 mg/m2/week for 4 consecutive weeks, followed by one additional injection every 3 months for one year. Remission was observed before the third rituximab injection. After a follow-up of 42 months, the patient was still in remission, i.e., microalbuminuria of 107 mg/day.
    Clinical nephrology 06/2008; 69(5):373-6. · 1.29 Impact Factor
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    ABSTRACT: In hepatitis C virus (HCV) positive kidney transplant (KT) patients, the use of alpha-interferon (alphaIFN) is contraindicated due to the risk of acute rejection (AR). Conversely, if these HCV(+) KT patients lose their allograft, re-transplantation might be contemplated provided alphaIFN therapy has been attempted. Between 01/01/1989 and 31/12/1994, 261 kidney transplantations were performed; of these 174 were HCV(-) (group I) and 87 were HCV(+) (group II). At last follow-up (2006), in group I, the number of patients with a functioning graft, the number of patients who died with a functioning graft, and the number of patients who lost their graft before or after month (M) 12 were 92 (52.8%), 14 (8%), 20 (11.5%) and 48 (27.7%), respectively. In group II, the corresponding figures were 22 (25.3%; P < 0.0001), 8 (9.1%; ns), 9 (10.3%; ns) and 48 (55.3%; P < 0.0001). In group I, 19 of 48 (39.5%) patients with failed allografts after M12 underwent transplantectomy (TX) compared to 14 of 48 (29%; ns) in group II. In group II, 11 of 48 (23%) patients were offered alphaIFN therapy after their allograft failed: of these, four (36.3%) developed AR during alphaIFN therapy leading to TX. Histology, in addition to chronic allograft lesions, showed acute cellular and vascular lesions. In patients who were not offered alphaIFN therapy, TX was performed less frequently, i.e. in only six cases (16.2%). We conclude that even alphaIFN-treated KT patients with a failed allograft can experience acute allograft rejection that requires transplantectomy during therapy.
    Nephrology Dialysis Transplantation 04/2008; 23(3):1043-7. · 3.37 Impact Factor
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    ABSTRACT: Renal involvement occurs in 75% of the patients with systemic necrotizing small-vessel vasculitis ie microscopic polyangiitis, Wegener's granulomatosis or Churg-Strauss syndrome. Small-vessel vasculitis may also be limited to the kidney. The hallmark of small-vessel pauci-immune vasculitides consists of necrotizing glomerulonephritis and resultant crescent formation, without immune-complex deposits in vessel walls. The resulting renal manifestations consist of haematuria, proteinuria and rapidly progressive renal failure. ANCA testing has a 90% sensitivity for renal-associated pauci-immune small-vessel vasculitis. Kidney biopsy is required for demonstrating necrotizing vasculitis. Early identification and prompt treatment are mandatory to avoid early mortality and end-stage renal failure. Induction therapy combines corticosteroids and IV cyclophosphamide. Plasma exchange in indicated in the patients presenting with active renal lesions and serum creatinine > 500 micromol/L. Maintenance of immunosuppressive therapy is required for 18 months. Twenty to 50% of the patients relapse during follow-up, and close monitoring is warranted for early detection.
    La Revue du praticien 03/2008; 58(5):499-506.
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    ABSTRACT: Linezolid is a recent oral antibiotic used in drug-resistant Gram-positive cocci infections. Herein, we report on the first case of linezolid-related acute renal failure in a kidney-transplant patient. A 60-year-old male having autosomic polycystic kidney disease with liver involvement, on cyclosporin A, mycophenolate mofetil and very low dose prednisolone, presented with an Enterococcus faecium abscess of a huge liver cyst, which was treated by percutaneous drainage and linezolid therapy. Eight days after starting linezolid, he presented with acute renal failure, i.e. serum creatinine increased from 136- 221 micromol/l, associated with mild hypereosinophilia, anemia and thrombocytopenia. There was no skin rash, arthralgia, eosinophiluria or proteinuria. The transplant kidney biopsy, performed 15 days after the beginning of linezolid therapy, showed interstitial nephritis and focal tubular atrophy. After linezolid withdrawal and increasing prednisolone daily dose to 20 mg/d, within a few days, serum creatinine had decreased; after 2 and 4 weeks post linezolid withdrawal, his serum creatinine was 166 and 159 micromol/l, respectively. Because of the potential side effects of linezolid, i.e. myelosuppression and possibly nephrotoxicity, we recommend close monitoring of these parameters when linezolid therapy is attempted in kidney transplant patients.
    Clinical nephrology 12/2007; 68(5):327-9. · 1.29 Impact Factor
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    ABSTRACT: The successful use of cinacalcet in dialysis patients and in patients with primary hyperparathyroidism has prompted transplant physicians to use it to treat renal-transplant patients with persisting hyperparathyroidism. However, in the setting of kidney transplantation, many questions remain unanswered, i.e. the time of initiation of cinacalcet after transplantation, its dosage and the side effects on kidney function all remain unknown. Herein, we report on a kidney-transplant recipient with persisting hyperparathyroidism who developed hypercalciuria afterreceiving high doses of cinacalcet. Cinacalcet was started 3 months after transplantation at a once-daily dose of 60 mg. Thereafter, the dosage was increased progressively because of persistant hyperparathyroidism and hypercalcemia. At a dose of 90 mg b.i.d, hypercalciuria occurred. The latter disappeared after reduction of cinacalcet dosage. Cinacalcet might be responsible for urinary calcium excretion, either by reduction of tubular calcium reabsorption via the reduction of PTH level, or by its direct effect on the calcium sensor receptor located in the upper thick ascending limb of the loop of Henle. We conclude that cinacalcet should be used with caution in renal-transplant patients. Further investigations are required to determine the best way to use this drug in this setting.
    Clinical nephrology 11/2007; 68(4):245-8. · 1.29 Impact Factor
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    ABSTRACT: Salmonella enteritidis-associated acute renal failure has often been described and is usually a result of dehydration or of rhabdomyolysis. A few cases of acute renal failure with glomerular syndrome, caused by S. enteritidis infection, have been reported in the literature, but none have been proven by histological findings. Herein, we report on a case of S. enteritidis-related glomerulonephritis that occurred in a 42-year-old male transplant recipient. He was admitted with fever, signs of urinary infection, diarrhea, and nephritic syndrome, i.e. edema, hypertension, increase in serum creatinine, microscopic hematuria, proteinuria. His urine culture tested positive for S. enteritidis. Under light microscopy, the graft biopsy showed proliferative and exudative endocapillary glomerulonephritis. In addition, there was polymorphonuclear infiltration of the interstitium, and extra-capillary proliferation in one glomerulus. Immunofluorescence showed granular deposits of C3 in the mesangium. Electron microscopy showed electron-dense deposits typical of humps. He fully recovered on a double antibiotic therapy that included ofloxacin and amikacin. Although acute renal failure related to non-typhoidal Salmonella infections are often related to dehydration or rhabdomyolysis, this case report shows that it might also be related to immune complex-mediated glomerulonephritis manifesting as nephritic syndrome.
    Clinical nephrology 06/2007; 67(5):321-4. · 1.29 Impact Factor
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    ABSTRACT: Many etiologies lead to thrombotic microangiopathy (TMA), amongst which are antineoplastic chemotherapies. Gemcitabine, a nucleoside analogue, has been approved for the treatment ofbladder and advanced non-small cell lung carcinomas (NSCLC). The reported incidence of gemcitabine-associated TMA in the literature is low, ranging from 0.015-0.31%. Herein, we describe the first reported case of gemcitabine-induced TMA in a renal transplant patient. This occurred in a 54-year-old male transplant recipient undergoing sirolimus-based immunosuppression. In February 2005, he was diagnosed to have NSCLC, for which he received dual chemotherapy, including carboplatin and gemcitabine. After the third cycle he developed TMA. On admission, he presented with weakness, edema, normal blood pressure, leucopenia (2440/mm3), thrombopenia (11,000/mm3), hemolytic anemia with hemoglobin at 8 g/dl, schistocytes between 18-33% per hundred, increase in lactate dehydrogenase at 600 IU/l (N <380), and decreased haptoglobin at 0.29 g/l. Renal function was stable: serum creatinine was 1.3 mg/dl, albuminemia 30 g/l, proteinuria was present at 3 g/l in association with microscopic hematuria, and sirolimus trough level was 6.4 ng/ml. Treatment included infusions of fresh frozen plasma, withdrawal of sirolimus, which was replaced by mycophenolate mofetil, and suspension of chemotherapy. He fully recovered from TMA within 4 weeks. The concomitant use of sirolimus, which inhibits vascular endothelial growth factor, plus gemcitabine may have resulted in TMA.
    Clinical nephrology 02/2007; 67(2):114-8. · 1.29 Impact Factor
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    ABSTRACT: We report what is to our knowledge the first case of severe isolated vertigo that developed after renal transplantation and was a manifestation of cryptococcal meningitis. Treatment with antifungal therapy resulted in the complete resolution of vertiginous symptoms. Immunosuppressed patients with an opportunistic infection of the central nervous system can present with extremely tenuous features of infection and atypical neurologic signs.
    Experimental and clinical transplantation: official journal of the Middle East Society for Organ Transplantation 01/2007; 4(2):525-7. · 0.59 Impact Factor
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    ABSTRACT: Systemic B-cell depletion and clinical remission of the systemic effects of cryoglobulins have been achieved in hepatitis C virus-positive immunocompetent patients with rituximab, a human/mouse chimeric monoclonal antibody that specifically reacts with the CD20 antigen. Thus, this provides a rationale for the use of rituximab for type III cryoglobulin-related graft dysfunction in renal-transplant patients. Seven patients, of whom five were hepatitis C positive, developed renal function impairment long after transplantation, as well as de novo nephrotic syndrome (n = 5), severe hypertension (n = 5), nephritic syndrome (n = 1), and increased serum creatinine (n = 1). This type III cryoglobulinemia was associated with membranoproliferative glomerulonephritis and with thrombi within the glomeruli in one case. In addition to their baseline standard immunosuppressive medications, the patients were given weekly rituximab infusions: 375 mg/m(2) for 2 weeks in four cases, for 3 weeks in one case, and for 4 weeks in two cases. This treatment resulted in a dramatic improvement in all renal parameters, particularly a sustained remission of nephrotic syndrome in three cases, the disappearance of nephritic syndrome in one patient, and improved nephrotic syndrome in two cases, as well as a sustained clearance of cryoglobulins in six cases. However, it also resulted in severe infectious complications in two cases. We concluded that rituximab therapy is effective in cryoglobulin-related renal dysfunction in renal transplant patients but, due to chronic immunosuppression, this may be achieved at the expense of infectious complications.
    Transplantation Proceedings 10/2006; 38(7):2308-10. · 0.95 Impact Factor
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    ABSTRACT: Type II or III cryoglobulins are fairly prevalent in renal-transplant (RT) patients, and are often related to chronic hepatitis C virus (HCV) infection. However, they rarely result in graft dysfunction. They are sustained by proliferation of oligoclonal B-cells. Systemic B-cell depletion and clinical remission of the systemic effects of cryoglobulins have been achieved in HCV-positive immunocompetent patients with a human/mouse chimeric monoclonal antibody that specifically reacts with the CD20 antigen (i.e., rituximab). Thus, this provides the rationale to use rituximab for cryoglobulin-related graft dysfunction in RT patients. Three RT patients, of whom one was HCV-positive, developed renal-function impairment long after transplantation, as well as de novo nephrotic syndrome (n=2) and severe hypertension (n=2). This latter case was related to type III cryoglobulinemia and was associated with membranoproliferative glomerulonephritis. In addition to their baseline standard immunosuppression, the patients were given weekly rituximab infusions of 375 mg/m (two infusions in patient and four infusions for the other two cases). This treatment resulted in a dramatic improvement in renal parameters, particularly in a sustained remittence of nephrotic syndrome, a sustained clearance of cryoglobulins in two cases, but also in severe infectious complications in two cases. We conclude that rituximab therapy is highly effective in cryoglobulin-related renal dysfunction in RT patients; however, due to chronic immunosuppression, this is at the expense of infectious complications.
    Transplantation 01/2006; 80(11):1560-4. · 3.78 Impact Factor
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    Nephrology Dialysis Transplantation 02/2005; 20(1):227-30. · 3.37 Impact Factor
  • Revue De Medecine Interne - REV MED INTERNE. 01/2002; 23.
  • Revue De Medecine Interne - REV MED INTERNE. 01/2002; 23.
  • Revue De Medecine Interne - REV MED INTERNE. 01/2002; 23.