PubMed Health⌕ Search

Biomedical subjects

Eric Rondeau

Publications and source records attributed to Eric Rondeau.

At least 19 recordsLinked to original sources
PubMed2007

Prognostic value of anti-ADAMTS 13 antibody features (Ig isotype, titer, and inhibitory effect) in a cohort of 35 adult French patients undergoing a first episode of thrombotic microangiopathy with undetectable ADAMTS 13 activity.

To study both the pathophysiologic and the prognostic value of ADAMTS13 in thrombotic microangiopathies (TMAs), we enrolled a cohort of 35 adult patients combining a first acute episode of TMA, an undetectable (below 5%) ADAMTS13 activity in plasma, and no clinical background such as sepsis, cancer, HIV, and transplantation. All patients were treated by steroids and plasma exchange, and an 18-month follow-up was scheduled. Remission was obtained in 32 patients (91.4%), and 3 patients died (8.6%) after the first attack. At presentation, ADAMTS13 antigen was decreased in 32 patients (91.4%), an ADAMTS13 inhibitor was detectable in 31 patients (89%), and an anti-ADAMTS13 IgG/IgM/IgA was present in 33 patients (94%). The 3 decedent patients were characterized by the association of several anti-ADAMTS13 Ig isotypes, including very high IgA titers, while mortality was independent of the ADAMTS13 inhibitor titer. In survivors, ADAMTS13 activity in remission increased to levels above 15% in 19 patients (59%) but remained undetectable in 13 patients (41%). Six patients relapsed either once or twice (19%) during the follow-up. High levels of inhibitory anti-ADAMTS13 IgG at presentation were associated with the persistence of an undetectable ADAMTS13 activity in remission, the latter being predictive for relapses within an 18-month delay.

ADAM Proteins↗
PubMed2006

Candida albicans arteritis transmitted by conservative liquid after renal transplantation: a report of four cases and review of the literature.

BACKGROUND: Mycotic arteritis and/or aneurysms are infrequent complications of renal transplantation. They are mostly secondary to bacterial infection and rarely to Candida albicans. We report four cases of mycotic arteritis due to C. albicans after renal transplantation but which have been inoculated during organ harvesting or conservation. METHODS: In all the four cases corresponding to two independent donors, C. albicans was isolated few days later in the systematic culture of the conservative liquid. We also review the clinical features and outcomes of 13 cases previously reported in the literature. RESULTS: In two cases, the diagnosis of fungal arteritis was confirmed only during autopsy after the patient's death due to massive bleeding. In the other two cases, the diagnosis was made on the arterial section of the anastomotic wall after detransplantation for massive bleeding for arterial leakage although an immediate antifungal treatment with fluconazole and caspofungin was given and was found to be inefficient. CONCLUSION: This is a serious complication of renal transplantation because it leads to graft loss in the majority of the cases and even to death in a few cases despite an efficient and rapid treatment. Routine fungal cultures of preservation media are important for early diagnosis and timely surgical interventions are life-saving.

Adult↗
PubMed2006

Thrombotic microangiopathy with acquired deficiency in ADAMTS 13 activity in lung transplant recipients.

BACKGROUND: Thrombotic microangiopathy may develop after solid organ transplantation, but it is usually not associated with severe deficiency in von Willebrand factor-cleaving metalloprotease (ADAMTS 13) activity. METHODS: We present the cases of two lung transplant recipients who experienced a thrombotic microangiopathy associated with an acquired severe (<5%) deficiency in ADAMTS 13 activity. RESULTS: A major feature of both cases was the occurrence of a diffuse alveolar hemorrhage. CONCLUSION: Our two cases of lung transplant patients, with thrombotic microangiopathy related to an acquired ADAMTS 13 deficiency recipients, confirm that this mechanism may also be involved in the pathogenesis of thrombotic microangiopathy developing after solid organ transplantation. Therefore, we consider that ADAMTS 13 activity should be assessed on a systematic basis in this setting.

ADAM Proteins↗
PubMed2005

Thrombotic microangiopathy in marginal kidneys after sirolimus use.

The increasing shortage of cadaver donor kidneys has prompted the use of expanded or marginal donor kidneys, ie, from older donors or those with a history of hypertension or diabetes. These marginal kidneys may be especially susceptible to calcineurin inhibitor (CNI)-mediated vasoconstriction and nephrotoxicity. Recipients of renal transplants from marginal donors therefore require non-nephrotoxic immunosuppression. Some investigators have proposed using sirolimus, a novel and potent immunosuppressant, instead of CNIs. Moreover, another complication of solid-organ transplantation is thrombotic microangiopathy (TMA), which affects 3% to 14% of patients on immunosuppression therapy treated with CNIs. Therefore, it was suggested that CNIs may be substituted by sirolimus in patients with posttransplantation CNI-induced TMA. We report 3 patients who received marginal cadaveric kidneys and were administered maintenance immunosuppression with sirolimus, prednisone, and mycophenolate mofetil. They each developed de novo TMA despite never having been previously administered a CNI. In these cases, TMA occurred in marginal kidneys with possible endothelial injury before transplantation. Sirolimus may have prevented recovery from these injuries and thus may have promoted TMA in these marginal kidneys. The risk for such a vascular complication should be kept in mind in patients who receive marginal kidneys and are administered sirolimus, even when sirolimus is used without CNIs.

Aged↗
PubMed2005

The clinical characteristics of HIV-infected patients receiving dialysis in France between 1997 and 2002.

BACKGROUND: In 1997, 0.38% of dialysis patients in France were infected by human immunodeficiency virus (HIV). No prevalence data were available in France since the widespread introduction of highly active antiretroviral therapy. METHODS: This was a cross-sectional epidemiologic survey. A questionnaire was sent to all French dialysis centers in July 2002. The centers that did not respond were sent 3 additional mailing reminders. Finally, the nonresponding centers were called early in 2004. RESULTS: Of the 27,577 patients on hemodialysis and 587 patients on peritoneal dialysis, 190 patients (0.67%) were infected by HIV. HIV-associated nephropathy was the cause of renal failure in 39.8% patients. Mean age was 44.6 +/- 10.9 years, the mean duration of dialysis was 4.9 +/- 5.9 years, the mean known duration of HIV infection was 8.9 +/- 5.6 years. Eighty-two percent of patients received antiretroviral therapy (ART). Fifty-eight percent of ART-treated patients had an undetectable HIV plasma viral load with a median CD4+ T-cell count 303/mm(3). CONCLUSION: The prevalence of HIV infection among French dialysis patients was 0.67% in late 2002, a 79% increase since 1997. Possible reasons for this large increase include increased access to dialysis, better general status of HIV dialysis patients, and increasing proportion of patients originating from Africa and the Caribbean. The current efficacy of ART makes renal transplantation a realistic option for these young patients.

AIDS-Associated Nephropathy↗
PubMed2005

Carnosine as a protective factor in diabetic nephropathy: association with a leucine repeat of the carnosinase gene CNDP1.

The risk of diabetic nephropathy is partially genetically determined. Diabetic nephropathy is linked to a gene locus on chromosome 18q22.3-q23. We aimed to identify the causative gene on chromosome 18 and to study the mechanism by which the product of this gene could be involved in the development of diabetic nephropathy. DNA polymorphisms were determined in 135 case (diabetic nephropathy) and 107 control (diabetes without nephropathy) subjects. The effect of carnosine on the production of extracellular matrix components and transforming growth factor-beta (TGF-beta) after exposure to 5 and 25 mmol/l d-glucose was studied in cultured human podocytes and mesangial cells, respectively. A trinucleotide repeat in exon 2 of the CNDP1 gene, coding for a leucine repeat in the leader peptide of the carnosinase-1 precursor, was associated with nephropathy. The shortest allelic form (CNDP1 Mannheim) was more common in the absence of nephropathy (P = 0.0028, odds ratio 2.56 [95% CI 1.36-4.84]) and was associated with lower serum carnosinase levels. Carnosine inhibited the increased production of fibronectin and collagen type VI in podocytes and the increased production of TGF-beta in mesangial cells induced by 25 mmol/l glucose. Diabetic patients with the CNDP1 Mannheim variant are less susceptible for nephropathy. Carnosine protects against the adverse effects of high glucose levels on renal cells.

Aged↗
PubMed2004

Plasminogen activator inhibitor type 1: the two faces of the same coin.

PURPOSE OF REVIEW: Plasminogen activator inhibitor type 1 is the primary inhibitor of plasminogen activators. It is often bound to vitronectin, an abundant component of extracellular matrix in many tissues. The aim of this review is to discuss the contradictory results reported concerning the impact of plasminogen activator inhibitor type 1 expression in the kidney and in the vessel wall during pathological conditions. RECENT FINDINGS: First described as a 'bad guy' promoting the persistence of fibrin deposition and the evolution towards organ fibrosis, plasminogen activator inhibitor type 1 was recently reported to serve an unexpected protective role during fibrin-dependent diseases, such as experimental glomerulonephritis, and during aortic atherosclerosis. SUMMARY: Plasminogen activator inhibitor type 1 is not only an inhibitor of plasmin generation. Recent data suggest that plasminogen activator inhibitor type 1 is required for the regulation of plasminogen activator-dependent, plasmin-independent processes, and that its expression in vivo critically modulates inflammation, potentially by its capacity to occupy vitronectin binding sites.

Animals↗
PubMed2004

Role of the coagulation/fibrinolysis system in fibrin-associated glomerular injury.

In the past decade, numerous experimental studies of genetically engineered mice have confirmed the involvement of the coagulation/fibrinolysis system during glomerular inflammation and repair, revealing many unexpected biologic effects far beyond fibrin formation and clearance. Resident glomerular cells and macrophages seem to act in concert to ensure the long-term consolidation of local injury and progression toward glomerulosclerosis. These recent advances will probably pave the way to a new therapeutic approach to renal diseases. However, the balance governing glomerular permeability is very delicate, and many issues will have to be dealt with before targeting this system.

Animals↗
PubMed2004

Regulation of vascular permeability factor/vascular endothelial growth factor (VPF/VEGF-A) expression in podocytes.

BACKGROUND: Vascular permeability factor/vascular endothelial growth factor (VPF/VEGF-A) is expressed constitutively in the adult glomerular podocytes at high levels; however, the regulation of its production is unclear. Recent data from podocyte-specific knockout mice suggest that VPF/VEGF-A is critical for the proper maintenance of glomerular filtration barrier and the glomerular endothelial fenestrae. We hypothesized that the glomerular basement membrane (GBM) matrix-podocyte interaction may play a role in the constitutive expression of VPF/VEGF-A in the adult glomerulus. METHODS: VPF/VEGF-A mRNA levels in a human podocyte cell line grown in the presence of various extracellular matrices were quantitated by real-time polymerase chain reaction (PCR) experiments. VPF/VEGF-A protein levels in the culture supernatant from the same conditions were measured by enzyme-linked immunosorbent assay (ELISA). Promoter activity of VPF/VEGF-A gene in these cells was performed by transfecting full length (2.6 kb) VPF/VEGF-A promoter, which is fused with luciferase reporter gene. Immunoprecipitation and Western blot experiments were carried out in order to detect the association of hypoxia-inducible factor-alpha (HIF-alpha) and p300 in podocyte cells. RESULTS: In this study, we provide preliminary evidence that signaling through the extracellular matrix proteins and, in particular, laminin and its receptor alpha(3)beta(1) integrin may regulate VPF/VEGF-A production in cultured podocytes in vitro. We also present data that increased activity of the transcription factor HIF-alphas in podocyte is not related to hypoxia and may lead to up-regulation of VPF/VEGF-A transcription. The classical type protein kinase C (PKC) may be a potential intermediate signaling molecule in this event. CONCLUSION: These data suggest a novel nonhypoxic regulation of VPF/VEGF-A production in the glomerulus of the kidney during physiologic states. These observations may form the basis of more elaborate studies that will finally provide the detailed signaling pathway for VPF/VEGF-A synthesis in podocytes and will help our understanding of the pathogenesis of various VPF/VEGF-A-related diseases in the glomerulus of the kidney.

Basic Helix-Loop-Helix Proteins↗