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Biomedical subjects

S Dard

Publications and source records attributed to S Dard.

8 recordsLinked to original sources
PubMed1981

[Isolated dissection of the renal artery. A rare cause of arterial hypertension (author's transl)].

During aetiological investigation of recently developed hypertension in a 31-year-old man, isolated dissection of the upper branch of the right renal artery was discovered. Injection, after sodium depletion, of saralasin, a competitive angiotensin II inhibitor, resulted in significant fall of the mean arterial pressure. During sodium depletion, the plasma renin activity was higher in the right renal artery (17.8 ng/ml/h) than in the left artery (9.4 ng/ml/h) and the infra-renal portion of the inferior vena cava (8.7 ng/ml/h). These figures suggested that surgical treatment of the dissection would have beneficial effects on blood pressure. Six months after resection of the pathological arterial segment and replacement by a graft from the internal saphenous vein, blood pressure had spontaneously returned to normal levels.

Adult↗
PubMed1981

[Acute renal failure induced by sulfinpyrazone (author's transl)].

We report on 4 cases of reversible acute renal failure (ARF), appearing within the first days after institution of a sulfinpyrazone treatment (600 mg p. day) early after a myocardial infarction. Urinary data were consistent with an acute tubular necrosis. A renal biopsy, performed in 3 patients, revealed only very discrete tubular and interstitial lesions, not helpful in the understanding of the ARF. Three pathogenetic mechanisms could be evoked. Data in favour of an acute tubular precipitation of uric acid or an immunologically induced acute interstitial nephritis are lacking. More probably this ARF is due to an inhibitory effect of sulfinpyrazone on the renal prostaglandin synthesis. Early after a myocardial infarction, renal prostaglandins could play an important protective role in maintaining the renal circulation. Renal function should be monitored closely when sulfinpyrazone is prescribed, especially early after a myocardial infarction.

Acute Kidney Injury↗
PubMed1981

[Compared metabolic effects of phosphorus or hydrochlorothiazide therapy in hypercalciuric stone-formers (author's transl)].

The hypocalciuric effect of phosphorus or hydrochlorothiazide therapy was evaluated in 26 hypercalciuric stone-formers after 2 to 4 months and 8 to 12 months treatment. After 2 to 4 months, a significant decrease of the urinary calcium to creatinine ratio was noted only in a group of 7 patients receiving phosphorus supplementation (1500 mg/day). The decrease was transient however, since in 5 of these patients, the calcium to creatinine ratio was found to be at pretreatment levels when the patients were reinvestigated after 8 to 12 months on phosphorus. In contrast, in 8 patients receiving hydrochlorothiazide (50 mg/day) during 8 to 12 months, this ratio was significantly lower (P less than 0.01) than before treatment. A group of patients maintained on high water intake alone for 8 to 12 months served as a control and no modification in calcium excretion was observed. This study indicates that long-term treatment with hydrochlorothiazide is more efficient in lowering urinary calcium excretion than phosphorus therapy.

Calcium↗
PubMed1979

[Idiopathic hypercalciuria: effects of acute phosphorus deficiency (author's transl)].

Eleven patients with kidney stone disease and idiopathic hypercalciuria (urinary calcium above 4 mg/kg/j), without phosphorus renal leak and 6 control subjects have been put for 3 days on a diet containing 1 g calcium and 1 phosphorus daily (period A), and then for 4 days on a diet containing 1 g calcium, 450 mg phosphorus and 3 g aluminium hydroxyde daily (period B). During period A, no significant difference in blood calcium, phosphorus and magnesium, not in phosphaturia, rate of phosphorus reabsorption (RPR) and ratio maximum RPR/creatinine clearance was found between the two groups. After 2 days on a low phosphate diet (period B) the blood phosphorus decreased significantly in the hypercalciuric patients but not in the control subjects, thus revealing among the forme a latent abnormality in the retention of phosphates. This abnormality could play an important role in the pathogenesis of hypercalciuria.

Adult↗
PubMed1975

Glomerular fibrinolytic activity after thrombin perfusion in the rat.

The effects of thrombin perfusion on glomerular fibrinolytic activity (GFA) have been assessed quantitatively in isolated rat glomeruli. Gfa was augmented by increasing total thrombin perfused to a maximal dose of 120 units per 100 gm. Fifty per cent maximal GFA occurred at a dose of 38 to 42 units of thrombin per 100 gm. independent of duration or rate of perfusion. After termination of infusion, GFA diminished and thrombi were no longer observed. Simultaneous administration of thrombin and epsilon-aminocaproic acid was associated with sustained high GFA and persistence of thrombi, presumably due to inhibition of the action of plasmin on fibrin, but it had no effect on tissue activators of plasminogen.

Aminocaproates↗