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Biomedical subjects

E Rondeau

Publications and source records attributed to E Rondeau.

At least 19 recordsLinked to original sources
PubMed2002

[False hyperchloremia in a bromide intoxication].

A false hyperchloremia in a patient with a history of depression suspected bromide intoxication. The diagnosis was confirmed by an increased bromide concentration > 20 mmoL.L-1. Rehydration was effective and allowed to decrease bromide concentration. In conclusion, hyperchloremia associated with a negative anion gap is a clue to the diagnosis.

Bromides↗
PubMed2002

[Hemolytic and uremic syndrome in the adult].

Hemolytic-uremic syndrome (HUS) is a rare disease but may be fatal in the absence of appropriate treatment. It is the first cause of acute renal failure (ARF) in children and is less frequently observed in adults. We report the case of a 50 years old woman who was first admitted in the surgery department for intestinal occlusion. Haematological and renal disorders were not recognised initially. Specific treatment with plasma exchanges was beneficial. This case was idiopathic but in 50% of HUS in adults, an aetiology can be found and sometimes treated: drugs, pregnancy, systemic diseases, hypertension or cancer. Although still debated, treatment is based on fresh frozen plasma infusion, associated or not to plasma exchanges. Some other therapies can be added: steroids, polyvalent immunoglobulin infusion, vincristin or splenectomy. In all cases, blood pressure control must be obtained, especially with ACE inhibitors. Response to treatment is often excellent, but chronic renal failure persists in about 25% of cases in adults. Recurrences are rare and occur mainly in patients with an hereditary factor H deficiency. The hemolytic-uremic syndrome should be diagnosed and treated immediately.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Prognostic value of plasminogen activator inhibitor type 1 mRNA in microdissected glomeruli from transplanted kidneys.

BACKGROUND: Plasminogen activator inhibitor type 1 (PAI-1) exerts antifibrinolytic and profibrotic activities. Inside the glomerulus, PAI-1 is mainly synthesized by mesangial cells. We hypothesized that thrombin, via its receptor protease activated receptor type 1 (PAR-1), present on the membrane of glomerular cells, is an important mediator of PAI-1 synthesis. METHODS: Using the technique of Peten et al., we microdissected the glomeruli of 23 kidney transplanted patients admitted in our department from 1993 to 1997, and we followed-up these patients for up to 5 years, with sometimes iterative renal biopsies. With this technique, we also microdissected the glomeruli of three patients who have had a nephrectomy for cancer (control patients). We investigated mRNA expression of the PAI-1, the thrombin receptor PAR-1, the alpha2 chain of type IV (alpha2 IV) collagen, and of a housekeeping gene (cyclophilin) by reverse transcription-polymerase chain reaction. The results were correlated with the renal function and the histological findings classified into acute rejection (9 biopsies), chronic rejection (22 biopsies), or normal (8 biopsies). RESULTS: A significant up-regulation of PAI-1 and alpha2 IV collagen mRNA was observed in acute rejection (P<0.05) when compared to normal kidneys. A positive correlation exists between alpha2 IV collagen mRNA level and the degree of cellular infiltration. A negative correlation was found between the level of mRNA of PAR-1 and the degree of vascular thrombosis (P=0.005) and glomerulosclerosis (P=0.04). A positive correlation was found between the degradation of renal function and the mRNA level of PAI-1 at the time of the renal biopsy (P<0.05). CONCLUSIONS: These results suggest that glomerular PAI-1 mRNA may be predictive of the long-term renal graft function.

Adolescent↗
PubMed2001

[Is there an age limit for organ donors?].

Nowadays organ transplantations suffer from a lack of donors. Thus the waiting list of patients is constantly growing. Several ways to increase organ procurement are being evaluated. About 50% of cerebral deaths are related to vascular cerebral in patients older than 60 years. For the last few years, organs have been harvested from these patients despite their age. As the quality of the grafts is reduced, transplantation of one kidney may be insufficient whilst transplantation of the two kidneys to the same recipient is technically possible. We report here a case of a 44-year-old patient who was transplanted with two kidneys in September 2000. The donor was 85-year-old patient who died after prolonged cardiac arrest. Kidney biopsy showed a 16% rate of sclerotic glomeruli and mild interstitial fibrosis. The creatinine clearance estimated by the Cockcroft formula was 50 mL.min-1. The double kidney transplantation was successful, without any surgical or anaesthetic complication. Restoration of urine production was immediate. Three months after the transplantation, creatinine clearance was 80 mL.min-1. This observation gives the opportunity to discuss the criteria for organ harvesting in patients with cerebral death. Donor age should not remain anymore a systematic contra indication for kidney or liver donation. Renal function, macroscopic examination and histological findings seem more important for making a decision in taking the graft. Double transplantation, here the second case in France, has been performed for several years in other countries, and has permitted to expand the pool of donors, thus increasing the number of transplanted patients.

Adult↗
PubMed2001

Idiopathic membranous glomerulonephritis is associated with altered patterns of self-reactive IgM and IgG antibody repertoires.

Idiopathic membranous glomerulonephritis (MGN) is an immune complex nephropathy characterized by the subepithelial deposition of immunoglobulin (Ig)G. The pathogenesis of the disease remains largely unknown, but recent evidence suggests that human MGN may involve an autoimmune component. In the present study, we have analyzed the IgM and IgG antibody repertoires of patients with MGN towards self- and nonself-antigens using a technique of quantitative immunoblotting on a panel of whole human tissue or solubilized bacterial cell extracts as sources of antigens. Data were compared by means of multiparametric statistical analysis. We demonstrate that the antibody repertoires of self-reactive IgM and IgG in plasma of patients with MGN exhibit significantly altered patterns of reactivity, as compared with those of healthy controls. In contrast, multiparametric statistical analysis does not discriminate the reactivity patterns of IgM and IgG in plasma of patients and healthy controls towards nonself antigens. These observations indicate that a failure in the regulation of physiological self-reactivity is associated with immune complex nephropathy in MGN.

Adult↗
PubMed2001

Multicenter trial of one HLA-DR-matched or mismatched blood transfusion prior to cadaveric renal transplantation.

BACKGROUND: The beneficial effect of blood transfusions before cadaveric renal transplantation on allograft survival, although previously well documented, has become controversial in light of their adverse effects. Recently, it has been suggested that their clinical benefits are due to HLA-DR sharing between the blood donor and recipient. METHODS: In this prospective study, 144 naive patients were randomly assigned to receive one unit of blood matched for one-HLA-DR antigen (N = 49), or one unit of mismatched blood (N = 48), or to remain untransfused (N = 47). Graft survival and acute rejection rate were analyzed in 106 cadaveric renal allograft recipients receiving the same immunosuppressive protocol. RESULTS: Graft survival was similar in the three groups at one and five years: 91.7 and 80% in untransfused patients, 90.3 and 79.3% in patients transfused with one DR-antigen-matched unit, and 92.3 and 83.7% in patients transfused with HLA-mismatched blood. The difference in the incidence of six-month post-transplant acute rejections was not statistically significant in the three groups: 12 out of 36, 33.3% in nontransfused patients; 6 out of 31, 19.4% in patients transfused with one DR-matched blood; and 13 out of 39, 33.3% in patients transfused with mismatched blood. CONCLUSION: The results of our prospective randomized trial showed that in a population of naive patients, one transfusion mismatched or matched for one HLA-DR antigen given prior to renal transplantation had no significant effect on the incidence and severity of acute rejection, and did not influence overall long-term graft outcome. Considering the potentially deleterious adverse effects of blood transfusions, the costs, and the considerable logistical efforts required to select and type blood donors, such a procedure cannot be recommended in a routine practice for patients awaiting cadaveric kidney transplantation.

Acute Disease↗
PubMed2001

No evidence for point mutations of the calcium-sensing receptor in familial idiopathic hypercalciuria.

BACKGROUND: Idiopathic hypercalciuria (IH) is frequently associated with nephrolithiasis. As 40% of patients have a positive familial history of IH, an autosomal dominant mode of inheritance has been suggested. Numerous genes have been studied in this regard but none have been found to be linked to IH. Mutation of the calcium-sensing receptor (CaR) has never been studied. Therefore, we conducted a study to detect such mutations. METHODS: Seven families with IH and nephrolithiasis were recruited in a prospective study. Forty-two family members underwent 24-h urine calcium measurement. Twenty-five of them with 24-h hypercalciuria also underwent extensive metabolic evaluation. Blood samples were collected in one or two affected family members in each family and exons 2-7 of the CaR gene were sequenced. RESULTS: In the seven families, at least one parent and more than half of the children had hypercalciuria (21/30), consistent with autosomal dominant inheritance. Among the nine affected family members whose CaR gene has been studied, all nine had absorptive hypercalciuria, three also had fasting hypercalciuria, and one had renal phosphorous leak. No mutation of the CaR gene was detected in these seven families. Two previously reported polymorphisms were detected, each of them in five families: A986S and C-to-T change at -60 in intron 5. CONCLUSION: In these seven families, IH is not related to the CaR gene mutation. Although we cannot exclude that point mutations can be found in other families, familial IH does not seem to be generally associated with CaR mutation.

Adult↗
PubMed2001

Induction of urokinase receptor expression in nephrotoxic nephritis.

The urokinase receptor (uPAR) is a multifunctional molecule involved in pericellular, fibrinolytic, and proteolytic activities, as well as in cell adhesion and chemotaxis and may play a role in the pathogenesis of tissue remodeling occurring during glomerulonephritis. We analyzed sequentially the expression of uPAR by immunohistochemistry and in situ hybridization in an accelerated model of nephrotoxic nephritis in rats. A strong induction of uPAR mRNA expression was observed in glomeruli as soon as 1 h after nephrotoxic serum injection. The intensity of glomerular uPAR mRNA and antigen expression increased and peaked at 24 h. At that time, numerous glomerular fibrin deposits, monocyte/marcrophage infiltration, and heavy proteinuria were observed. Fibrin deposition was detected at 6 h, peaked at 24 h, and progressively declined over the next 3 weeks, while uPAR antigen expression remained elevated until the end of the study (3 weeks). By double labeling, we showed that the expression of uPAR was mediated by both intrinsic glomerular cells and infiltrating macrophages. Severe podocytic lesions developed within 3 days after antiserum injection, and glomerulosclerosis rapidly progressed within 2-3 weeks. These results show that glomerular uPAR expression is induced in nephrotoxic nephritis and suggest that uPAR may promote local proteolysis and also tissue remodeling, leading to the late development of glomerulosclerosis.

Animals↗
PubMed2001

Internalisation of the protease-activated receptor 1: role of the third intracellular loop and of the cytoplasmic tail.

To analyse the mechanisms of PAR-1 internalisation, we constructed several PAR-1 mutants and stably expressed them in CHO cells. Our study shows that the Ser(306)-->Ala mutation (S306A), which eliminates a potential site of phosphorylation by PKC in the third intracellular loop of PAR-1, did not change the rate of phosphorylation but reduced the rate of thrombin-induced internalisation of the PAR-1 mutant (58 versus 78% of membrane PAR-1 in 15 min, p<0.005). Deletion of the last 43 amino acid residues of the PAR-1 cytoplasmic tail completely suppressed the thrombin phosphorylation of the mutated receptor and significantly reduced its internalisation upon activation. This deletion also inhibited the PMA-induced and the agonist-independent internalisation of the receptor. The Tyr(371)--> Ala mutation (Y371A), in a NPXXY motif of the seventh transmembrane domain of the receptor had no effect on the receptor behaviour. Our results indicate that both the C-tail and the third intracellular loop are involved in PAR-1 internalisation induced by thrombin while only the C-tail plays a role in the PMA-induced and in the agonist-independent PAR-1 internalisation.

Alanine↗
PubMed2001

Role of the third intracellular loop and of the cytoplasmic tail in the mitogenic signaling of the protease-activated receptor 1.

The activation of the protease-activated receptor 1 (PAR-1) by thrombin has been shown to induce an activation of the MAP kinase cascade and to stimulate cell proliferation. To examine the mechanisms of signal transduction by PAR-1, we constructed several PAR-1 mutants which were stably expressed in CHO cells. When compared to wild-type PAR-1, mutation of Ser306-->Ala (S306A) in the third intracellular loop of PAR-1 inhibited MAP kinase activation and cell proliferation stimulated by thrombin. The thrombin activation of MAP kinase was inhibited by pertussis toxin, suggesting a role for a Gi-like protein. As shown by calcium signaling and inosotol trisphosphate generation, the Ser306-mutated PAR-1 induced a strong activation of phospholipase C after thrombin addition. Deletion of the cytoplasmic tail of PAR-1 also inhibited thrombin-induced DNA synthesis but the MAP kinase pathway was activated as with wild-type PAR-1. In contrast, the deletion of the C-tail of PAR-1 prevented almost completely the activation of the phospholipase C pathway. Taken together these results suggest that the C-tail of PAR-1 is a critical site for PAR-1 coupling to phospholipase C activation, while the third intracellular loop of PAR-1 is implicated in PAR-1 coupling to Gi and MAP kinase activation. In addition, these results also show that MAP kinase activation is necessary but not sufficient for thrombin to induce cell proliferation.

Animals↗
PubMed2001

[Plasminogen activator inhibitor type 1: physiology and role in renal physiopathology].

Plasminogen activator inhibitor type 1 plays a prominent part in the regulation of extra and intra-vascular fibrinolysis through the inhibition of plasmin formation. In addition to its role in the resolution of blood clots, PAI-1 is involved in a variety of other biological processes including extracellular remodeling, cellular mobility, embryo implantation, development and tumoral proliferation. Moreover, PAI-1 is also implicated in various pathological processes such as thromboembolic diseases, atherosclerosis and fibrosis formation, particularly in the kidney and the lung. Inhibition of PAI-1 activity or of PAI-1 synthesis by specific antibodies, peptidic antagonists, antisens oligonucleotides or decoy oligonucleotides has been obtained in vitro but need to be evaluated in vivo. All these findings may have new therapeutical implications, explaining the importance of studies on PAI-1 production and regulation.

Aldosterone↗
PubMed2000

Regulation of the paired type IV collagen genes COL4A5 and COL4A6. Role of the proximal promoter region.

Tissue-specific expression patterns of the paired type IV collagen genes COL4A5 and COL4A6 form the basis for organ involvement in X-linked Alport syndrome, a disorder in which these genes are mutated. We investigated the proximal promoter region of COL4A5 and COL4A6 using glomerular visceral epithelial cells, in which COL4A5 alone is transcribed; keratinocytes, in which the genes are co-transcribed; and additional model cell lines. By RNase protection assays, the intergenic region is 292 base pairs. Transcription start sites for two 5' splice variants of COL4A6 are 1 kilobase apart. Transient transfections with reporter gene constructs revealed that the minimal promoters for COL4A5 and COL4A6 are within 100 base pairs of their respective transcription start sites and are functionally distinct. In further transfection, gel shift and footprinting assays, we defined a bidirectional positive regulatory element, which functions in several cell types, but not in glomerular visceral epithelial cells selectively transcribing COL4A5. The existence of separate promoters for COL4A5 and COL4A6 permits fine control over their expression. Activation through the bidirectional element can bring about co-expression of the genes, exploiting their paired arrangement. Features of the proximal promoter region frame its roles in a hierarchy regulating type IV collagen gene expression.

Base Sequence↗
PubMed2000

[Rapidly progressive acute renal failure. A rare complication of primary Sjogren syndrome].

BACKGROUND: Renal impairment, usually due to tubulointerstitial and rarely glomerular disorders occurs in 10 to 30% of patients with primary Sjögren's syndrome. Extracapillary proliferation may also be observed. CASE REPORT: A 62-year-old woman with primary Sjogren's syndrome diagnosed 12 years earlier, developed microscopic polyangeitis leading to rapidly progressive renal failure. Antipolynuclear anticyclosine antibody (ANCA) serology was positive (pANCA, anti MPO) and the renal biopsy evidenced necrotizing glomerulonephrities with extracapillary proliferation. Outcome was favorable despite a recurrence one year after onset. DISCUSSION: Extracapillary proliferative glomerulonephritis is characterized by hematuria and proteinuria associated with renal failure. Renal impairment may worsen rapidly, sometimes leading to an emergency situation because the renal prognosis is directly related to delay to treatment. This case illustrates an uncommon complication of Sjögren's syndrome, compared with the usual tubulointerstitial disorders. The mechanism remains unknown, but outcome can be favorable with rapidly initiated immunosuppressor treatment.

Acute Kidney Injury↗