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H Beaufils

Publications and source records attributed to H Beaufils.

120 records · Page 7Linked to original sources
PubMedDate not supplied

Behcet's syndrome and renal involvement: a histological and immunofluorescent study of eleven renal biopsies.

The finding of focal glomerulonephritis in a patient with Behcet's syndrome led us to perform systematic renal biopsies in ten other patients with the disease. None of the patients had symptoms of renal disease. Proteinuria was found in five, two of whom had associated leukocyturia. By light microscopy mesangial and extramembranous glomerular deposits were observed in eight patients. Arterioles in ten patients showed subendothelial and medial hyaline deposits. A granular pattern of fluorescent staining identified the presence of the third component of complement in these deposits. Circulating immune deposits were sought and found in six out of seven patients. The finding of circulating immune complexes and deposition of complement in glomerular and arteriolar tissues supports an immune complex mediated nephropathy and is consistent with the hypothesis of an immunological pathogenesis in Behcet's syndrome.

Adult↗
PubMedDate not supplied

Hemolytic and uremic syndrome after heart transplantation.

Two cases of hemolytic and uremic syndrome in heart transplant recipients are reported. Among solid organ transplantations, this complication mainly occurred in renal transplantation and only 1 case was reported in heart transplantation in the literature. Cyclosporine was the only etiologic factor found. The renal outcome was severe with end-stage renal failure and no recovery of the renal function despite stopping cyclosporine, corticoids and plasma exchange.

Adult↗
PubMedDate not supplied

Sodium restriction decreases AP-1 activation after nephron reduction in the rat: role in the progression of renal lesions.

Renal hyperplasia and hypertrophy are early events after nephron reduction which precede progressive destruction of the remnant kidney. Restriction of dietary sodium content was shown to reduce renal lesions following nephron reduction. AP-1 is a transcription factor, resulting from heterodimerization of fos and jun proteins, which mediates the effects of mitogenic growth factors. To elucidate the role of AP-1 in growth processes involved in renal deterioration, we evaluated whether restriction of dietary sodium content (0.25 vs. 0.50% sodium w/w) affected AP-1-DNA binding and hyperplasia in the remnant kidney after nephron reduction (70% nephrectomy). Cell proliferation, evaluated by PCNA immunostaining, increased progressively from day 7 to day 60 in glomeruli, proximal and distal tubules and loops of Henle of nephrectomized (Nx) rats compared to control sham-operated (C) animals. AP-1-DNA binding activity increased 7 and 14 days after surgery, but it was reduced below C values at day 60. c-fos and c-jun expression were also reduced in Nx rats at day 60. Sodium restriction significantly reduced the number of PCNA-stained cells in glomeruli and tubules at days 14 and 60, but not at day 7, whereas it decreased AP-1 activation at all times of the study. This effect was associated to a marked reduction of renal lesions in Nx rats. In conclusion, we showed that, after nephron reduction, the beneficial effect of sodium restriction was associated with a reduction of hyperplasia and AP-1 activation, but that the latter did not parallel delayed cell proliferation rate in remaining nephrons. Thus, we propose that different transduction pathways are involved in cell proliferation after nephron reduction, according to the time of evolution of renal lesions.

Animals↗
PubMedDate not supplied

Morphology of cyclosporine nephrotoxicity in human heart transplant recipients.

The morphologic findings of renal biopsies (four cases studied by electron microscopy) and renal specimens obtained from 44 autopsies of patients who died after heart transplantation are reviewed. Eight patients treated postoperatively with cyclosporine (serum concentration of 100 to 150 ng/ml), with a survival rate of 1 to 24 months, constantly had renal lesions of variable severity. Correlated with functional renal disturbances, these changes predominantly affect the proximal convoluted tubule: vacuolization, calcifications, and tubular atrophy. The interstitial fibrosis, increasing parallel to tubular alterations, occurs only after 3 months after transplantation. The hypertrophy of juxtaglomerular apparatus and the arteriolar sclerosis noted on and after the fourth month were associated with arterial hypertension. Among the other inconstant and mild lesions (attrition of vascular endothelium and arteriolar or glomerular thrombi), the partial sclerosis of glomerular flocculus, probably correlated with tubular lesions, seems more significant. Thus these findings corroborate the nephrotoxicity of cyclosporine (principally against the proximal convoluted tube), the increase of lesions with time, and the possible irreversibility of the lesions despite appropriately decreasing the dosage of cyclosporine to eliminate toxic side effects.

Acute Kidney Injury↗
PubMedDate not supplied

Renal function and blood pressure in heart transplant recipients treated with cyclosporine.

Cyclosporine, a cyclic endecapeptide of fungal origin, has been used for nine years in clinical transplantation to suppress allograft rejection. Nephrotoxicity represents the most frequent and severe complication associated with its use and may ultimately define the limits of its utility as a drug for long term immunosuppression. However, this nephrotoxicity cannot be truly assessed in kidney transplant recipients for obvious reasons. It has recently been reported in heart transplant recipients. In addition, cyclosporine therapy is responsible for a persistent elevation of blood pressure requiring intensive and combined anti-hypertensive regimens. This hypertension develops within the first weeks post-transplantation in 60% to 90% of heart allograft recipients. This study analyzes the renal function and blood pressure of patients operated on in our department where cyclosporine was introduced in 1981.

Actuarial Analysis↗
PubMedDate not supplied

Malignant hypertension in antiphospholipid syndrome without overt lupus nephritis.

The antiphospholipid syndrome is usually defined by the association of a clinical manifestation (recurrent venous and/or arterial thrombosis, recurrent spontaneous miscarriages) and a biological abnormality (anticardiolipin antibody, lupus anticoagulant). We retrospectively analyzed the records of 5 patients (4 females, 1 male, aged 30 +/- 12 years) with antiphospholipid syndrome, primary (n = 1) or secondary to systemic lupus erythematosus (n = 4), who developed malignant systemic hypertension with renal insufficiency, in the absence of lupus nephritis. Before the episode of malignant hypertension, all patients had normal systemic blood pressure and renal function. During malignant hypertension the systolic pressure was 206 +/- 39 mmHg and the diastolic pressure 130 +/- 25 mmHg, peak serum creatinine was 204 +/- 95 mumol/l, daily proteinuria was 1.1 +/- 0.8 gr, and complement serum levels were normal in all patients. Renal angiography found normal proximal renal arteries. Renal biopsy showed ischaemic glomeruli without proliferative lesions (n = 5), focal intimal fibrosis either isolated (n = 3) or associated with thrombosis (n = 2) of the intrarenal vessels, and the absence of vasculitis. Immunofluorescence study did not reveal typical lupus deposits. Patients were treated with antihypertensive agents, increasing doses of prednisone (n = 3), and anticoagulant (n = 2) or anti-aggregant therapy (n = 1). After a mean follow-up of 6.8 +/- 5.2 years, 4 patients were still alive with normal blood pressure and renal function, whereas 1 patient died of a probable catastrophic antiphospholipid syndrome. Patients with antiphospholipid syndrome, primary or secondary to systemic lupus erythematosus, may develop malignant hypertension with renal insufficiency and intrarenal vascular lesions, in the absence of lupus nephritis.

Adolescent↗
PubMedDate not supplied

[Reversible nephrotic syndrome in Crohn's disease complicated with renal amyloidosis].

A 24-year-old woman suffered from ano-rectal Crohn's disease and nephrotic syndrome due to glomerular amyloidosis AA. She received azathioprine and colchicine for two years. Both Crohn's disease and nephrotic syndrome resolved. However amyloid renal lesions were still present. This course is exceptional, and leads to a discussion of the treatment of amyloidosis associated with Crohn's disease.

Adult↗