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Biomedical subjects

F Bayle

Publications and source records attributed to F Bayle.

At least 37 records · Page 2Linked to original sources
PubMed1995

[Hematotoxicity caused by azathioprine genetically determined and aggravated by xanthine oxidase deficiency in a patient following renal transplantation].

Azathioprine is an immunosuppressor used with ciclosporin and corticosteroids after organ transplantation. Azathioprine is rapidly transformed into 6-mercaptopurine which in turn is metabolized by three competitive pathways: a) intracellular hypoxanthine guanine phosphoribosyl transferase leads to 6-thioguanine nucleotides which can damage chromosome DNA; b) thiopurine methyltransferase produces inactive methylated derivatives; c) xanthine oxidase produces thiouric acid. Due to inter-individual variations in the later two pathways, azathioprine dose must be adapted to each patient. A 48-year-old female patient underwent renal transplantation in 1994 and was given immunosuppressive therapy combining thymoglobulins, azathioprine and ciclosporin. Severe leukopenia (< 3000/mm3) occurred on day 5 requiring withdrawal of azathioprine. Known hypouricaemia (< 50 mumol/l) suggested xanthine oxidase deficiency. Laboratory results confirmed xanthine oxidase deficiency and also revealed reduced thiopurine methyltransferase activity (14.9 pmol/h/mg Hb). Azathioprine toxicity was confirmed by regression of the leukopenia after withdrawal and recurrence at rechallenge. Xanthine oxidase deficiency occurs in 2% of the general population. Reduced thiopurine methyltransferase activity affects 11% of the population. The combined presence of these two genetic anomalies led to early and sudden intolerance to azathioprine and emphasize the need to develop new immunosuppressor agents degraded by other metabolic pathways.

Azathioprine↗
PubMed1995

Beneficial effect of one HLA haplo- or semi-identical transfusion versus three untyped blood units on alloimmunization and acute rejection episodes in first renal allograft recipients.

Acute allograft rejection is the major risk factor of renal function decline and graft loss. Beside histocompatibility matches and pharmacological immunosuppression, blood transfusion is empirically used to detect responder subjects and to induce immune tolerance. Alloimmunization associated with blood transfusions readily detected by anti-HLA antibodies could induce acute vascular rejection episodes during the early period after grafting. Our open prospective study was aimed at analyzing the 1 year follow-up of 105 successive first cadaver renal transplant recipients according to the transfusion protocol as assessed by anti-HLA antibody production, acute rejection episodes, and graft survival. Our conventional transfusion protocol involved 3 nonphenotyped blood transfusions set up at least 20 days before grafting in a control cohort (group A) and was compared with a single pretransplant HLA haplo- or semi-identical blood transfusion in a successive group of patients (group B). Our results suggest that both protocols were associated with similar 1-year graft survivals (> 96% in both groups) and number of patients experiencing rejection episodes (20.7% in group A; 9.6% in group B; P NS). HLA haplo- or semi-identical transfusion was significantly beneficial in naive patients without previous alloantigen contact by pregnancy or blood transfusions during dialysis. Naive patients in group B did not develop post-transfusion anti-HLA antibodies compared to naive patients in group A (16.6%; P < 0.001), and they experienced significantly less acute rejection episodes (2.7%) compared to group A naive patients (20.8%; P = 0.02).

Blood Transfusion↗
PubMed1994

[Influence of kidney procurement techniques on urologic and vascular complications of the transplantation].

Surgical complications of renal transplantation, rejection and infectious diseases are factors contributing to poor renal graft survival. Factors directly concerning the donor can be involved in graft failure: age, medical history, causes of donor brain death. Urologic or arterial anatomic variations are often the source of difficult surgical conditions during renal transplantation. Technical errors during graft procurement must be avoided such as excess of traction or coagulation. Failure in perfusion preservation. As few renal grafts are available, it is thus essential to obtain optimal conditions to avoid failure in cadaver donor graft linked to technical errors during organ procurement.

Adolescent↗
PubMed1986

[Primary microvascular lesions of the kidney or pre-hypertensive nephroangiosclerosis. 25 cases].

Isolated non inflammatory lesions of renal microarteries (eventually with mild thickening of tubular basement membranes, but with negative immunofluorescent glomerular studies) were observed in 25 patients (22 males) in whom renal biopsy have been performed for proteinuria (P). Selection criteria were: pathological lesions by definition; absence of hypertension (HT) in clinical and at the time of biopsy; minimum follow up of 4 years after the first statement of the proteinuria (4 to 29 years; mean 14 years). Three groups have been isolated: 1. 3 patients have had an acute glomerulonephritis followed by disappearance of proteinuria. It reappears 1 to 5 years later. HT was discovered 2, 8 and 11 years after the proteinuria. Renal failure occurred 1 and 3 years after HT. 2. 14 patients had hereditary or acquired vascular risk factors (obesity, smoking, ethylism). In 7, HT occurred 3 to 15 years after P. In 2, renal failure occurred 4 to 8 years later. 3. 8 patients had no vascular risk factor; in 3 of them Ht developed 7, 13 and 20 years after the first statement. A positive immunofluorescence with IgM or C3 on renal arterioles had been found in only 3 of the 10 patients who in group 2 and 3 became hypertensive. A proteinuria may precede the occurrence of HT without being induced by glomerulonephritis. Group 2 and 3 suggest that these renal lesions of arterial sclerosis precede and may be a factor of HT. Indeed, this entity may be considered as a prehypertensive condition.

Arterioles↗
PubMed1985

[Nephrotoxicity of mitomycin C (apropos of 25 case reports). Results of a multicenter survey organized by the Society of Nephrology].

We have studied 25 cases of hemolytic and uremic syndrome (H.U.S.) induced by mitomycin C, collected from 1976 to 1982 in 12 Nephrology Centers. Mitomycin C was administered in successive cures at a cumulative dose higher than 50 mg/m2. This H.U.S. is characterized by its slow and late occurrence, by extra-renal, mainly respiratory, manifestations that may reveal the disease, and finally by its pathological aspects. Mesangiolysis and endothelial or mesangial enlarged and atypical nuclei are observed in addition to the usual lesions of thrombotic micro-angiopathy. The prognosis was very poor in the first cases reported. It was better, however, in the patients studied more recently, because the cumulative dose was lower. In severe cases, plasma exchange might improve long-term prognosis. The disease might be due to a direct toxic effect of mitomycin C on the vascular endothelium.

Adult↗
PubMed1985

Macrophage function in primary and secondary glomerulonephritis.

The function of the mononuclear phagocyte system was assessed in vivo in 85 patients with primary and secondary glomerulonephritis, by measuring the clearance of IgG - sensitised 51Cr-labelled autologous erythrocytes. Eleven per cent of patients in clinical remission were found to have a delayed clearance, whereas impaired macrophage function was present in 62.5 per cent of the patients with major urinary abnormalities. Blockade of mononuclear phagocyte system, induced at least in part by unidentified factors, might have a role in development and perpetuation of glomerular injury.

Adult↗
PubMed1984

[Nephrotoxicity of antitumor chemotherapy].

The renal toxicity of antitumoral drugs is an increasingly disturbing problem. These drugs are now prescribed in an ever wider variety of cases, and delayed renal reactions, previously unknown, are revealed by the longer survivals obtained. For a number of years, patients whose cancer had been cured have been placed under haemodialysis on account of drug-induced renal failure. The renal toxicity of cisplatinum, nitrosoureas and methotrexate is well-known, but mitomycin C is also capable of inducing permanent renal failure; the delayed toxicity of this drug explains that it has long been underestimated. This example emphasizes the need for close co-operation between oncologists, nephrologists and pharmacologists in order to determine, for each patient, the most effective treatment with the minimum of side effects.

Antineoplastic Agents↗
PubMed1983

Papillary plasma flow in rats. II. Hormonal control.

Papillary plasma flow (PPF) was measured by the albumin accumulation technique in Wistar rats. PPF was significantly lower in male (293 +/- 5 microliter X min-1 X g-1) than in female (499 +/- 17) rats. Castration in male rats increased PPF; testosterone administration in gonadectomized rats returned PPF to control. Acute indomethacin administration equalized PPF in both sexes to low values close to those found in normal males (320 +/- 5 in males, 326 +/- 17 in females). Conversely, captopril administration equalized PPF in both sexes by raising PPF in males (505 +/- 21) without significant change in females (526 +/- 88). Dehydration decreased PPF slightly in males (255 +/- 28) but more markedly in females (349 +/- 11). This decrease was prevented by captopril administration (520 +/- 34 and 609 +/- 61 in males and females, respectively). In captopril-treated male rats, angiotensin II (AII) was continuously infused by osmotic minipumps at a rate of 5 micrograms/h. This did not restore PPF (405 +/- 12) to basal values. In contrast, AII infusion together with indomethacin administration completely restored PPF (322 +/- 22) in captopril-treated rats whereas indomethacin alone did not normalize PPF (425 +/- 18). We suggest that male sex hormones and AII decrease PPF, and account for the low PPF measured in male rats. Vasodilator PGs are involved in the high PPF found in female rats. The vasodilator action of captopril on papillary circulation is explained by both decreased AII formation and increased PG synthesis.

Angiotensin II↗