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Biomedical subjects

M Beaufils

Publications and source records attributed to M Beaufils.

At least 91 records · Page 5Linked to original sources

Angiotensin II binding to renal glomeruli from sodium-loaded and sodium-depleted rats.

125I-labeled angiotensin II (125I-labeled AII) and [3H]angiotensin II ([3H]AII) bind specifically to isolated rat glomeruli. Three groups of receptor sites could be defined by the KD value (7.1 +/- 0.3 X 10(-11, 3.4 +/- 0.2 X 10(-10), and 1.6 X 10(-9) M, respectively) and the number of receptor sites (11.6 +/- 1.2, 29.4 +/- 3.9, and 113.8 +/- 3.8 fmol/mg glomerular protein, respectively). Both association and dissociation constants for 125I-labeled AII were greater than those for [3H]AII, but their ratio (KD) remained unchanged. Specificity of binding to these three groups of receptor sites was demonstrated by the following: 1) inhibition of binding of labeled AII by unlabeled hormone or by antagonists; and 2) reversibility of binding, independent of either hormone or receptor degradation. Binding was increased in glomerular preparations from acutely and chronically sodium-loaded rats, compared with glomerular preparations from acutely and chronically sodium-depleted rats. This change in binding resulted from both a change in the number of receptor sites and modification of the affinity of AII for its receptors. KD was higher in preparations from sodium-depleted rats (12.9 +/- 3.3 and 14.6 +/- 3.9 X 10(-11) M in chronically and acutely depleted rats, respectively) than in those from sodium-loaded rats (2.7 +/- 0.2 and 3.9 +/- 1 X 10(-11) M in chronically and acutely sodium-loaded rats, respectively). Changes in the binding of AII to its glomerular receptors could play a role in the adaptation of glomerular filtration rate to the sodium balance.

Angiotensin II↗

Enhanced antiplasmin activity in acute renal failure.

Plasmatic slow plasmin-inhibitor activity was assessed in 20 patients with acute renal failure and 12 controls with the fibrin plate method. The area of fibrinolysis was 250-5 +/- 5 mm2 in the patients and 289 +/- 6mm2 in the controls (P less than 0.001) and was negatively correlated with antiplasmin activity. Thirteen patients had areas of lysis equal to or inferior to the minimal lysis observed in the controls. No correlation was found between antiplasmin activity and serum fibrin-fibrinogen related antigen titres, the presence or absence of disseminated intravascular coagulation, or the causative disease.

Acute Kidney Injury↗

Increased plasma calcitonin in early acute renal failure.

1. High plasma immunoreactive calcitonin concentrations were observed in ten of eleven patients with acute renal failure, particularly in the oliguric phase. 2. Immunoreactive calcitonin decreased progressively with time, independently of recovery of renal function. 3. Radioimmunoassay curves obtained with serial dilutions of plasma from these patients were parallel to or superimposed upon those obtained with calcitonin standards.

Acute Kidney Injury↗

Late streptokinase therapy in thrombotic microangiopathy: a case study.

A 42 year woman presented with malignant hypertension, anuria and hemolytic anemia with schistocytosis. The diagnosis of thrombotic microangiopathy was confirmed by early renal biopsy. Purely symptomatic treatment (peritoneal dialysis and hypotensive drugs) was supplemented by administration of heparin and Dipyridamole. Gastro-intestinal bleeding prevented early thrombolytic therapy. Microangiopathic anemia rapidly disappeared but anuria persisted. Three months later a second renal biopsy showed persistence of active lesions and absence of irreversible parenchymal damage. Streptokinase treatment was then instituted and followed by a rapid return of urinary output. Hemodialysis was stopped and renal function continued to improve over the following months. Two years later the patient remains well despite persistence of hypertension difficult to control. Creatinine clearance is stable at 20 ml/min. This observation suggests that late thrombolytic therapy may be effective in patients with thrombotic microangiopathy when histological findings do not indicate extensive irreversible lesions.

Adult↗

[Is hypertension related to the number of nephrons?].

The kidney has a key role in blood pressure control, and an abnormal regulation of sodium balance is involved in essential hypertension. It has been suggested that a reduced nephron number at birth could be one possible mechanism. Indeed various strains of hypertensive animals exhibit a reduced nephron number. In human beings, two autopsy studies have clearly shown a lower (about 50%) nephron number in hypertensive subjects. The glomeruli are also enlarged, indicating hyperfiltration. This could be the cause of both high blood pressure and later nephrosclerosis. A low number of nephrons is part of the perinatal programming which occurs together with fetal growth retardation, and this has been reproduced experimentally. There is a negative correlation between birth weight and glomerular number. Such a situation is associated with a largely increased risk of cardiovascular complications in adulthood.

Animals↗

[Does hyperuricemia involve a specific cardiac or renal risk? (author's transl)].

Hyperuricemia, commonly found in hypertensive patients, is a daily problem for the practitioner, especially those induced by diuretic therapies. The most divergent opinions are being given about the cardiovascular potential risk of hyper-uricemia. This article raises the problem of the use of those substances which change the metabolism of uric acid, whether they are hyper- or hypo-uricemic. It serves to remind that one must not prescribe hypo-uricemic diuretics to patients whose uricemia is increased, because they may involve serious risks, especially renal ones.

Heart Diseases↗

[Aspirin during pregnancy. Indications and modalities of prescription after the publication of the later trials].

Aspirin, an inhibitor of cyclo-oxygenase, is prescribed in a number of conditions related to abnormal production of prostaglandins including gravidic hypertension. Results of the most recent trials demonstrate that in patients with a past history of pre-eclampsia or intra-uterine growth retardation, a pathological Doppler examination of the uterus, a pathological angiotensin test or an antiphospholipid syndrome, prescription of aspirin at the dose of 100 mg/day can prevent recurrence or development of pre-eclampsia or intra-uterine growth retardation. Treatment should begin as soon as possible during pregnancy, certainly before development of clinical manifestations. After history taking and identification of possible contraindications, bleeding time (Ivy method) is recorded before and after prescription and should be lower than 8 minutes. In case bleeding time exceeds 10 minutes 10 to 15 days after initiating aspirin, doses may be reduced to 50 mg per day or even 50 mg every two or three days to reach the target level. Treatment should generally be continued up to 36 weeks gestation.

Angiotensin II↗