PubMed Health⌕ Search

Biomedical subjects

Eric Rondeau

Publications and source records attributed to Eric Rondeau.

27 records · Page 2Linked to original sources
PubMed2003

Primary brain lymphomas after kidney transplantation: presentation and outcome.

BACKGROUND: Non-Hodgkin's lymphoma is the second most frequent neoplasia following solid-organ transplantation. The objective of this study is to describe the clinical, histologic, and radiologic features of primary posttransplantation brain lymphomas (PTBL) in addition to their outcome. METHODS: Twenty-five kidney transplant patients with histologically proven PTBL from 11 French centers were retrospectively investigated. RESULTS: Immunosuppressive regimen included induction with antithymocyte globulins (ATG) in 20 patients. Median overall delay between transplantation and lymphoma was 18 months (4-264). Six of 10 patients with late posttransplantation brain lymphomas (PTBL) occurrence (>3 years) had been recently switched from azathioprine to mycophenolate mofetil (median switch lymphoma delay 14 months). Cerebral computed tomography (CT) scans and magnetic resonance imaging (MRI) revealed multifocal lesions (n=18), with a ring contrast enhancement (n=20) similar to cerebral abscesses, as observed in HIV-related brain lymphomas. Histology showed large B-cell non-Hodgkin's lymphoma in 87.5% of cases; Epstein-Barr virus (EBV) was detected in 95%. After lymphoma diagnosis, immunosuppressive treatment was reduced in all patients, and all but one received complementary treatment by surgery (n=2), anti-CD21 antibodies (n=2), chemotherapy including high-dose intravenous methotrexate (n=7), encephalic radiotherapy (n=5), or chemotherapy plus radiotherapy (n=8). Median overall survival was 26 months. Patients with a radiotherapy-based regimen seemed to have a longer survival (36 vs. 7 months, P<0.005). CONCLUSIONS: Our study showed that PTBL are EBV-induced large B-cell lymphomas, which mimic cerebral abscesses on imaging and whose occurrence may be influenced by immunosuppression modifications. Treatment by radiotherapy is associated with better survival.

Adult↗
PubMed2003

Type 1 plasminogen activator inhibitor deficiency aggravates the course of experimental glomerulonephritis through overactivation of transforming growth factor beta.

Type 1 plasminogen activator inhibitor (PAI-1) is the primary inhibitor of tissue-type plasminogen activator (tPA) and urokinase-type plasminogen activator (uPA). Whereas PAI-1 is not expressed in normal kidneys, it is strongly induced in glomerular diseases and thus could promote the local accumulation of fibrin. To study the role of PAI-1 in the development of inflammatory glomerular injury, passive antiglomerular basement membrane (GBM) glomerulonephritis (GN) was induced in PAI-1 knockout mice and in wild-type mice of the same genetic background. Unexpectedly, PAI-1 deficiency was associated with an early and severe exacerbation of glomerular injury: Infiltration by CD4 T cells, proportion of fibrinous crescents, and renal function impairment were significantly more pronounced in PAI-1 -/- mice. Interestingly, activation of transforming growth factor (TGF)- beta, which is known to be dependent on the PA/plasmin system in vitro, was dramatically enhanced in the kidneys in the absence of PAI-1. Moreover, administration of neutralizing antibodies against TGF-beta significantly attenuated the disease in PAI-1 -/- mice. This suggests that the poor outcome of GN in PAI-1 -/- mice is consecutive to an uncontrolled activation of TGF-beta and confers PAI-1 with a new, immunomodulatory role.

Animals↗
PubMed2002

Risk factors for nephrolithiasis in patients with familial idiopathic hypercalciuria.

PURPOSE: About 40% of patients with nephrolithiasis have idiopathic hypercalciuria, sometimes associated with a family history of kidney stones. In these families, little is known about the frequency of, and risk factors for, stone formation among hypercalciuric patients. We therefore conducted a prospective study of 216 subjects from 33 families with idiopathic hypercalciuria. MATERIALS AND METHODS: We recorded the age, weight, and history of calcium stones in all subjects, and measured 24-hour urine volume and excretion of calcium, uric acid, sodium, magnesium, urea, citrate, phosphate, and sulfate on a nonrestricted diet. We performed a more complete metabolic evaluation in many of the hypercalciuric subjects (calciuria/weight >0.1 mmol/kg/d). Multivariate logistic regression analysis was performed to identify independent risk factors for stone formation. RESULTS: The prevalence of self-reported nephrolithiasis was 46% (61/132) in hypercalciuric subjects and 11% (7/63) in normocalciuric subjects (P <0.0001). In multivariate analysis, age (odds ratio [OR] per 10 years of age = 1.3; 95% confidence interval [CI]: 1.1 to 1.6), urine calcium excretion (OR = 1.3 per mmol/d increase; 95% CI: 1.2 to 1.5), and uric acid excretion (OR = 3.3 per mmol/d increase; 95% CI: 1.4 to 7.5) were independent risk factors for nephrolithiasis. The risk of nephrolithiasis increased progressively with greater levels of hypercalciuria. CONCLUSION: We found a significant dose-effect association between calciuria and stone disease in patients with familial hypercalciuria. Other factors associated with stone formation included higher uric acid excretion, probably reflecting higher food intake, and age, probably reflecting the length of exposure to hypercalciuria and hyperuricosuria.

Adult↗
PubMed2002

Chronic graft dysfunction in renal transplant patients: potential role of plasminogen activator inhibitor type 1.

BACKGROUND: Chronic allograft nephropathy is the main cause of long-term kidney graft loss. The plasminogen activator inhibitor type 1 (PAI-1) is a potential fibrogenic molecule whose secretion is regulated by several metabolic, inflammatory, and genetic factors. We aimed to determine whether PAI-1 secretion in renal transplant patients is correlated with the decline in renal function after transplantation. METHODS: Renal transplant patients (145 male/71 female) were included in the study 1-27 years after transplantation (median of follow-up: 7.35 years). At inclusion, routine clinical and biological data were collected, the 4G/5G polymorphism of the recipient PAI-1 gene was determined, and the PAI-1 plasma level was measured. RESULTS: The mean rate of decline in renal function was -4.26+/-0.30 ml/min/year. By multiple linear regression analysis, the rate of decline in renal function was significantly correlated with proteinuria (P=0.0176), occurrence of late acute rejection episodes (P=0.0001), and PAI-1 plasma level (P=0.0051). In addition, PAI-1 plasma level was also significantly correlated with body mass index (P=0.038), insulin (P<0.0001), platelet count (P<0.0001), and fibrinogen (P=0.024). The PAI-1 gene polymorphism tested did not influence the rate of decline in renal function after transplantation nor the plasma level of PAI-1 antigen. CONCLUSION: We conclude that PAI-1, whose secretion is determined in large part by metabolic and inflammatory factors, may be implicated in the rate of decline in renal function after transplantation.

Adult↗
PubMed2002

Adult haemolytic and uraemic syndrome: causes and prognostic factors in the last decade.

BACKGROUND: Haemolytic uraemic syndrome (HUS) is a rare and severe disease of various aetiologies in adults. The effect of fresh frozen plasma (FFP) infusion in adults suffering from HUS is not well defined. The aim of this retrospective study was to analyse the causes of HUS in adults admitted in a single renal intensive care unit (ICU) and to determine the life and renal prognosis factors, while most patients (78%) received FFP infusion. METHODS: We recorded clinical, biological, and histological data of 55 adults admitted in our renal ICU for HUS between 1990 and 1998, 49 of them having had a renal biopsy. By stepwise logistic regression analysis, we examined the parameters that were associated with the in-hospital mortality and renal function at discharge. RESULTS: HUS complicated different diseases in 40 patients (HIV infection n=18, nephropathies n=10, allotransplantation n=7, malignant diseases n=5) and appeared as a primary in 15 patients. Factors influencing the in-hospital mortality were positive HIV serology (odds ratio (OR) >20, P=0.0002) and requirement for haemodialysis (OR >35, P=0.004). A pre-existing nephropathy was a bad prognosis factor for renal function (OR >99, P=0.02), while fever was associated with better renal prognosis (OR=1/10, P=0.033). CONCLUSIONS: HUS in adults remains a severe disease, with a high mortality rate in HIV patients and in those who required haemodialysis. However, as compared with previous studies, we observed an improvement in renal outcome, particularly in patients with primary HUS, suggesting a beneficial effect of FFP infusion, at least in these forms.

Acquired Immunodeficiency Syndrome↗
PubMed2000

Characterization and localization of the neonatal Fc receptor in adult human kidney.

The binding of Fc fragments of Ig on glomerular epithelial cells (GEC) was observed previously, but the receptor could not be identified. In immunofluorescence and immunohistochemical studies using normal adult human kidney sections, the presence of the so-called neonatal Fc receptor (FcRn) was demonstrated on GEC as well as in the brush border of proximal tubular cells. FcRn transcripts were also detected on isolated glomeruli by reverse transcription-PCR. Using an immortalized GEC line, the presence of the FcRn was confirmed by flow cytometry, reverse transcription-PCR, Western blotting, and by the pH dependence of the binding of heat-aggregated IgG. Because it is well established that the FcRn is involved in IgG transcytosis, it is hypothesized that the FcRn in the kidney may play a role in the reabsorption of IgG. Ongoing studies should clarify the role of the FcRn as a potential target for immune complexes on GEC and should assess its relevance in physiology and pathology.

Adult↗