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Gilbert Deray

Publications and source records attributed to Gilbert Deray.

At least 37 records · Page 2Linked to original sources
PubMed2006

[Statins in patients with kidney failure: efficacy, tolerance, and prescription guidelines in patients with chronic kidney disease and renal transplant].

BACKGROUND: Chronic kidney disease (CKD) is extremely common in adults, although often undiagnosed and thus untreated. Cardiovascular disease is the leading cause of death among patients with CKD and reducing its risk in this population is an important priority. Dyslipidemia is almost always present when proteinuria is above 3 gr/24 hours. Roughly two thirds of all patients with end-stage renal failure and kidney transplants suffer from dyslipidemia and should receive lipid-lowering therapy, as suggested by recent Afssaps (French drug agency) and NKF-K/DOQI (National Kidney Foundation-Kidney Disease Outcomes Quality Initiative) guidelines. We reviewed recent studies on efficacy, tolerability and prescription recommendations of statins in CKD and renal transplant patients. METHODS: We searched Medline, the international medical database, to conduct a systematic review of the literature on the efficacy and tolerability of statins in CKD and renal transplant patients and on specific recommendations for dosage adjustments in this population. RESULTS: The efficacy of statins in decreasing total cholesterol and LDL-cholesterol levels in dialysis and renal transplant patients is similar to that in the general population. On the other hand, large-scale randomized clinical trials among CKD (4D) and renal transplant (ALERT) patients do not demonstrate that statins significantly decrease rates of cardiovascular disease. They have a beneficial effect on proteinuria and lower the rate of kidney function deterioration in patients with dyslipidemia. Early introduction of a statin in transplant patients did not lead to improved kidney function or prevent loss of the graft. Although most statins are not excreted by the kidneys, the dosage of some must be adapted in CKD patients because of pharmacokinetic modifications induced by renal impairment. CONCLUSION: Statins at appropriately adapted doses have the same efficacy in CKD patients as in subjects with normal kidney function, and tolerance is not a problem. Their effectiveness in cardiovascular prevention in this population has not been demonstrated to date. Results about statin-induced kidney protection are encouraging but further and more specific studies are needed.

Adult↗
PubMed2006

Loss of podocyte dysferlin expression is associated with minimal change nephropathy.

We report a case of limb-girdle muscular dystrophy type 2B (LGMD2B) associated with minimal change disease. Immunohistochemical examination of quadriceps muscle showed a deficiency in dysferlin in sarcolemma, and dysferlin gene analysis showed 3370 G missense mutation, leading us to the diagnosis of LGMD2B. The patient also developed glomerular proteinuria. We also explored urinary protein levels in 3 other patients with dysferlinopathy and found microalbuminuria with albumin excretion of 0.14 to 0.18 g/d in 2 patients. Renal abnormalities during LGMD2B and kidney dysferlin expression have never been reported. Renal biopsy showed a lack of glomerular dysferlin expression compared with a positive immunohistochemical marking in patients with idiopathic minimal change nephropathy and healthy controls. We therefore suggest that dysferlin is present in glomeruli and may be associated with glomerular permeability.

Adult↗
PubMed2006

Drug-induced glomerulopathies.

Normal renal function depends upon an intact glomerular apparatus. Many drugs and chemicals are capable of damaging the glomerulus, causing its increased permeability to large molecules. Glomerular lesions are usually responsible for proteinuria and the nephrotic syndrome. This also holds true for the drug-induced glomerulopathies, of which membranous glomerulo-nephritis is the most frequent type of lesion encountered. Apart from this, several cases of different glomerular changes such as focal segmental glomerulosclerosis and crescentic glomerulonephritis have also been reported. The drug-induced glomerulopathies are probably immune mediated. This is, for instance, reflected in the fact that patients with drug-induced nephritic syndrome frequently have the HLA-B8 and DR3 antigens. In depth information is provided for the previously mentioned disorders.

Glomerulonephritis, Membranous↗
PubMed2006

[What do we know about the cardiovascular toxicity of the NSAIDs?].

Following the arterial thrombotic risk of rofecoxib (myocardial infarct and cerebral ischemic accidents) that led to its withdrawal from the market, the other coxibs then the NSAIDs have also been blacklisted. The factors responsible for the cardiovascular risk associated with the ingestion of the NSAIDs, selective or not, are not clearly identified. The objective of this review was to collect the available data from the literature, in order to better evaluate of the risk and its causes, principally on the basis of the results of randomised studies, but also of case reports and meta-analyses. There is an increase in the risk of arterial thrombotic events under coxibs and traditional NSAIDs, however the risk is variable for both classes. The cardiovascular risk linked to celecoxib seems variable and modest, and at a standard dose and for usual treatment durations, the risk is probably inexistant. While the real risk of classical NSAIDs is difficult to appreciate from the available results, it can be concluded that the cardiovascular risk of naproxen is low. While part of the cardiovascular consequences of rofecoxib could be associated with increased arterial pressure, these effects are not exclusive to the coxibs since they have been observed with the conventional NSAIDs. However the increase in arterial pressure cannot probably explain everything. Similarly the cardiac insufficiency associated more particularly with rofecoxib, especially in some groups of patients (very old subjects) is not a new type of complication and does not seem to be more frequent with coxibs than with classical NSAIDs. No short-term arterial thrombotic risk of the coxibs and NSAIDs has been clearly demonstrated.

Aged↗
PubMed2006

[Are there any differences in the cardiovascular tolerance between classical NSAIDs and coxibs?].

Three placebo-controlled studies have demonstrated deleterious cardiovascular (CV) effects of rofecoxib, celecoxib, and pare/valdecoxib. It remains to be determined whether this CV toxicity is specific to coxibs, or shared with all non-steroidal anti-inflammatory drugs (NSAIDs). Seven meta-analyses show that, in comparison with non-specific NSAIDs, the risk of thrombotic CV accident is increased with rofecoxib and celecoxib, but not with valdecoxib or lumiracoxib. Concerning the risk of thrombotic CV accident, seven of the ten observational studies which have evaluated the risk have found an increased risk for the non-specific NSAIDs in comparison with non-exposed subjects. The seven observational studies, which evaluated the risk of coxibs, have all found an increased risk with rofecoxib, and two with celecoxib. Three studies out of six have shown on increase of risk with rofecoxib and one study out of five with celecoxib. Two of the three studies, which have compared rofecoxib with celecoxib, have found on increased risk with rofecoxib. Concerning the risk of arterial hypertension, aedemas or congestive cardiac insufficiency, a meta-analysis and a randomised trial have shown a deleterious effect of rofecoxib in comparison with celecoxib and non-specific NSAIDs. Two studies have shown a deleterious effect of the non-selective NSAIDs and three a deleterious effect of rofecoxib in comparison with non-exposed subjects. Three studies have demonstrated a deleterious effect of rofecoxib in comparison with non-specific NSAIDs. No study has shown any deleterious effect of celecoxib in comparison with subjects non-exposed or exposed to non-specific NSAIDs. These studies suggest that all the NSAIDs, specific or not, increase the CV and renal risk. This risk seems variable from a compound to another one and must be evaluated, for each patient, according to the susceptibility and associated risk factors. While waiting for other long-term controlled studies, the available data show the existence of a risk of CV secondary effect linked to the class of NSAIDs, specific (coxibs) or not.

Age Factors↗
PubMed2006

[How to watch over a patient treated with a NSAID in relation to the cardiovascular and renal risk?].

Despite the cardiovascular risk attributable to the NSAIDs, these drugs are among the most prescribed treatments in the world. Recently to manage this risk during chronic inflammatory rheumatisms a surveillance plan has been developed based on a decision algorithm. Given that the arterial thrombotic risks (myocardial or cerebral) are observed essentially during long-term treatments, two types of situation have been envisaged, short-term treatments and long-term treatments. Before any short-term NSAID prescription (less than one month), the cardio-renal risk should be evaluated. A pre-therapeutic check-up should include the search for risk factors and the treatment surveillance should imply a clinical and biological check-up carried out after 2 to 3 weeks of treatment. Before any long-term NSAID prescription (more than one month), the arterial thrombotic risk (cardiac or cerebral) should be evaluated and the patient's history determined. Pre-therapeutic check-up and surveillance should be carried out and reconsidered at least every three months. In the case of high risk the advice of a cardiologist or a nephrologist should be obtained and drastic therapeutic measures taken. There are cases where the prescription of NSAIDs or coxibs is possibly not recommended.

Adult↗
PubMed2006

[Which information should be given to the patient concerning the cardiovascular and renal risk of the NSAIDs?].

OBJECTIVE: Patient information is a topical subject. The aim of this review is to present the rare studies concerning the degree of patient information on the cardiovascular and renal risks of the non-steroidal anti-inflammatory drugs and to suggest some recommendations on this subject. METHODOLOGY: After analysis of the literature (Medline search - January 2006), a series of recommendations has been drown up following discussion among experts from different specialties (clinical epidemiology rheumatology cardiology nephrology gastroenterology). RECOMMENDATIONS: It appears necessary to warn all patients of the potential risk of hyperkolemia, renal insufficiency and/or hydrosodium retention (decompensation of an arterial hypertension or a cardiac insufficiency), especially subjects who present risk factors such as age over 75 years, a dehydration, a pre-existing renal disorder etc. Concerning the risk of arterial thrombotic incident (coronary or cerebral), it is important to indicate that this risk is rare and seems to be observed particularly during prolonged treatments and at high dose.

Age Factors↗
PubMed2005

Regional citrate anticoagulation during hemodialysis: a simplified procedure using Duocart biofiltration.

BACKGROUND: Regional citrate anticoagulation during hemodialysis is promising, but its clinical implementation is routinely cumbersome because a continuous adjustment of calcium infusion at the dialyzer outlet is needed. Duocart biofiltration (DCB) is a new hemodialysis method using a calcium and magnesium-free dialysate containing only sodium chloride and bicarbonate combined with the infusion into the venous line of a solution containing the ionic complement (K, Ca, Mg) and glucose. Since the dialysate is calcium- and magnesium-free and infusion rate of the solution containing calcium is automatically determined by the dialysis delivery system according to the on-line measured value of ionic dialysance, DCB seems a technique especially suitable for citrate anticoagulation procedure. METHODS: Thirty DCB sessions were performed in 10 patients with increased risk of bleeding. A commercially available mixture of trisodium citrate, citric acid and glucose was infused into the arterial line at a rate equal to 3% of dialyzer blood flow. The ionic complement (K: 48 mM, Ca: 42 mM, Mg: 14 mM, glucose: 110 mM) was infused at a rate equal to 1/24 ionic dialysance value automatically determined each 15 min by the dialysis monitor. DCB sessions were compared to 21 conventional bicarbonate hemodialysis (BHD) sessions with low-molecular-weight heparin anticoagulation. RESULTS: Whole blood activated clotting time (WBACT) measured in the venous line (before infusion of ionic complement) was 200% of the WBACT value in the arterial line. Clotting and citrate-related adverse events were not observed. Postdialysis compression time of the arteriovenous access is significantly (p<0.001) shorter after DCB sessions (3.9+/-1.1 min) compared with BHD sessions (8.7+/-4.6 min). CONCLUSION: Citrate anticoagulation during Duocart biofiltration is effective, safe and suitable for routine use because calcium infusion rate is automatically adjusted without the need of monitoring degree of anticoagulation and level of ionized calcium.

Adult↗
PubMed2005

[Tubular transporters OAT1 and MRP2 and clearance of adefovir].

Adefovir is transported by the organic anion transporter (OAT1) and the multidrug resistant protein (MRP2, 4 and 5). We studied adefovir clearance in rat after inhibition of transporters by probenecid and in TR- rats, in which MRP2 is lacking. After treatment by probenecid or placebo, pharmacokinetics of adefovir 10 mg/kg was studied via population modeling (NONMEM). The fraction of drug excreted in the urine was low. Renal clearance of adefovir was significantly lower (P < 0.05) in probenecid TR- rats (0.03 +/- 0.02 l/hour) than in normal control (0.09 +/- 0.05 l/hour), in normal probenecid (0.10 +/- 0.07 l/hour) and in TR- control rats (0.13 +/- 0.07 l/hour). In vivo in rats MRP2 mutation alone did not affect adefovir clearance suggesting that MRP2 does not play a critical role in the secretion of adefovir. Additional pharmacological inhibition of transporters decreased renal clearance, which may reflect inhibition of compensating transport mechanisms activated when MRP2 is lacking.

Adenine↗
PubMed2005

[Drug-induced nephrotoxicity: bibliography from January 2003 to December 2004].

Drug-induced kidney injury is a major side effect in clinical practice. Renal injury associated with drugs may involve several components of the kidney: glomerulus, tubules, interstitium and blood vessels. Acute renal failure may occur as a major reaction to many drugs. Moreover, therapeutic agents may induce an allergic reaction leading to interstitial inflammation and tubular damage. In this article, we present an updated version of the bibliography containing the case reports of nephrotoxicity published in the international literature from January 2003 to December 2004.

Drug-Related Side Effects and Adverse Reactions↗
PubMed2005

FHD: an index to evaluate drug elimination by hemodialysis.

BACKGROUND: In hemodialyzed patients, physicians have to (1) adjust drug dosage for a creatinine clearance lower than 10-15 ml/min and (2) know whether or not the drug will be removed by the dialysis session to decide whether it may be administered before or after the session on dialysis days. However, of several indices being used to evaluate drug removal by dialysis none is appropriate and we suggest a novel index named F(HD), which reflects the role of hemodialysis clearance of a drug in its overall clearance during the session. METHODS: Pharmacokinetic simulations were performed to test the influence of dialysis on the pharmacokinetics of some drugs, whether F(HD) was considered or not, to determine when to administer the drug. F(HD) was then calculated for several drugs and its value compared with other indices. Five hemodialysis patients from our department for whom the time of drug administration was determined according to F(HD) were included in a small study and their drugs' trough concentrations were monitored. RESULTS: F(HD) emphasized that considering hemodialysis clearance alone may lead to false interpretations of the potential dialyzability of some drugs. In our patients, who received their treatment according to the 'F(HD) rule', monitoring of trough levels gave satisfactory results. CONCLUSION: The use of the 'F(HD) rule' should be tested on a long-term administration basis to confirm our conclusion. F(HD )could be the index of choice to determine when to administer a drug, before or after the session, in hemodialysis patients.

Adult↗
PubMed2005

[Is dialysis efficient in the prevention of ionic contrast agent-induced nephropathy?].

UNLABELLED: A FREQUENT AND EXPENSIVE PROBLEM: Ninety percent of contrast media nephrotoxicity (CMN) occur in patients with pre-existing kidney failure. Its aggravation may require early chronic dialysis. PREVENTIVE MEASURES: CMN prophylaxis is important in these patients. Pre- and post-hydration, with infusion of isotonic saline solution or sodium bicarbonate, and reduction of contrast medium (CM) volume to the strict minimum are essential for preventing CM-induced kidney failure. THE INTEREST OF PROPHYLACTIC HEMODIALYSIS AND HEMOFILTRATION: An interesting approach in preventing CMN is the early elimination of the CM with dialysis techniques. Preventive hemodialysis does not reduce the risk of CMN, but hemofiltration has shown significant efficacy in a population of patients with kidney failure. THE INTEREST OF IMMEDIATE HEMODIALYSIS IN CHRONIC HEMODIALYSIS PATIENTS: Although nephrotoxicity is no longer a problem in patients undergoing chronic hemodialysis, CM, especially in high-dose injections, may be responsible for fluid and electrolyte abnormalities and/or volemic expansion. No data yet justify a conclusion that a hemodialysis session immediately after injection of a CM in chronic dialysis patients might be helpful.

Contrast Media↗
PubMed2005

[Anticancer drug-induced nephrotoxicity].

Nephrotoxicity is an inherent adverse effect of certain anticancer drugs. Anti neoplasic drugs have a narrow therapeutic index and the amount of drug necessary to produce a significant reduction in tumour burden usually produces significant nephrotoxicity. The dosage used in clinical trials represents often the maximum tolerated doses determined during phase I drug evaluation. Greater toxicity is acceptable during curative therapy than during palliative therapy. But cancer patients often exhibit excretory reduced organ function. Modulation of pharmacokinetics and pharmacodynamics of these drugs in cancer patients is therefore necessary in order to improve tolerance. Patients with malignancies are particularly vulnerable to development of renal abnormalities. Conversely, patients with renal abnormalities who have undergone kidney transplantation are at high risk for malignancy. Clinical syndromes of renal involvement are diverse and sometimes insidious. Despite the recent advances in understanding the mechanism of anticancer drug nephrotoxicity, prevention still relies on drug dosage decrease and active screening for renal abnormalities as part of the usual biological work up in patients treated with anticancer drugs.

Antineoplastic Agents↗
PubMed2005

Statins' dosage in patients with renal failure and cyclosporine drug-drug interactions in transplant recipient patients.

Dyslipidemia is frequent in patients with renal failure and in transplant recipient patients. This lead to a wide use of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) in patients with impaired renal function or in patients treated with cyclosporine as post-transplantation immunosuppressive therapy. As a result, it is crucial for those patients' physicians to be aware of how to handle these drugs when renal function is impaired and/or when cyclosporine is co-administered. Most statins have an extensive hepatic elimination and the renal route is usually a minor elimination pathway. However, pharmacokinetic alterations have been described for some of these drugs in patients with renal insufficiency. Cyclosporine is a widely used immunosuppresive therapy in solid organ transplant patients and drug-drug interactions are likely to occur when statins and cyclosporine are administered together. Those interactions may theoretically result in increased statins and/or cyclosporine serum levels with potential muscle and/or renal toxicity. As a result, caution is warranted if concurrent administration is performed. In this review, we synthesized the data from the literature on (1) the pharmacokinetics and dosage adjustment of atorvastatin, fluvastatin, pravastatin, rosuvastatin, and simvastatin in patients with renal failure and (2) the potential drug-drug interactions between these drugs and cyclosporine in transplant recipient patients.

Cyclosporine↗