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Biomedical subjects

G Deray

Publications and source records attributed to G Deray.

At least 181 records · Page 10Linked to original sources
PubMed1988

Renal function and blood pressure in patients treated with cyclosporin A for uveitis.

Renal function has been evaluated in 21 patients treated with cyclosporin A (CyA) for 9 months for idiopathic uveitis. Serum creatinine, which was 82 mumol.l-1 before treatment, was significantly elevated after 1 month (111 mumol.l-1). After 9 months of treatment, and despite a decrease in CyA dosage, the mean plasma creatinine remained elevated at 132 mumol.l-1. Hypertension developed in 6 patients, five of them being concomitantly treated with corticosteroids. In 8 patients serum creatinine 3 months after CyA had been stopped had decreased from 148 to 93 mumol.l-1. Two of those patients remained hypertensive 3 months after CyA treatment had ceased. In patients with idiopathic uveitis CyA induces a reversible increase in serum creatinine. However the reversibility of such a biochemical marker does not preclude a histopathological lesion. Chronic renal damage may be responsible for the persistence of hypertension after cessation of CyA treatment.

Adult↗
PubMed1988

Plasma concentrations of atrial natriuretic peptide in patients with artificial and transplanted hearts.

Plasma atrial natriuretic peptide (ANP) concentrations were measured by radioimmunoassay 1 to 12 days after operation in six patients with artificial hearts. The mean levels were significantly higher in artificial heart recipients (58.2 pg.ml-1) than in controls (12.6 pg.ml-1). The mechanism underlying the raised values is not clear, although it is suggested that elevated atrial pressure may have been the stimulus for higher ANP release. In 3 patients plasma ANP concentrations were also measured 1 to 5 days after orthotopic transplantation. In all of them ANP concentrations had increased by 20 to 74% despite lower right atrial pressure. An increase in atrial tissue mass may have contributed to the raised plasma ANP after orthotopic transplantation. It also suggests that the functioning sympathetic nervous system is not a necessary condition for ANP release.

Adult↗
PubMed1988

Effects of ciclosporin on plasma renin activity, catecholamines and prostaglandins in patients with idiopathic uveitis.

Animals and humans undergoing treatment with ciclosporin (CS) show a reversible increase in renal vascular resistance and a decrease in glomerular filtration rate. The causes of these abnormalities have not yet been established. We evaluated the effects of a 1-week treatment with CS on creatinine clearance, renal arachidonic acid metabolites, plasma renin activity (PRA), plasma aldosterone levels, urinary excretion and plasma levels of catecholamines in 7 patients with idiopathic uveitis. We show that CS treatment induces a significant (p less than 0.05) decrease in creatinine clearance (from 132 +/- 0.5 to 108 +/- 8 ml/min); urinary 6-keto-PGF1 excretion (from 17.8 +/- 4.9 to 10.9 +/- 3.3 ng/mmol creatinine), urinary thromboxane B2 excretion (from 7.0 +/- 1.0 to 3.6 +/- 0.9 ng/mmol creatinine), upright PRA (from 4.2 +/- 0.9 to 2.3 +/- 0.8) and supine PRA (from 2.0 +/- 0.5 to 1.1 +/- 0.3). We found no change in plasma aldosterone levels and plasma levels and urinary excretion of catecholamines. We suggest that the reversible renal vasoconstriction observed in patients treated with CS may be induced by inhibition of renal prostacyclin synthesis. In this setting inhibition of PRA and angiotensin II formation may impair autoregulation of effective filtration pressure and therefore glomerular filtration rate.

Adult↗
PubMed1988

Acute renal failure induced by foscarnet: 4 cases.

Foscarnet (FC) is a new antiviral agent which has been recently proposed for the treatment of severe cytomegalovirus (CMV) infections in immunocompromised patients. When used intravenously (i.v.), main adverse effects of FC are a fall in hemoglobin, and an increase in liver enzymes and serum calcium. Although increased serum creatinine have been noted in several patients, deterioration of renal function is often accounted for by the concomitant use of other nephrotoxic drugs, the severity of underlying disease or the presence of graft rejection. Consequently FC is often considered as a non or poorly nephrotoxic drug. We report 4 cases of acute renal failure (ARF) which can be exclusively attributed to FC. FC was used for CMV chorioretinitis in 3 AIDS patients and in one non-immunocompromised patient. ARF was diagnosed between the 6th and 15th day of treatment, with oligoanuria in two patients (one of whom required two hemodialysis periods). ARF was most likely secondary to acute toxic tubulopathy. Three patients did not receive any other nephrotoxic drug. The fourth patient received concomitantly sulfadiazine but renal function returned to baseline value after FC completion although sulfadiazine was continued. In conclusion, our 4 observations suggest that FC may be responsible for acute tubulopathy. We suggest that in these patients renal function should be carefully monitored and dehydration promptly corrected to limit the risk of nephrotoxicity.

Acquired Immunodeficiency Syndrome↗
PubMed1988

[Functional renal effects of cyclosporin. Physiopathological mechanisms].

Animals and humans undergoing a treatment with cyclosporin (CsA) show a reversible increase in renal vascular resistance and decrease in glomerular filtration rate. The causes of these abnormalities have not yet been established. In animals potential mechanisms for CsA induced renal functional impairment are an increase in urinary thromboxane A2 excretion, plasma renin activity and renal sympathetic nervous system activity and an enhancement of vasopressin stimulated Ca++ mobilisation and cell contraction in vascular smooth muscle cells. In human, the problem is far less clear. CsA induces an inhibition in PRA and urinary prostaglandins excretion. Furthermore CsA does not modify urinary and plasma levels of catecholamines. Whatever the mechanism underlying the vasoconstriction induced by CsA, the inhibition of PGI2 synthesis and angiotensin II formation may participate in the decrease in renal blood flow and glomerular filtration rate which is observed in patients receiving CsA.

Animals↗
PubMed1988

[Clinical aspects of continuous ambulatory peritoneal dialysis in diabetics].

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). 81 patients, mean age 51.3 years, were treated over the past nine years by CAPD-CCPD. Extrarenal complications, mainly vascular lesions, account for qualifying these patients as a high risk population. The technique was modified in order to inject insulin intraperitoneally, four times per day, to control blood glucose level. Peripheral vascular disease was prospectively studied in 19 patients. Actuarial survival was 92% at one year, 50% at four years mainly influenced by age: 85% survival at two years in 35 patients aged less than 50 years and 62% at two years in 46 patients aged more than 50 years. The main causes of death were of cardiovascular origin: arteritis, myocardial infarction, stroke. The main causes for transfer to an alternative method of treatment were technical complications. Peritonitis rate was one episode ever 14 months. Satisfactory control of blood pressure, blood glucose levels, main biological parameters, visual status were the clear advantages of the method. Peripheral vascular disease is not influenced by the technique. CAPD can be the technique of first choice in young diabetics awaiting a kidney transplant and the reference technique for home dialysis.

Adult↗
PubMed1988

Effects of nifedipine on cisplatinum-induced nephrotoxicity in rats.

The effects of calcium channel blockade with nifedipine (N) on cis-diammine dichloroplatinum II (CDDP)-induced nephrotoxicity were tested in male Sprague-Dawley rats. Renal function was evaluated before and five days after CDDP administration (5 mg/kg). The rats were treated with various doses of N (0.1; 0.3; 0.6 mg/kg/day) 2 days before CDDP administration and throughout the study. The severity of CDDP-induced acute renal failure was markedly modified in N-treated animals according to the daily dosage of N. At 0.3 and 0.6 mg/kg BW/day, N enhanced CDDP nephrotoxicity. Serum creatinine was 637 +/- 45 and 611 +/- 71 mumoles/liter, respectively, 5 days after CDDP administration (vs. 313 +/- 24 mumoles in animals treated with CDDP alone; p less than 0.05). In these animals the plasma potassium level was significantly elevated at day 7 when compared with CDDP-treated and control rats. In contrast, at the dose of 0.1 mg/kg BW/day N attenuated CDDP nephrotoxicity with a serum creatinine of 214 +/- 35 mumoles at the end of the study. The pathologic changes were also more severe in the groups receiving 0.3 and 0.6 mg/kg of nifedipine. We postulate that at the higher doses (0.3 and 0.6 mg/kg) the systemic hemodynamic effects of nifedipine may override the potentially beneficial intrarenal effect which may account for the favorable results recorded with a dosage of 0.1 mg/kg.

Acute Kidney Injury↗
PubMed1987

[Hemolytic-uremic syndrome in adults].

Haemolytic uraemic syndrome is a rare condition easily diagnosed from biochemical data. Numerous forms consecutive to pregnancy, systemic diseases, carcinomas (notably mucin-secreting gastric adenocarcinoma), infections and medications have been described. The physiopathology of the syndrome, although more elaborate, is not entirely clear. The fundamental anatomical lesions (fibrin-platelet microthrombi) develop from vascular endothelial injuries. They persist and extend due to the non-functioning of physiological regulatory systems, in particular the coagulation-fibrinolysis system. In spite of frequently heavy and expensive treatments empirically applied, the course of the disease is generally unfavourable, with a mortality of about 50%.

Hemolytic-Uremic Syndrome↗
PubMed1987

Evidence of an endogenous digitalis-like factor in the plasma of patients with acromegaly.

Evidence suggests that plasma-volume expansion leads to the release of a digitalis-like factor, which is thought to act on the renal tubular cells and cause natriuresis. We postulated that this factor might be present in patients with acromegaly (in whom plasma volume is elevated) and might return to normal levels when the disease was treated successfully. We measured the ability of plasma extracts from patients with acromegaly to inhibit the binding of ouabain to the sodium pump in normal red cells and to inhibit the enzymatic activity (sodium-potassium-ATPase) of the sodium pump in membrane preparations from normal kidneys. In 21 patients with active acromegaly, the mean (+/- SE) level of ouabain-binding inhibition (1.56 +/- 0.38) was higher (P less than 0.01) than that in either 11 successfully treated patients (0.18 +/- 0.05) or in 27 normal controls (0.19 +/- 0.03). The inhibition of sodium-potassium-ATPase activity by plasma was also greater in patients with active acromegaly (38.1 +/- 6.8 percent) than in successfully treated patients (18.4 +/- 5.6 percent, P less than 0.05) or controls (21.1 +/- 2.7 percent, P less than 0.05). Significant correlations were found between plasma volume and ouabain-binding inhibition in 23 patients (r = 0.72, P less than 0.01) and sodium-potassium-ATPase inhibition in 19 patients (r = 0.62, P less than 0.01). Pituitary adenomectomy decreased plasma volume and the inhibition by plasma of ouabain binding. We conclude that an endogenous digitalis-like factor is present in the plasma of patients with chronic volume expansion due to acromegaly. These results are consistent with the hypothesis that this natriuretic factor may have a physiologic role in water and sodium homeostasis.

Acromegaly↗