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Biomedical subjects

L Potaux

Publications and source records attributed to L Potaux.

At least 37 records · Page 2Linked to original sources

[Prostacyclin in the treatment of hemolytic-uremic syndrome: apropos of a case].

A 52 year-old man was hospitalised for acute renal failure with thrombocytopenia and hemolytic anemia without oliguria. A haemolytic-uremic syndrome was diagnosed and prostacyclin infusion was started. Twenty-four hours later, the renal function improved as well as thrombocytopenia and anemia. Recovery occurred after 11 days of treatment. Haemolytic-uremic syndrome treatment is not well codified: plasmaphoresis, fresh frozen plasma, transfusions showed inconstant efficiency and data about prostacycline treatment are rare and often contradictory. Multicentric studies must be started in order to determine the precise benefit of this treatment.

Epoprostenol↗

Improvement in lipid profiles and triglyceride removal in patients on polyamide membrane hemodialysis.

Cardiovascular morbidity and mortality in hemodialyzed patients are increased due to the frequently abnormal lipid metabolism. It has been reported that this abnormal lipid metabolism could be partially corrected by some highly permeable membranes, such as polysulfone or cellulose triacetate. We investigated the influence of 4 months of dialysis with a polyamide membrane upon the course of lipid parameters in 6 patients presenting a hypertriglyceridemia > 2 mmol/l while on bicarbonate dialysis with a cellulose membrane. Lipid parameters improved after 4 months of hemodialysis with a polyamide membrane. Serum triglyceride and cholesterol levels decreased, while HDL cholesterol and HDL levels rose significantly (p < 0.05). Apolipoprotein B decreased significantly (p < 0.05). Following heparin administration, lipoprotein lipase activity improved (p < 0.02), associated with a decrease apolipoprotein C3 (p < 0.05). The fractional clearance rate of triglycerides rose significantly (p < 0.01). The use of highly permeable polyamide membranes results in a significant improvement in lipid disturbances of dialysis patients due to an increased lipoprotein lipase activity, induced perhaps by the removal of circulating inhibitors such as apolipoprotein C3.

Apolipoproteins↗

[Cysto-ileal diversion by Y loop of a compressive pseudocyst after segmental pancreatic transplantation].

We report the case of a young female patient who underwent dual segmentary pancreatic and renal transplantation in May 1990. The immediate post-operative course was marked by the peri pancreatic collections normally noted with this technique. However, a peculiarity was a long-lasting pseudocyst of the grafted tissue which could not be drained externally despite several attempts. This was compressing the splenic vein of the tissue, thereby causing a reflux. Fear of losing tissue functionality led us four and a half years later to perform an internal cysto-ileal derivation on a bowel loop. In this way, normal endocrine function of the pancreatic graft tissue has now been maintained for over a year.

Adult↗

Long-term control of hyperparathyroidism in advanced renal failure by low-phosphorus low-protein diet supplemented with calcium (without changes in plasma calcitriol).

Phosphorus (Pi) retention linked to chronic renal failure (CRF) favors secondary hyperparathyroidism (HPT). Reduction of Pi and protein intake has been shown to prevent the development of HPT in CRF. The aim of the present study was to assess in patients with advanced CRF the long-term effects on phosphate and calcium metabolism of a low-Pi (5-7 mg/kg/day), low-protein (0.4 g/kg/day) diet providing 300 mg/day calcium (Ca) and supplemented with amino acids and ketoacids, Ca carbonate (400-800 mg/day) and vitamin D2 (1,000 IU/day). Twenty-nine patients with advanced CRF (glomerular filtration rate (GFR) 13.7 +/- 4.5 ml/min) were selected for the study, on the basis of a follow-up of a least 2 years and a satisfactory compliance to the prescribed diet. At the start of the study, biological evidence of HPT was present with increased plasma PTH concentration (144 +/- 95 pg/ml), increased plasma Pi (1.57 +/- 0.33 mmol/l), an increase in alkaline phosphatase activity and plasma osteocalcin concentration. Plasma PTH concentration was positively correlated with plasma Pi and inversely with plasma Ca concentrations and GFR. Pi and protein restriction induced a significant correction of HPT within 3 months after starting the diet. After 2 years of diet, despite the diminution of GFR (11.1 +/- 3.7 ml/min, p < 0.0001), plasma PTH was still lower than at the start of the diet (88 +/- 57 pg/ml, p < 0.01), as was plasma Pi (1.32 +/- 0.24 mmol/l, p < 0.001), total plasma Ca being higher (p < 0.01). Plasma PTH levels were correlated only to plasma Ca concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Correction of chronic metabolic acidosis in haemodialysed patients by acetate-free biofiltration does not influence parathyroid function.

In eight patients remaining acidotic after more than 1 year of bicarbonate haemodialysis, we studied the effect of correcting the chronic metabolic acidosis using acetate-free biofiltration for 4 months on the course of secondary hyperparathyroidism. An AN69 capillary membrane was employed with a bicarbonate infusion rate initially set at 1.8 l/h in all patients and then adjusted in each one to obtain a predialysis bicarbonate of > or = 23 mmol/l. Standard blood chemistry parameters were determined every 2 weeks. Measurements of PTH, calcifediol and calcitriol, as well as calcium-PTH curves were determined at the beginning and end of the study. While acetate-free biofiltration appears to be an adequate technique for the correction of chronic metabolic acidosis when bicarbonate dialysis fails, this study indicates that it does not influence secondary hyperparathyroidism in haemodialysed patients. The level of intact PTH did not vary significantly and the calcium-PTH curves at 0 and 4 months were superimposable with no significant differences in the set point and the slope of the curves.

Acidosis↗

One-year enzyme-linked immunosorbent assay follow-up of human interleukin for Da cells/leukemia inhibitory factor in blood and urine of 22 kidney transplant recipients.

The cytokine human interleukin for Da cells/leukemia inhibitory factor (HILDA/LIF) exerts multiple biological effects in vitro. In mice, high circulating levels of HILDA/LIF induce a wide range of pathophysiological events, some of them closely involved with immunological and inflammatory responses. Using a sandwich ELISA recognizing the natural human HILDA/LIF molecule with a threshold of 50 pg/ml in urine and 150 pg/ml in plasma, we monitored the urine and plasma HILDA/LIF levels of 22 patients in their first year after a kidney transplant. HILDA/LIF urine excretion is increased during acute rejection, and infections also trigger heavy HILDA/LIF plasma concentrations or urine excretion. In addition, this study raises the question of HILDA/LIF involvement in post-kidney-transplant phenomena such as hypercalcemia, osteoporosis, or the reversal of anemia.

Adolescent↗

Granulocyte activation and adhesion molecules during hemodialysis with cuprophane and a high-flux biocompatible membrane.

Hemodialysis with complement-activating membranes, such as cuprophane, induces neutropenia and expression of the granulocyte adhesion receptor Mac-1 (CD11b/CD18), while hemodialysis with noncomplement-activating membranes does not. Increased expression of CD11b by neutrophils may mediate cuprophane-induced leukopenia. However, the rebound granulocytosis that follows leukopenia is not fully understood. Ten patients on regular hemodialysis were included in a cross-over study. Hemodialysis was performed for 2 weeks with cuprophane and 2 weeks with polyamide, a high-flux noncomplement-activating membrane. At the end of each period, the following parameters were determined during a hemodialysis session: C5a concentration by enzyme immunoassay and the neutrophil expression of CD11b, LFA-1 (CD11a/CD18), and the antigen recognized by MoF11 (MoF11 Ag), a monoclonal antibody that recognizes activated neutrophils, by immunofluorescence flow cytometry. Hemodialysis with cuprophane induced an increase in C5a concentration and in the expression of CD11b and MoF11 Ag, which were maximal after 15 minutes of hemodialysis, at the nadir of neutropenia. CD11b expression was maintained throughout hemodialysis, despite the reversal of neutropenia. Conversely, after peak expression, C5a and MoF11 Ag decreased as the neutrophil count increased to baseline values. Polyamide hemodialysis did not induce variations in C5a concentration, nor in CD11b and MoF11 Ag expression. CD11a/CD18 expression remained stable during hemodialysis with both membrane types. Neutrophil activation, as determined by MoF11 Ag expression, was correlated with the evolution of neutrophil count and C5a concentration during cuprophane hemodialysis, while CD11b expression was not correlated with neutrophil count throughout dialysis. A decrease in neutrophil activation could explain in part the detachment of neutrophils previously bound to endothelium and, therefore, the reversal of neutropenia.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Protective effect of verapamil in cyclosporin-incubated human and murine isolated glomeruli.

Cyclosporin A (CsA)-induced nephrotoxicity is characterized by a decrease in the glomerular filtration rate (GFR) which is associated with a large increase in renal vascular resistance (RVR). Using a video image analyzer, we have demonstrated CsA-induced glomerular vasoconstriction in rat isolated glomeruli as assessed by a significant reduction of glomerular area. This vasoactive response explains in part the renal hemodynamic changes and the development of CsA-induced reversible decline in renal function. To confirm the direct vasoactive effect of CsA on glomeruli and to determine if calcium-blocking agents modified this response, we compared the changes in area of isolated rat and human glomeruli incubated either with CsA alone or with CsA plus verapamil. The area of the isolated glomeruli was quantitatively evaluated by a camera video image analyzer; each glomerulus served as its own control. Area kinetics were studied at 5 min intervals over 30 min. CsA-induced glomerular size reduction is dose dependent (-4.2% for 10(-10) M and -10.2% for 10(-6) M) and time dependent (-2.3% at 5 min, -4.7% at 10 min, and -12.1% at 30 min for 10(-6) M). With verapamil pretreatment, CsA-induced reduction in glomerular size was reduced (-0.6% and -3.6%, respectively, for 10(-6) M and 10(-7) M verapamil). Thus, verapamil can be considered as a protective agent against CsA-induced vasoconstriction in rat and human isolated glomeruli.

Adult↗

Effect of cyclosporin and the prostacyclin analogue iloprost on human glomerular vasoreactivity.

Cyclosporin is known to cause a decrease in renal blood flow and glomerular filtration rate in both humans and animals. These acute modifications are reversible if the drug is withdrawn, and seem to be caused by a local hormonal imbalance between vasoconstricting and vasodilating substances. We studied human glomeruli incubated with either CsA alone, iloprost alone, or CsA + iloprost. Photomicrographs of glomeruli were taken at t0, t1, t2 and t5 min and glomerular areas were measured with a videoanalyser linked to a computer. Results show a significant vasoconstriction with CsA alone, and no significant modification of glomerular areas with iloprost or CsA + iloprost. We conclude that iloprost prevents CsA-induced vasoconstriction in human glomeruli in vitro.

Cyclosporine↗

[Comparison of different monitoring techniques for vascular access in chronic hemodialysis].

Aim of the study was to compare different techniques of monitoring for vascular accesses in our chronic hemodialysis patients. Twenty seven patients (14 men, 13 women) were investigated. The accesses studied consisted of 19 arteriovenous fistulas and 8 vascular protheses. Twenty-four were trouble free, venous pressure was high in two, one was difficult to puncture. Three measurements of recirculation percentage were made for each patient, as well as a color Doppler flow imaging, and a digital angiography of the access. Recirculation measurements were normal for all patients including those with functional abnormalities. A stenosis was found 9 times with the Doppler and 10 times by angiography, there being disagreement between the two techniques in one case. The location of the stenosis was the same in the 9 concordant cases. There was a very strong correlation between the degree of stenosis found using the two techniques (p < 0.0001). In conclusion, measurement of recirculation appears to us to be of no interest for verifying a vascular access. On the other hand, the color Doppler seems to be an excellent choice for detecting an abnormality. An arteriographic confirmation seems necessary before correction.

Adolescent↗

Detection of single cells secreting IFN-gamma, IL-6, and IL-10 in irreversibly rejected human kidney allografts, and their modulation by IL-2 and IL-4.

The frequency of isolated low-density graft-infiltrating cells (GIC) secreting IFN-gamma, IL-6, and IL-10 was studied in 8 cases of irreversible rejection of human renal allografts, using ELISA and SPOT-forming cells (ELISPOT) assays. The GIC were mostly CD8+ T cells, although CD4+ T cells, B cells, and macrophages could also be detected. On the average, in 10(6) cells, 189 secreted IFN-gamma, 747 IL-10, and 17114 IL-6. Culture of GIC in the presence of IL-2 resulted in an increase in the frequency of IFN-gamma-producing cells (IFN-gamma-PC), in a dose-dependent manner, with an optimal 6.5-fold increase at 50 U/ml. In contrast, 25 U/ml IL-4 decreased the frequency of spontaneous and IL-2-induced IFN-gamma-PC by 71.3% and 52.8%, respectively. Furthermore, IL-4 reduced the frequency of IL-6-PC (56.8%). By this new approach to graft rejection, it becomes easier to determine cytokine profiles within an allograft and to study their modulation by different agents. It could be a useful model of study for the development of new treatment.

Adjuvants, Immunologic↗

Tumor necrosis factor alpha in human kidney transplant rejection--analysis by in situ hybridization.

Macrophagic infiltration and necrosis of rejected kidney transplants represent two pejorative patterns. It has been assumed that the macrophagic toxicity is mediated partly by secretion of tumor necrosis factor alpha. On the other hand, TNF is also involved in many inflammatory and immunological phenomena. We thus evaluated the expression of TNF mRNA by in situ hybridization in 6 rejected kidney transplants using a radiolabeled TNF-c DNA probe. Then the synthesis of TNF alpha protein was studied by immunohistochemistry using an anti-TNF alpha antibody. In severely rejected kidney grafts, TNF mRNA is expressed in some monomorphic infiltrating cells, mostly located in the deepest part of the cortex and around the tubes. These cells do not bind other probes, such as dopa-decarboxylase DNA or preproenkephalin RNA. They are also recognized by a monoclonal antibody directed against TNF alpha. What is more, this antibody binds with some glomerular endothelial and tubular epithelial cells that do not express TNF mRNA. These cells are likely target cells for TNF. In the normal kidney, there are no cells expressing TNF-alpha mRNA.

Gene Expression↗