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Biomedical subjects

G Deray

Publications and source records attributed to G Deray.

At least 163 records · Page 9Linked to original sources
PubMed1990

Interaction between angiotensin II and adenosine in mediating the vasoconstrictor response to intrarenal hypertonic saline infusions in the dog.

Intrarenal artery infusion of hypertonic saline induces a sustained renal vasoconstriction that is most likely mediated by tubuloglomerular feedback. The purpose of this study was to investigate the contribution of angiotensin II and adenosine to this response in normal-salt and salt-deplete states. Intrarenal infusions of hypertonic saline to sodium-deplete dogs caused a renal vaso-constrictor response that was observed between 5 and 10 min into the infusion. This response was attenuated in dogs on a normal-salt diet and in salt-deplete dogs receiving captopril. Intravenous infusion of subpressor doses of angiotensin II to dogs either on a normal-salt intake or on a salt-deplete diet but receiving captopril, restored the vasoconstrictor response to hypertonic saline. The vasoconstrictor response in the presence of an angiotensin II infusion in each of these two groups of dogs was abolished by an intrarenal artery infusion of the adenosine receptor blocker, theophylline. These experiments are consistent with the hypothesis that intrarenal infusion of hypertonic saline enhances the endogenous production of adenosine and that the ability of adenosine to reduce renal blood flow is dependent on the presence of angiotensin II.

Adenosine↗
PubMed1989

Adenosine inhibits renin release induced by suprarenal-aortic constriction and prostacyclin.

The purpose of this study was to determine whether adenosine can attenuate the renin release response to a reduction in renal perfusion pressure. To this end, the secretion rate of renin was measured in six beta-blocked dogs at ambient arterial blood pressure and after a reduction of renal perfusion pressure to 80 mm Hg. These measurements were made during a control period, an intrarenal infusion of adenosine at 10 and 30 micrograms/min, and a recovery period. During the control and recovery periods renal artery hypotension significantly increased the secretion rate of renin. However, during the intrarenal infusions of adenosine, renin secretion rate did not increase significantly. Analysis of variance indicated that both doses of adenosine reduced the renin response to renal artery hypotension. In another six dogs with a single nonfiltering kidney, we again measured renin secretion during a control period, the intrarenal infusion of adenosine at 10 and 30 micrograms/min, and a recovery period; however, in this study PGI2 was used to stimulate renin release. Adenosine also significantly attenuated the renin release response to PGI2. We conclude that adenosine can inhibit the renin release response to both renal artery hypotension and PGI2 and that this effect is most likely mediated by a direct action of adenosine on juxtaglomerular cells. Also, since PGI2 may be a mediator of the renin response to renal artery hypotension, the data are consistent with the hypothesis that adenosine inhibits the renin response to renal artery hypotension by attenuating the response of juxtaglomerular cells to PGI2.

Adenosine↗
PubMed1989

Methylxanthines augment the renin response to suprarenal-aortic constriction.

In a previous study we discovered that the adenosine receptor antagonist, caffeine, increases plasma renin activity and blood pressure in renin-dependent renovascular hypertension. The purpose of the present investigation was to determine whether methylxanthines augment the increase in renin secretion induced by a reduction in renal perfusion pressure and, if so, whether this effect is mediated by a direct action on juxtaglomerular cells. Accordingly, we examined the effects of infusions of caffeine and theophylline directly into the renal artery on the increase in renin secretion induced by suprarenal aortic constriction. All studies were conducted in dogs receiving an intravenous infusion of propranolol to prevent changes in renin secretion mediated indirectly via the sympathetic nervous system. Caffeine (5 mg/min) increased the renin response to suprarenal aortic constriction about 10-fold without significantly affecting renal hemodynamics or excretory function. Theophylline (5 mg/kg), on the other hand, did not significantly increase the renin response to a reduction in renal perfusion pressure, but did increase urine flow and sodium excretion about 10-fold. However, in the non-filtering, beta-adrenoceptor blocked, canine kidney, theophylline markedly increased the renin response to suprarenal aortic constriction. These results indicate that methylxanthines can potentiate the renin response to a reduction in renal perfusion pressure most likely by directly affecting the juxtaglomerular cells; however, since increased sodium delivery to the macula densa inhibits renin release, the extent to which methylxanthines affect the renin response to renal artery hypotension depends on how vigorous the diuretic response is to a given methylxanthine.

Adrenergic beta-Antagonists↗
PubMed1989

The effects of diltiazem on methotrexate-induced nephrotoxicity.

We have tested the effects of calcium channel blockade with diltiazem on methotrexate-induced nephrotoxicity in patients with biopsy-proven malignant disease. The patients were randomized in a cross-over fashion to receive MTX (4 g.m-2 body surface area) with or without Diltiazem (360 mg per day orally) during two consecutive periods separated by a 3-week interval. Methotrexate caused reversible acute renal failure, with an increase in serum creatinine from 89 (7)mumol.l-1 on day 0 to 150 (6)mumol.l-1 on Day 6. The patterns of beta 2-microglobulin and N-acetyl glucosaminidase urinary excretion were similar, with a sharp increase from Day 0 to Day 3. Urinary beta 2-microglobulin excretion increased from 161 (57) micrograms.l-1 on Day 0 to 1160 (840) micrograms.l-1 on Day 3 and fell to 918 (530) micrograms.l-1 on Day 10. Urinary N-acetyl glucosaminidase excretion increased from 250 (100) mmol.h-1 per mg of creatinine on Day 0 up to 655 (261) on Day 3 and fell to 285 (82) on Day 10. The evolution of renal function was not influenced by diltiazem. In patients receiving diltiazem, serum creatinine increased from 93 (0) mumol.l-1 on Day 0 to 151 (68) mumol.l-1 on Day 6 (p = NS when compared with control values). Urinary enzyme excretion also markedly increased from Day 0 to Day 3 to the same extent as in the group not receiving diltiazem. Our data indicate that acute deterioration in renal function caused by methotrexate is accompanied by tubular damage. Diltiazem was ineffective in preventing the acute renal failure induced by methotrexate.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1989

Disopyramide-induced hypoglycemia: case report and review of the literature.

Disopyramide is a group I antiarrhythmic drug which is mainly used for the treatment of ventricular and supraventricular rhythm disturbances. Commonest side effects result from disopyramide's anticholinergic activity. Other side effects such as hypoglycemia have been reported less frequently. We report one observation of disopyramide induced hypoglycemia, and a review of the literature is presented. Including our observation, 14 cases (9 men and 5 women, aged from 41 to 88) have so far been reported. Doses of disopyramide ranged from 200 to 1,200 mg per day, administered from one day to one year. Symptomatology was mainly neurologic (12 patients) and two patients were clinically asymptomatic. The outcome was favorable in all but the 2 patients who died with persistent hypoglycemia after a single dose of 250 mg in one patient and after 400 mg daily during 4 days in the other (without stopping the drug). Renal function was markedly impaired in 9 patients, two of these patients being on a long term dialysis therapy. Blood levels of disopyramide were measured in 7 patients and ranged from 1 to 11.4 ng/ml. In five patients it was in the normal range (1-4 ng/ml). Three patients were rechallenged for disopyramide: hypoglycemia occurred in all, without clinical symptoms in two of them. The main risk factors of disopyramide induced hypoglycemia are a preexisting chronic renal failure, advanced age, and malnutrition. In these patients normally non toxic disopyramide blood levels, as defined in normal subjects, seem to be inappropriately high. We suggest that in patients at risk, disopyramide blood levels should be maintained at the lower range of therapeutic level.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1989

Foscarnet nephrotoxicity: mechanism, incidence and prevention.

Foscarnet is a pyrophosphate analogue that has been successfully used in severe cytomegalovirus (CMV) infections. Little is known of the incidence and mechanisms of foscarnet-induced nephrotoxicity as most data comes from recipients of renal allografts or from patients with severe underlying disease or with other nephrotoxic drugs. We have retrospectively analyzed the evolution of renal function after 56 courses of foscarnet. In addition, we have prospectively studied the protective effects of hydration on foscarnet nephrotoxicity (2.5 liters of saline/day during the night before the foscarnet therapy and throughout the course of treatment). Foscarnet-induced acute renal failure was defined as a rise in serum creatinine of at least 25% from the basal value. An increase in serum creatinine occurred in 37 cases out of the 56 courses of foscarnet (66%). The mean serum creatinine prior to foscarnet was 80.5 +/- 3.3 mumol/l and the mean increase was 190 +/- 28.3 mumol/l (range 80-1,000). Peak serum creatinine was higher than 200 and 300 mumol/l in 16 and 13 patients, respectively. Kidney obtained at autopsy from a 30-year-old male with AIDS, CMV pneumonitis and acute renal failure secondary to foscarnet administration showed an extensive tubular necrosis. In the group which was prospectively hydrated only 1 patient had an acute renal failure. The mean serum creatinine at the peak (96 +/- 4 mumol/l) and at the end of the treatment (83 +/- 4 mumol/l) was significantly lower (p less than 0.05) than in non hydrated patients. In conclusion, foscarnet is a highly nephrotoxic drug which induces acute tubular necrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Kidney Injury↗
PubMed1989

Clinical aspects of continuous ambulatory and continuous cyclic peritoneal dialysis in diabetic patients.

The treatment of end-stage renal diabetic nephropathy remains a challenge. A large experience allows us to clearly outline the advantages and the drawbacks of continuous ambulatory peritoneal dialysis (CAPD) and continuous cyclic peritoneal dialysis (CCPD). Eighty-one patients, mean age 51.3 years, were treated over the last 9 years by CAPD-CCPD. Extrarenal complications, mainly vascular lesions, were present in this high-risk group of patients. The technique was modified in order to inject intraperitoneally, 4 times per day, insulin to control blood glucose level in CAPD patients. Actuarial survival was 92% at 1 year, 50% at 4 years mainly influenced by age: 85% survival at 2 years in 35 patients aged less than 50 years old and 62% at 2 years in 46 patients aged more than 50 years old. The main causes of death were of cardiovascular origin: myocardial infarction, stroke, atherosclerotic vasculopathy. The main causes of transfer to hemodialysis were due to technical complications. Peritonitis rate was one episode every 14 patient-months. Control of blood pressure, blood glucose levels, main biological parameters, and visual status were the clear advantages of the method. Peripheral vascular disease is not influenced by the technique. CAPD-CCPD is the technique of first choice in young diabetics and the preferential technique for home dialysis.

Actuarial Analysis↗
PubMed1989

Idiopathic acute interstitial nephritis associated with anterior uveitis in adults.

Concomitant renal and ocular lesions have been described in a few systemic diseases. The association of acute interstitial nephritis (AIN) and anterior uveitis without determined cause was first described in children. Recently, the same clinical association has been reported in adults. We report 3 cases of this association and present a review of the literature. Including our 3 patients, 7 cases of this association have been reported in adults. All patients were females aged 27-74 years. Initial symptoms were either ocular, or pseudoviral (fever, myalgia and fatigue). Histological renal studies revealed acute interstitial nephritis with tubular lesions. Immunofluorescence and electron microscopy were not contributive. Ocular prognosis was always good. In 5 patients, the evolution of renal function was excellent with complete resolution of acute renal failure within a few weeks. Chronic renal failure developed in two of the four patients who did not receive systemic steroid therapy (with evolution towards terminal renal failure in one patient). Three of the patients received 60 mg per day of prednisone and none of them developed chronic renal failure. Despite the small number of patients reported and the possibility of spontaneous regression, these data suggest a beneficial effect of systemic steroid therapy to prevent or reduce interstitial inflammation and subsequent fibrosis.

Acute Disease↗