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Biomedical subjects

G Deray

Publications and source records attributed to G Deray.

At least 73 records · Page 4Linked to original sources
PubMed1999

Renal effects of low and isoosmolar contrast media on renal hemodynamic in a normal and ischemic dog kidney.

RATIONALE AND OBJECTIVES: The authors investigated the comparative effects of a nonionic dimer contrast medium (iodixanol) with an ionic low osmolar contrast media (locm) (ioxaglate) on renal blood in a normal and an ischemic dog kidney. METHODS: Six dogs were studied for two periods. During the first period (the control period) a renal arteriography was performed with either iodixanol (Visipaque) or ioxaglate (Hexabrix) in a randomized order. Twenty minutes after applying a suprarenal clamp just above the right renal artery, two selective intrarenal contrast media administrations were performed at 30-minute intervals in a randomized order (ischemic period). RESULTS: During the control period ioxaglate and iodixanol induced no change in mean arterial blood pressure and pulse rate. The maximum decrease in renal blood flow (rbf) observed with ioxaglate was 19 +/- 4%. The maximum decrease in rbf observed with iodixanol was 51 +/- 16% versus control period (P = 0.05 compared with ioxaglate). During the ischemic period, renal perfusion pressure was 72 +/- 2 mm Hg and 73 +/- 2 mm Hg before iodixanol and ioxaglate administration, respectively (P = NS). Iodixanol induced a 61 +/- 11% decrease in RBF. These changes were significantly higher than those observed with ioxaglate during the control period and with the control ischemic period. Ioxaglate induced a maximum 11 +/- 6% decrease in RBF at 1 min (P < 0.05 versus iodixanol). These modifications were not significantly higher than those observed during the control period. CONCLUSIONS: In this study the authors found that the renal effect of iodixanol are markedly more pronounced than that of ioxaglate. In the setting of ischemia the effects of iodixanol were only slightly enhanced whereas those of ioxaglate were not modified.

Analysis of Variance↗
PubMed1999

[Are the antagonists of angiotensin II AT1 receptors protectors of the kidney?].

A lot of evidence points to the important role of the renin-angiotensin system in the physiopathology of hypertension and the progression of chronic renal failure. In this review, the authors report the data concerning the protective effects of antagonists of angiotensin II AT1 receptors (AT1ra). The AT1 ra have been shown to have beneficial effects in most experimental models of nephropathy in which they have been tested (renal ischaemia, essential or induced hypertension, glomerulonephritis, 5/6 nephrectomy, renal transplantation, induced diabetes, toxic and radiotherapy-induced nephropathy). Clinical trials confirm these beneficial effects. In healthy subjects and hypertensive patients, the AT1 ra have identical effects to those of angiotensin converting enzyme (ACE) inhibitors on renal haemodynamics. In hypertensives, Candesartan and Irbesartan increase renal blood flow and the glomerular filtration rate and decrease the filtration fraction. Two studies have also shown that Candesartan and Irbesartan reduce proteinuria in diabetic patients. Similar results have been reported in essential hypertension with renal failure. These data suggest that AT1 ra have beneficial effects on the progression of experimental kidney disease and on proteinuria in the clinical setting. Of the pharmacological agents available for use in this class, it is essential to propose molecules whose efficacy in antagonising the effects of angiotensin II lasts throughout the 24 hour period. Clinical trials are under way to evaluate the effects of AT1 ra on renal function in man over a long period.

Angiotensin Receptor Antagonists↗
PubMed1998

[Nephrotoxicity of ritonavir].

A RECOGNIZED COMPLICATION: Ritonavir is an antiprotease used in the treatment of HIV-positive patients. Among the known side effects, nephrotoxicity can be severe. We have observed acute renal failure in 8 patients. CIRCUMSTANCES: Renal failure occurs early after introducing ritonavir (3-21 days). It is often severe with major creatinine elevation. One patient was dialyzed for 16 days. In these patients, saquinavir was usually associated with ritonavir. RITONAVIR ALONE: We retrospectively analyzed creatinine levels in 87 patients treated with ritonavir without saquinavir. Twelve of these 87 patients (13.7%) developed renal failure. Creatinine clearance (Cockcroft) was reduced 116 to 71 ml/min in 12 patients. Finally, it was demonstrated in 6 patients that ritonavir can reduce creatinine clearance by 25% after only 3 days of treatment. VIGILANCE: Ritonavir has a known nephrotoxic potential. Acute renal failure may be severe and can occur with ritonavir alone or in combination with saquinavir. The pathogenic mechanism has not been demonstrated from renal biopsies or experimental studies. Renal function should be followed in these patients and risk factors controlled.

Acute Kidney Injury↗
PubMed1998

[Calcium inhibitors in the management of hypertensive patients on cyclosporine].

Cyclosporine (CsA) is an immunosuppressor widely used in all postoperative transplantation protocols. Nephrotoxicity and hypertension are the major secondary effects of cyclosporine. The CsA acts on two essential regulatory mechanisms of the blood pressure: the extracellular volume and the systemic vascular resistances. The incidence of hypertension in patients treated with CsA varies from 10% to 80% in the literature. In view of two main mechanismes implicated in CsA-induced hypertension the most logical therapeutic approach would be to use diuretics and calcium inhibitors. The major drawback of diuretic therapy is the risk of hyperuricaemia and attacks of gout, the predisposition to which is already increase by treatment with CsA. In addition, renal failure may rarely be observed. The calcium channel blockers are the drugs of choice in the treatment of CsA-induced hypertension. Not only are they effective in decreasing the blood pressure, but they also have a major advantage of having a nephroprotective effect against CsA. Cyclosporine is metabolised in the liver by cytochrome P450 3A4 dependant enzymes. Many pharmacological interferences have been described with this drug and other pharmacological agents. This type of interaction has been described with certain calcium inhibitors which inhibit hepatic and digestive degradation of cyclosporine and therefore increase its plasma concentrations. The choice of calcium inhibitors should be based on criteria of efficacy and tolerance and on the drug's pharmacokinetics. The interaction between cyclosporine and some calcium inhibitors exposes the patients to the risk of overdosage when treatments is instituted and of underdosage when the treatment is withdrawn.

Blood Pressure↗
PubMed1997

[Urinary calculi and crystalluria in HIV+ patients treated with indinavir sulfate].

OBJECTIVES: Anti-proteases, a new class of anti-HIV drugs used in combination with reverse transcriptase inhibitors have led to spectacular improvement in the patients' clinical status. Since April 1996, indinavir is the most widely prescribed anti-protease in France. PATIENTS AND METHODS: From July 1996 to July 1997, we analyzed 46 spontaneously expulsed stones in 45 HIV+ patients (35 men and 10 women; age range 25 to 64 years) given indinavir in combination with other drugs since one week to ten months. Only six patients were known to have a past history of renal lithiasis. RESULTS: Forty-one calculi contained indinavir monohydrate (INDM) identified by mass spectrometry and infrared spectrophotometry. INDM was the only component excepting proteins in 39/45 calculi. In the 12 others, other compounds were also identified. Among the 114 urine samples collected 2 to 3 hours after an 800 mg dose of indinavir, 38 (33%) monohydrate indinavir crystals, identified by infrared microscopy. Mean urinary pH was significantly higher than in samples without INDM crystals (6.53 +/- 0.68 versus 5.96 +/- 0.71, p < 0.001). CONCLUSION: Two measures could possibly reduce the risk of crystalization: administration of urine acidifiers and increased fluid intake to raise diuresis. Alkalinisation is not indicated. Long-term increased fluid intake should be preferred over acidification which could be reserved solely for the treatment of drug-induced lithiasis.

Adult↗