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Biomedical subjects

B Mougenot

Publications and source records attributed to B Mougenot.

At least 55 records · Page 3Linked to original sources
PubMed1992

Nephropathy associated with infection by human immunodeficiency virus: a report on 11 cases including 6 treated with zidovudine.

The human immunodeficiency virus (HIV) was recently suggested to be involved in generating kidney lesions in HIV-associated nephropathy (HIVN). The possibility that antiretroviral agents can slow down the usually explosive evolution of HIVN to end-stage renal failure (ESRF) has not been studied in many of the series of cases published. The present work is a retrospective analysis of 11 patients with histologically proven HIVN, 6 of whom were treated with zidovudine. Seven patients (group 1) either required dialysis at the outset, when HIVN was diagnosed, or progressed very fast to ESRF within 15-45 days. Two patients of this group were treated with zidovudine, but it had no effect on kidney function. In the remaining 4 patients (group 2), HIVN progressed more slowly than in group 1. All 4 patients were treated with zidovudine at an earlier stage of the disease than ESRF. Only 1 deteriorated to ESRF in 9 months. The 3 others, who did not have ESRF, were followed up for 13, 10 and 32 months, respectively. Although this is a preliminary study, its results do suggest that zidovudine can slow down the evolution of HIVN to ESRF. They highlight the need to screen HIV-positive patients regularly for proteinuria, in order to detect HIVN by renal biopsies at an early stage of renal lesion formation.

AIDS-Associated Nephropathy↗
PubMed1992

Association of chronic interstitial cystitis, protein-losing enteropathy and paralytic ileus with seronegative systemic lupus erythematosus: case report and review of the literature.

We report the case of a female patient with seronegative lupus and predominant bladder and intestinal involvement in the form of interstitial cystitis and protein-losing enteropathy. This association is exceptional in the literature but may be underestimated because of frequent latency of interstitial cystitis. It may define a peculiar subgroup of lupus patients usually responsive to steroid therapy. In this case, only cyclophosphamide markedly improved the protein-losing enteropathy but did not influence the bladder disease.

Adult↗
PubMed1991

[Necrotizing extracapillary glomerulonephritis without immunoglobulin deposits. Renal localization of systemic vasculitis with anti-cytoplasm polynuclear antibodies].

Necrotizing and crescentic glomerulonephritis without immunoglobulin deposits (also called pauci-immune glomerulonephritis) is the cause of approximately 50 percent of acute renal failures of glomerular origin. Our study, based on 40 case-records selected on histological criteria, and on data from the literature, shows that in most cases, if not all, this type of glomerulonephritis is part of a wider systemic vasculitis which predominantly affects the glomerular capillaries. Anti-neutrophil cytoplasm antibodies are detected in three-quarters of the cases, with a specific distribution that varies according to the clinical features. In spite of the patients' age (mean: 62 years), the severity of glomerular lesions and the extra-renal diffusion of the disease, 60 percent of these patients can be cured and recover a normal, or at least acceptable renal function, provided the corticosteroid and sometimes immunosuppressive therapy is initiated at an early stage.

Adolescent↗
PubMed1990

[Renal cholesterol embolism. Apropos of 13 cases].

Between January 1981 and April 1988, histologically proven renal cholesterol embolism was diagnosed in 13 men over 60 years of age with a previous history of hypertension and atherosclerosis. Six patients developed acute renal failure, usually induced by a triggering factor such as angiographic procedure or anticoagulation, and associated with peripheral and visceral cholesterol embolism, eosinophilia and a high sedimentation rate. In this group of patients, whose protean clinical manifestations and laboratory data mimicked necrotizing angiitis despite the absence of antineutrophil cytoplasmic antibodies, skin lesion biopsy established the diagnosis and made renal biopsy unnecessary. Six patients had chronic renal failure and elevated sedimentation rate, and the last patient had isolated microhematuria. In these 7 patients, percutaneous renal biopsy was an adequate procedure for the diagnosis of cholesterol embolism. As medical management of cholesterol embolism is essentially preventive, these unusual presentations must be emphasized.

Acute Kidney Injury↗
PubMed1990

Systemic and renal fibrinolytic activity in a patient with anticardiolipin syndrome and renal thrombotic microangiopathy.

A 24-year-old white woman with a past history of recurrent venous thromboses of the lower extremities was admitted for hypertension and renal failure. She had a chronic cutaneous ulcer on the anterior side of the left leg and oral ulcers of the palatum. Laboratory tests demonstrated rapidly progressive renal failure and the presence of an anticardiolipin antibody (ELISA). Thrombosis of the inferior vena cava was shown by phlebocavography. Renal biopsy revealed typical thrombotic microangiopathy. Tissue-type plasminogen activator (tPA) was visualized by immunofluorescence in endothelial cells of renal arterioles and glomeruli. Normal plasma levels of tPA, urokinase and plasminogen activator inhibitor 1 were found by ELISA, and tPA antigen levels rose after desmopressin acetate infusion. Thus, in this case, the diffuse thrombotic process was not related to defective circulating or renal fibrinolytic systems and could be promoted by the procoagulant effect of antiphospholipid antibodies.

Adult↗
PubMed1990

Plasminogen activator inhibitor 1 in renal fibrin deposits of human nephropathies.

The persistency of fibrin deposits in the kidney during renal diseases could reflect either a defective release of plasminogen activators (PA) or a local excess of PAI. In order to investigate this question, we studied human renal biopsies by immunofluorescence technique with specific antibodies for fibrin, tissue-type plasminogen activator (t-PA), urokinase (u-PA), PAI-1 and PAI-2. By this technique t-PA could be detected in the glomerular flocculus and the endothelium of small arteries of the normal control kidneys. We failed to detect significant fluorescence with other antibodies in normal kidneys. Conversely, in cases of vascular nephropathy with thrombosis the positive fluorescence obtained with anti-fibrin antibodies at the site of thrombosis was associated with a positive fluorescence with anti-PAI-1 and to a lesser extent with anti-t-PA antibodies. u-PA and PAI-2 were not detected in these lesions. Similarly in the most severe forms of crescentic glomerulonephritis, extracapillary fibrin deposits were associated with PAI-1. In one case u-PA was also detected. This is in agreement with our previous findings that glomerular epithelial cells release both PAI-1 and the inactive form of u-PA (pro u-PA). Thus, our results support the hypothesis that PAI-1, which is able to inhibit both t-PA and u-PA, may play a major role in the persistency of fibrin deposits in the human kidneys during pathological conditions.

Female↗
PubMed1990

Fibrin deposition and adaptive changes in glomerular procoagulant and fibrinolytic activities in rat renoprival nephropathy.

To investigate the mechanisms which may influence fibrin deposition in the remnant kidney, glomerular morphology and the haemostatic properties of isolated glomeruli were assessed in two groups of rats, 30 days after surgical removal of three-quarters of the total renal parenchyma, and compared to glomeruli in sham-operated controls. One group was given the thromboxane synthetase inhibitor OKY 046 and the other was not. Fibrin deposition occurred in about 20% of glomeruli, of which 4% exhibited segmental necrotizing lesions. Concomitantly, glomerular procoagulant activity dropped to 40% of the control level and glomerular fibrinolytic activity rose to 120-130% of this level. Inhibition of thromboxane synthesis did not affect fibrin deposition, glomerular haemostasis or the development of renal insufficiency. In an additional group of unilaterally nephrectomized rats, procoagulant activity also markedly decreased in the remaining kidney. These results indicate that in the rat remnant kidney, alterations in glomerular haemostatic properties tend to have antithrombotic effects which seem to constitute an adaptive reaction by an autacoid system to glomerular fibrin deposition.

Adaptation, Physiological↗
PubMed1989

Plasma exchange and immunosuppression for rapidly progressive glomerulonephritis: prognosis and complications.

Rapidly progressive glomerulonephritis frequently leads to death or dialysis. In 21 cases treated by plasma exchange and immunosuppression we observed seven deaths, with 12 others progressing to chronic renal failure within 3 months. Patients who died were older than those who survived (57.5 +/- 17.7 vs 40.5 +/- 16.5 years, mean +/- SD, P = 0.05), but had similar clinical symptoms (hypertension, haematuria, proteinuria, extrarenal signs) and biochemical presentation (initial creatininaemia). They required the same degree of haemodialysis, of plasma exchanges and of bolus methylprednisolone. The causes of death were infection (three cases), cardiac arrhythmia (two cases) and gastrointestinal bleeding (two cases). Among the 14 remaining patients, only two recovered normal renal function. Twelve had chronic renal failure, six of them requiring chronic dialysis or transplantation. Severe renal failure at entry and anuria were more frequently observed in patients whose renal function did not improve during treatment. Plasma exchange and steroid bolus infusions also seemed to have a beneficial effect on renal function.

Adult↗
PubMed1989

Tamm-Horsfall protein accumulation in glomeruli during acetazolamide-induced acute renal failure.

A patient with ocular hypertension was treated with acetazolamide. Acute renal failure developed rapidly and renal biopsy showed mild tubular lesions and crystal formation in a tubular lumen. By immunofluorescence studies with a monoclonal antibody, Tamm-Horsfall protein, normally absent from the proximal segments of the nephron, was detected in most glomeruli. This strongly suggests that tubular obstruction plays a major part in some cases of acetazolamide-induced acute renal failure.

Acetazolamide↗
PubMed1988

[Renal disease associated with heroin abuse].

Thirteen patients developed a renal disease after using heroin alone or in combination with other drugs, for a period of 3 to 12 years. Eleven were IV drug addicts, 2 were sniffers. Six patients had acute tubular necrosis, due to rhabdomyolysis in 5 and to prolonged gentamicin therapy for bacterial endocarditis in 1. Five patients manifested a nephrotic syndrome, and renal biopsy showed various types of glomerulonephritis (GN) without glomerular sclerosis. The two last patients had hypertension with intrarenal vascular lesions and HBsAg was present in their serum. Chronic hemodialysis and/or renal transplantation were required in 2 cases with GN; all other patients recovered normal serum creatinine. There was no specific pathologic picture of heroin abuse in this series.

Adult↗
PubMed1987

Multiple myeloma and severe renal failure: a clinicopathologic study of outcome and prognosis in 34 patients.

Renal failure (RF) occurring in the course of multiple myeloma is often judged irreversible and generally considered an ominous complication. The aim of the present study was to re-evaluate the outcome, triggering conditions and prognostic factors of severe RF in a series of 34 patients, 33 to 90 years old. RF was totally reversible in 7 patients and partially reversible in 9 although 6 of them had to be temporarily dialyzed. However, the improvement in renal function was often very slow as indicated by an average recovery time of 115 days. The high rate of RF reversibility was associated with markedly lengthened survival. Review of triggering events confirmed the leading role of dehydration and hypercalcemia, but further suggested that intake of nonsteroidal anti-inflammatory drugs and renal infection might play a part in the development of RF. Systematic statistical analysis of potential prognostic factors showed that the outcome was significantly more severe in females, but age, myeloma characteristics including tumor mass, calcemia, and triggering events had no predictive value. The most reliable prognostic indicators were provided by analysis of kidney biopsy performed in 30 patients. Complete recovery from RF was observed only in the absence of global tubular atrophy and interstitial damage. In contrast, cast-induced tubular obstruction detected by the presence of Tamm-Horsfall protein in urinary space of glomeruli did not seem to influence the outcome of RF. Finally, we analyzed the prognostic value of immunochemical properties of light chains (LC). Lambda LC were unexpectedly detected in 2 of 3 patients, as compared to a ratio of 1 to 3 in the population of normal and monoclonal Ig, but LC type did not correlate with the course of RF. Isoelectric points of LC measured in 32 patients were dispersed from 5.2 to 8.9 and bore only weak prognostic significance. These results underline the value of kidney biopsy and justify aggressive treatment including dialysis and chemotherapy.

Acute Kidney Injury↗
PubMed1987

Piridoxilate-associated nephrocalcinosis: a new form of chronic oxalate nephropathy.

Piridoxilate is an association of glyoxylic acid and pyridoxine in which pyridoxine is supposed to facilitate in vivo transformation of glyoxylic acid to glycine rather than to oxalic acid. However, it has recently been shown that long-term treatment with piridoxilate may result in overproduction of oxalic acid and in calcium oxalate nephrolithiasis. We report a patient in whom piridoxilate induced both oxalate nephrolithiasis and chronic oxalate nephropathy with renal insufficiency, an association that has not been previously described. Therefore, piridoxilate should be added to the list of chemicals responsible for chronic oxalate nephropathy.

Aged↗
PubMed1987

[Interstitial nephropathies induced by meticillin: demonstration of distal tubule functional anomalies].

Renal tubular dysfunction was investigated in two patients with meticillin-induced interstitial nephritis. Some degree of renal failure persisted after the acute episode in both cases. The first patient was investigated 10 weeks after the onset of the nephropathy. Nephrogenic diabetes insipidus and distal tubular acidosis were demonstrated. The second patient was investigated 7 months after the onset of the nephropathy. A major impairment in urinary concentration ability was demonstrated. Neither patient had proximal tubular dysfunction. These data show that meticillin-induced interstitial nephritis may be responsible for distal tubular abnormalities, namely nephrogenic diabetes insipidus and distal tubular acidosis, which may persist long after the onset of the nephropathy.

Adult↗