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J Bariéty

Publications and source records attributed to J Bariéty.

At least 19 recordsLinked to original sources
PubMed1995

Role of endothelin in acute renal failure due to rhabdomyolysis in rats.

Rhabdomyolysis and other causes of massive myoglobin release are often complicated by an acute ischemic renal failure. We tested the hypothesis that endothelin-1, the most potent renal vasoconstrictor known, plays a role in the renal toxicity of myoglobin. For this purpose, we induced rhabdomyolysis (8 ml/kg i.m. of a 50% glycerol solution) in rats pretreated or not pretreated with bosentan, a novel potent nonpeptide endothelin receptor antagonist. Glycerol decreased renal function dramatically, increased proteinuria and induced a massive tubular necrosis. This effect was associated with a 22% increase in plasma endothelin concentration. Bosentan prevented the decrease in creatinine clearance (1.12 +/- 0.07 ml/min vs. 0.83 +/- 0.05 ml/min, P < .01), the increase in proteinuria (19.9 mg/24 hr vs. 31.8 mg/24 hr, P < .001) and the tubular necrosis induced by glycerol (as assessed by histopathological evaluation), without affecting myoglobinuria. Involvement of endothelin was further suggested by the observation that myoglobin could markedly increase endothelin-1 release by rat mesangial cells in culture. We conclude that endothelin is, at least in part, responsible for the massive tubular necrosis observed in myoglobinuric nephropathy.

Acute Kidney Injury↗
PubMed1994

[Renal involvements in human immunodeficiency virus infection].

Two main types of renal disorder may affect the HIV-infected patients. The first type characterized by acute renal failure is not related directly to HIV infection, but results from complications secondary to diagnosis and therapeutic intervention in patients with severe immunodepression. The second type of renal complication includes three quite specific histological renal patterns. The typical "HIV-associated nephropathy" (HIVN), involves essentially the black population, both in Europe (84%) and in North America (83%) and could represent a pathogen-induced disease occurring on a specific genetic background. The two other types of nephropathy, i.e. immune complex-type glomerulonephritis and tubulointerstitial nephritis, involve both black and white seropositive populations and might be the consequence of dysregulation of the immune system.

AIDS-Associated Nephropathy↗
PubMed1994

Preeclampsia associated focal and segmental glomerulosclerosis and glomerular hypertrophy: a morphometric analysis.

Renal biopsies from hypertensive pregnant women performed 8 to 10 days postpartum were processed by morphometric analysis. We allocated the 74 patients into four groups according to the respective forms of pregnancy hypertension, i.e. preeclampsia and gestational hypertension. Groups I and II included preeclamptic women, with (group I) or without (group II) de novo FSGS. Groups III and IV included biopsies of women with isolated gestational hypertension, appeared during the third trimester (group III) or earlier (group IV). The control group included 17 biopsies from age-matched nonpregnant women presenting with isolated hematuria. Glomerular lesions of typical preeclampsia were seen in all the biopsies of groups I and II, and in some of women with gestational hypertension of groups III and IV. Our morphometric analysis of these renal biopsies showed a progressive increase in glomerular size from early gestational hypertension, gestational hypertension of the 3rd trimester, isolated preeclampsia, and finally preeclamptic nephropathy associated with FSGS. The largest glomeruli were seen in preeclamptic women with severe hypertension and histologic lesions of preeclampsia with FSGS. Thus, both systemic hypertension and glomerular hypertrophy seem necessary to induce FSGS in this type of pathology.

Adult↗
PubMed1994

Colocalization of myocardial fibrosis and inflammatory cells in rats.

BACKGROUND: Left ventricular overload and aging lead to an increase in fibrosis in the rat cardiac interstitium. The relationship between fibrosis, fibroblast activity, and inflammatory cell infiltration, was explored in spontaneously hypertensive rats (SHR) and Wistar controls. EXPERIMENTAL DESIGN: The left ventricle of three groups of eight SHR and eight Wistar controls hearts were sectioned for light microscopy, immunohistochemistry, and in situ hybridization with a cDNA probe encoding the murine alpha 1 chain of type I collagen. Fibrosis was measured morphometrically. Monoclonal antibodies directed against Ia antigen, CD8+ cytotoxic, CD4+ helper lymphocytes and monocyte/macrophages were used to localize and quantify the inflammatory cells. RESULTS: In 2-month-old rats, with nearly normal interstitial cardiac tissue, fibroblasts expressing collagen mRNA were located around coronary vessels. The areas of fibrosis and interstitial cellular infiltration were more extensive in 22-month-old rats than in 12-month-old rats and greater in SHR than in Wistar. Fibroblasts expressing collagen mRNA were mainly found at the border between fibrosis and myocytic cells, and were always colocalized with lymphocytes and macrophages. The interstitial areas of fibrosis and collagen I expressing fibroblasts had the same pattern of infiltrating cells in normotensive rats than in SHR. Fibrosis and the density of macrophages and CD4+ lymphocytes were correlated. CONCLUSIONS: Thus, fibroblast activity could be closely related to the presence of lymphocytes and macrophages in the myocardium of spontaneously hypertensive and aged rats.

Aging↗
PubMed1994

[The transplanted kidney. Role of imaging in early non-functioning grafts].

Renal failure following transplantation can be classified in two groups: initial non function characterized by the absence of renal function after transplantation and delayed secondary non function after an initial improvement. In the first group, the most frequent etiology is an acute tubular necrosis (30 to 50% of the cases) which usually heals within three weeks. Arterial thrombosis are rare but of very bad prognosis. In the second group, the most frequent cases are acute rejection, urological complications, renal artery stenosis, urinary infections and cyclosporine, intoxication. Diagnostic imaging, and especially the color Doppler flow, is very effective in obtaining diagnosis. Vascular or urological complications are to be confirmed by contrasted opacifications. In the absence of vascular or urological obstruction renal failure must be related to a renal parenchymal disease. This may be acute tubular necrosis, a rejection, a pyelonephritis or a medicinal intoxication depending on clinical symptoms, the time of their apparition and the results of biological examinations.

Acute Kidney Injury↗
PubMed1991

[Extramembranous glomerulopathies].

Membranous nephropathy is defined by the presence of immune deposits localized on the epithelial side of the glomerular basal membrane. Its mechanism has been elucidated through numerous experimental models and is thought to be the consequence of in situ formation of immune complexes. Membranous nephropathy is clinically discovered by a nephrotic syndrome of unknown long-term evolution: 25% of the patients undergo complete spontaneous remission and 20% show progressive renal failure. As of today, no prognostic criteria are available. Numerous studies using steroids, immunosuppressive agents, or a combination of both, have tried to modify the natural history of the disease, but none of these protocols clearly seem to have changed the course of the disease.

Adrenal Cortex Hormones↗
PubMed1991

The influence of age on renal prostaglandin synthesis in man.

The purpose of our study was to determine influence of age on renal prostaglandin (PG) synthesis in man. Urinary prostaglandins 6-Keto-PGF1 alpha, TxB2, PGE2 and PGF2 alpha were measured in 45 normotensive subjects aged from 20-95 years. Urinary 6-Keto-PGF1 alpha excretion, reflecting mainly renal cortical prostacyclin synthesis, decreased significantly with age, while urinary TxB2 showed the opposite development. The ratio of urinary 6-Keto-PGF1 alpha/TxB2 decreased with age. PGE2 excretion was preserved in old subjects probably because the age-dependent decrease in renal function concerns mainly the cortex and spares the medulla. PGF2 alpha synthesis was least influenced by age. This age-dependent decrease in renal prostacyclin synthesis may play a role in the renal alterations of the elderly.

Adult↗
PubMed1987

Bartter's syndrome with normal chloride reabsorption during indomethacin treatment.

A 17-year-old male patient with Bartter's syndrome was admitted for renal function studies. This patient had persistent hypokalemia, first found at age 5; the diagnosis of Bartter's syndrome with renal hypersecretion of prostaglandins E2 and F2 alpha had been established at age 13. A congenital defect of chloride reabsorption was expected, but after 4 years of indomethacin treatment no such defect was found. Withdrawal of indomethacin for 1 week resulted in profound hypokalemia and the appearance of a chloride reabsorption defect, with an excessive urinary PGE2 and PGF2 alpha excretion, and a parallel decrease in plasma prostaglandin precursors. The cause of Bartter's syndrome in this patient seems to be renal hyperprostaglandinism.

Adolescent↗
PubMed1985

[A very unusual case of amyloidosis].

This case report describes a patient with IgG lambda myeloma and vascular amyloidosis. Remarkable is the presence of mesangial granular deposits revealed by electron microscopy and positive with anti-IgG and anti-kappa anti-serum in an immunofluorescence study. Granular dense deposits were also found at the inner side of the basement membrane of the skin and were positive with anti-kappa anti-serum in immunofluorescence study. Because no L kappa q light chain proliferation could be demonstrated, the nature and significance of these kappa deposits are not clear.

Amyloidosis↗
PubMed1984

[Changes in plasma prostaglandins in normal subjects in an orthostatic position. Comparison with the response of the renin-aldosterone system].

Changes in blood pressure, plasma concentrations of PGE2, PGF2 alpha, G-keto-PGF1 alpha, thromboxane B2, aldosterone and plasma renin activity were evaluated in 13 normotensive subjects passing from supine to upright position. Orthostatism resulted in slight elevation of blood pressure and increase of all plasma prostaglandins (except PGE2), plasma aldosterone and plasma renin activity. A positive correlation was found in supine position between systolic arterial pressure and thromboxane B2 level (p less than 0.001). In upright position, however, blood pressure did not correlate with any of the hormones assayed. Orthostatism is a powerful stimulant of renin and aldosterone secretion but not so much of prostaglandin secretion. Basal arterial pressure is significantly influenced by thromboxane A2.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

[Anuria caused by perianeurysmal retroperitoneal fibrosis. Medical treatment. A case report].

After 3 sessions of haemodialysis, renal function returned to normal, but the bilateral ureteral obstruction recurred 11 months later with signs of compression of the inferior vena cava. Corticosteroid therapy in doses of 0.5 mg/kg/day resulted in disappearance of the pyeloureteral dilatation at intravenous urography and regression of the fibrosis on CT sections. From a review of the literature the authors describe the clinical symptoms, diagnostic methods and main treatments of perianeurysmal retroperitoneal fibrosis, a not uncommon disease.

Aged↗
PubMed1983

Thromboxane B2 in borderline and essential hypertensive patients.

Thromboxane B2 (TxB2) was measured in the venous and arterial plasma and in the urine of 15 borderline and 15 sustained essential hypertensive patients, and in the plasma and urine of 12 control normotensive age-matched subjects. Plasma and urine thromboxane B2 were significantly higher in both the borderline and sustained hypertensives than in the control normotensives. There was a significant positive correlation between urinary (i.e. renal)TxB2 excretion and the glomerular filtration rate, and between urinary TxB2 excretion and sodium excretion in the hypertensive but not in the normotensive subjects. Thromboxane A2 participates in pressure natriuresis.

Adolescent↗
PubMed1982

[Urinary thromboxane B2 in hypertensive patients].

UNLABELLED: Thromboxane A2 (TxA2) is a vasoconstrictor synthetized by the kidney. Its role in hypertension is unknown. We measured urinary TxB2 (the metabolite of renal TxA2) by radioimmunoassay and studied renal functions in 15 borderline, 15 sustained essential hypertensive patients and 12 age-matched normotensive subjects (6 young and 6 older adults). Results were as follows: Normotensive subjects: Mean arterial blood pressure (MBP) 97 +/- 2 mmHg, urinary TxB2 (UTxB2V) 159 +/- 12 pg/min, glomerular filtration rate (GFR) 120 +/- 8 ml/min, sodium excretion (UNaV) 73 +/- 9 mueq/min. Hypertensive patients: MBP 115 +/- 2 mmHg (p less than 0,001 vs controls), UTxB2V 298 +/- 24 pg/min (p less than 0,005), GFR 128 +/- 6 ml/min, UNaV 51 +/- 4 mueq/min (p less than 0.02). There was a positive significant correlation between UTxB2V and GFR (p less than 0,005) and between UTxB2V and UNaV (p less than 0,005) in hypertensive but not in normotensive subjects. There was no correlation between GFR and UNaV in either group. CONCLUSION: 1. Urinary (i.e. renal) TxB2 is significantly elevated in hypertensive patients; 2. TxA2 may be a mediator of pressure natriuresis.

Adolescent↗
PubMed1980

Distribution of blood group antigen A in normal and pathologic human kidneys.

We tested this distribution with an indirect immunofluorescent technique using purified rabbit anti-A antiserum on 21 whole normal kidneys (a group, N equal to 18; AB group, N equal to 1; O group, N equal to 2) and on 349 kidney biopsy samples (A group, N equal to 140; AB group, N equal to 14; O or B group, N equal to 195) representing a large spectrum of renal diseases. In normal kidneys from A and AB groups, the A antigen was detected in the whole vascular endothelium and in the convoluted distal tubules. In secretors, collecting tubules were brightly positive. Epithelial staining was more diffuse in the inner part than it was in the outer part of the medulla. The basement membrane of the inner collecting tubules was positive in frozen sections but not in paraffin sections. In pathologic kidneys, modifications were obvious: (1) The thickened basement membrane of atrophic convoluted distal tubules was brightly stained. (2) Endothelial staining allowed a precise appreciation of the glomerular and interstitial vasculature. (3) In proliferative changes such as arterial intimal proliferation, proliferative glomerulonephritis, and interstitial cell infiltration, endothelial cells do not proliferate. This routine staining technique of endothelial cells by anti-A antiserum provide information not obtainable with light microscopy.

ABO Blood-Group System↗