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Biomedical subjects

B Mougenot

Publications and source records attributed to B Mougenot.

At least 73 records · Page 4Linked to original sources
PubMed1986

[Rapidly progressing glomerulonephritis with mesangial IgA deposits in sarcoidosis].

This report concerns a patient with sarcoidosis who developed acute renal failure due to rapidly progressive glomerulonephritis. Renal biopsy revealed severe endo and extracapillary proliferation with diffuse mesangial deposits of IgA, C3 and beta 1-H on immunofluorescence. The possibility of a common immunopathogenic pathway between sarcoidosis and IgA nephritis is briefly discussed.

Adult↗
PubMed1985

[AA amylosis and the nephrotic syndrome complicating a pulmonary epidermoid carcinoma].

A 59 year-old male developed the nephrotic syndrome in the course of squamous-cell lung carcinoma with metastases. Renal biopsy disclosed amyloid deposits. Immunofluorescence was positive with an anti-SAA antiserum. Amyloidosis complicates exceptionally lung tumors, despite extremely high serum levels of SAA in this type of malignancy. This infrequency shows that determinants other than high SAA serum levels are necessary to create tissue amyloid deposits.

Adrenal Gland Neoplasms↗
PubMed1984

Renal failure in myeloma: relationship with isoelectric point of immunoglobulin light chains.

Renal failure is a frequent but inconstant complication of myeloma related to light chain excretion. Since it has been suggested that cationic light chains (lc) are most likely to induce renal damage, we have studied the isoelectric point (pI) of light chains produced by 17 patients with myeloma and related the results to the type and severity of renal damage assessed clinically and pathologically. In order to do so, we have applied immunoenzymatic techniques which allow identification of light chain types as well as measurement of pI without prior purification. Ten of fifteen patients with renal failure produced lambda light chains. There was no simple relationship between the isoelectric point and nephrotoxicity. However, light chains with the lowest pI observed in this series were associated with normal renal function in two cases and with acute reversible but severe renal failure requiring dialysis in five cases. By contrast, pI values above 6.0 observed in the remaining patients were associated with moderate renal failure in six patients with recently diagnosed myeloma and with irreversible renal failure, and in two patients in whom myeloma had been evolutive for several years. We thus suggest that further pI measurements may help to identify light chains with different nephrotoxic potentials.

Acute Kidney Injury↗
PubMed1984

[Renal involvement in scleroderma].

Renal biopsies were carried out in 29 patients with scleroderma to study the early vascular lesions and their eventual clinical significance. Haemolytic acute renal failure was present in 9 patients. The biopsies showed early vascular lesions on interlobar arteries. The main biological change was proliferative or fibrous endarteritis. Mucoid infiltration was found in 3 biopsies. The arterioles were spared or only slightly affected without major fibrinoid necrosis. These lesions were therefore distinct from those of malignant hypertension. However, at autopsy of 2 of these cases, the vascular lesions were undistinguishable from those of malignant hypertension. The biopsies in 13 out of 14 patients with scleroderma without obvious renal involvement (9 cases) or with moderate proteinuria and/or hypertension without renal failure (5 cases) showed interlobar endarteritis with associated mucoid infiltration in 3 patients. This lesion was isolated but sometimes extensive even in young patients without hypertension. One patient died within one year, of disseminated colonic carcinoma, and 4 of cardio-respiratory failure due to scleroderma without hypertension, renal failure or proteinuria. Eight of the 9 remaining patients were traced 6 to 16 years after biopsy. Two were moderately hypertensive but none had renal failure. Cutaneous and internal organ scleroderma had regressed in the majority and proteinuria had disappeared in 3 cases.

Acute Kidney Injury↗
PubMed1984

Familial idiopathic membranous glomerulonephritis.

2 brothers with identical HLA antigens presented an idiopathic membranous glomerulonephritis. This is, to our knowledge, the first report of familial membranous glomerulonephritis. The fact that both brothers had identical HLA antigens suggests a genetic predisposing background.

Adolescent↗
PubMed1984

[Hypocomplementemic urticarial vasculitis with glomerulopathy and renal venulitis].

A 58 year-old woman had atypical chronic urticaria, arthralgias and abdominal pain. Attacks of angioneurotic edema occurred. Proteinuria was discovered. She had clinical and biological signs of inflammation, leukoneutropenia , antileukocyte antibodies and low CH 50, C1q and C4 levels without functional C1 esterase deficiency. C1q precipitins were not detectable. Skin biopsy disclosed angiitis and by immunofluorescence a lupus band test was positive. Serologic investigations in search of SLE were negative. Renal biopsy showed mesangial deposits, capillary loop thickening and mesangial fixation of anti-IgG, C3 C1q and C4 antisera. In the interstitium, voluminous perivenular inflammatory infiltrates were visible. With corticosteroid treatment clinical manifestations subsided and proteinuria disappeared. This observation of McDuffie 's angiitis with renal venulitis leads to a review of the literature with discussion of the mechanisms of hypocomplementemia.

Biopsy↗
PubMed1978

[Renal atrophy in a child].

An acquired small kidney in a girl of 10 is reported. Interstitial pyelonephritis was the main cause for the shrinkage of the kidney, but very localised areas of renal dysplasia have also been found in this kidney, which happened to be completely destroyed in 34 months. In this meanwhile, the child had recurrent febrile urinary tract infections (clinically acute pyelonephritis). No malformation of the lower urinary tract was found in this child.

Atrophy↗
PubMedDate not supplied

Plasma cell dyscrasia-related glomerulopathies and Fanconi's syndrome: a molecular approach.

Considerable advances in the understanding of renal complications of dysglobulinemia have occurred in the last 10 years. They mostly result from sequence studies of nephritogenic immunoglobulin chains and comparison with sequence database, and from a careful analysis of clinicopathological features including electron microscopy characteristics of immunoglobulin deposits. These advances should help define subpopulations of patients with plasma cell dyscrasia at risk of developing renal complications and to design novel therapeutic approaches. Although renal complications of plasma cell dyscrasias may be considered as anecdotal diseases, understanding their pathophysiology may help dissect the mechanisms of glomerular and proteinuria-induced interstitial fibrosis.

Amyloidosis↗