Biomedical subjects
Vincent Launay-Vacher
Publications and source records attributed to Vincent Launay-Vacher.
Why is a shrunken bladder and a nephrotic kidney an expression of the same disease?
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Ear and kidney syndromes: molecular versus clinical approach.
The association between ear and kidney anomalies is not usually due to an insult to the embryo. In recent years, many essential development control genes that coordinate the assembly and function of kidney and ear have been discovered through the generation of animal mutants and have increased our understanding of the mechanisms of human oto-renal diseases. Here, we describe ear and kidney clinical syndromes and their molecular expression.
Antiretroviral and immunosuppressive drug-drug interactions: an update.
With the introduction of highly active antiretroviral therapy (HAART), human immunodeficiency virus (HIV) infection has become a chronic disease with more frequent end-stage organ failures. As a result, the question of transplantation in HIV patients is raised more often. However, some of the HAART regimen medications require elimination or metabolism via the P-glycoprotein (P-gp) and multidrug-resistant protein (MRP) transporters or via the cytochrome P450 enzyme system. Since these transporters and enzymes are also responsible for the clearance of immunosuppressive drugs, drug-drug interactions are likely to occur. Indeed, profound drug-drug interactions between protease inhibitors and immunosuppressive drugs have been observed and they required reductions in drug dosage. In contrast, HAART using nucleoside or nonnucleoside reverse transcriptase inhibitors without the use of protease inhibitors has been shown to produce less significant drug-drug interactions. It is thus crucial to take into account those potential pharmacokinetic and/or pharmacodynamic drug-drug interactions in order to avoid drug toxicity or a lack of efficacy. The aim of this work was to review and synthesize the international literature on this field in order to give practical recommendations on how to manage immunosuppressive drugs in HIV patients who get transplanted and on how to handle HAART therapy in transplant-recipient patients who get infected with HIV.
Renal safety of adefovir dipivoxil in patients with chronic hepatitis B: two double-blind, randomized, placebo-controlled studies.
BACKGROUND: The incidence of adefovir dipivoxil (ADV) nephrotoxicity has been previously reported with the 60 and 120 mg daily dose in human immunodeficiency virus (HIV). We report a complete analysis on the renal tolerance of ADV at the currently approved dose of 10 mg daily for the treatment of chronic hepatitis B. METHODS: To investigate the efficacy, safety, and the tolerability of two dosing regimens of ADV (10 mg daily or 30 mg daily), two double-blind, placebo-controlled studies were performed in patients with chronic hepatitis B and compensated liver disease who were not undergoing current treatment and who had evidence of hepatitis B virus (HBV) replication. RESULTS: There was no overall median change from baseline at week 48 in serum creatinine or serum phosphorus levels in the ADV 10 mg group. In the ADV 30 mg group there was a slight increase of 0.2 mg/dL in median serum creatinine levels, and decrease of 0.1 mg/dL in serum phosphorus levels at week 48. Serum creatinine increase and hypophosphatemia were more frequently observed in patients receiving ADV 30 mg daily compared with ADV 10 mg and placebo. There were no grade 4 proteinuria, hematuria, or glycosuria events. CONCLUSION: Mild nephrotoxicity was demonstrated with the dose of 30 mg daily. Nephrotoxicity, as defined by an increase >/=0.5 mg/dL from baseline in serum creatinine or a serum phosphorus value of <1.5 mg/dL on two consecutive occasions, was not observed in patients treated with ADV 10 mg for a median follow-up period of approximately 64 weeks.
Epidemiology of microscopic polyarteritis: a 16-year study.
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Antiretroviral drugs and the kidney: dosage adjustment and renal tolerance.
BACKGROUND: Acquired immunodeficiency syndrome (AIDS)-related kidney disorders concern 30% of those patients and can lead to end-stage renal disease (ESRD; 0.6 to 1%). Therefore, administration of antiretroviral drugs in human immunodeficiency virus (HIV) patients with nephropathy is not uncommon. AIM OF THE REVIEW: Since renal insufficiency is not uncommon among HIV-infected patients treated with antiretroviral drugs, guidelines on how to use these drugs in the pattern of an altered renal function are mandatory. This review provides such guidelines established on the basis of pharmacokinetic and clinical studies reported in the international literature. In addition, some of these drugs may be nephrotoxic. Mechanisms and clinical and/or biological manifestations are reviewed to help monitor renal tolerance in patients receiving these drugs. CONCLUSION: Antiretroviral drugs' dosage in HIV-infected patients with altered renal function should be cautiously determined. Drug dosage should not be systematically reduced since dosage adjustment is not mandatory for all therapies (ie. protease inhibitors). Furthermore, when dose reduction is necessary, pharmacokinetic and clinical data from the literature allows to establish practical guidelines on how to use these drugs in such patients.
Inadequacy of antiretroviral drugs dosage adjustment in HIV patients receiving dialysis.
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Drug-induced Fanconi's syndrome.
Fanconi's syndrome (FS) was first described by Lignac in 1924. Associated with numerous varieties of inherited and acquired conditions, FS is characterized by a generalized transport defect in the proximal tubules, leading to renal losses of glucose, phosphate, calcium, uric acid, amino acids, bicarbonates, and other organic compounds. Cardinal symptoms of the syndrome are hyperaminoaciduria, glucosuria in the face of a normal serum glucose level, and phosphate wasting. Other symptoms may be associated, such as defects in bicarbonate reabsorption; renal acidification; urate reabsorption; urinary concentration; potassium conservation; reabsorption of sodium, calcium, and low-molecular-weight proteins; and secretion of p-aminohippuric acid. Acquired renal tubular defects resulting in FS also have been described in association with many exogenous agents, whether administered or accidentally ingested. This review concentrates on drug-induced FS.
Pharmacokinetics of tenofovir in haemodialysis.
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Dosing guidelines for fluconazole in patients with renal failure.
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Eye and kidney: from clinical findings to genetic explanations.
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Retroperitoneal fibrosis due to Wegener's granulomatosis: a misdiagnosis as tuberculosis.
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Clinical review: use of vancomycin in haemodialysis patients.
Following intravenous administration, vancomycin is poorly metabolized and is mainly excreted unchanged in urine. Total body clearance is thus dependent on the kidney, and is correlated with glomerular filtration rate and creatinine clearance. Accumulation of vancomycin in patients with renal insufficiency may therefore occur, and this may lead to toxic side effects if dosage is not modified according to the degree of renal failure. Furthermore, vancomycin easily diffuses through dialysis membranes. The aim of the present review is to establish guidelines for handling this drug in such patients. We indicate how and when plasma concentrations of vancomycin should be determined in dialysis patients.
Angiotensin-converting enzyme inhibitor-induced syndrome of inappropriate secretion of antidiuretic hormone: case report and review of the literature.
Seventeen cases of severe hyponatremia induced by angiotensin-converting enzyme (ACE) inhibitor therapy have been reported in the literature. The mechanism of severe hyponatremia induced by ACE inhibitor is not clear. A 60-year-old white man with a history of idiopathic dilated cardiomyopathy was treated with enalapril, 20 mg daily, that had been started 2 weeks before heart transplantation. The serum sodium level was 138 mmol/L before initiation of enalapril therapy and 127 mmol/L just before cardiac surgery. In the post-heart transplantation period, enalapril therapy was withdrawn for the perianesthesia period, and the serum sodium level increased from 127 to 140 mmol/L. One month later, viral myocarditis developed in the patient and enalapril was reintroduced at 20 mg daily. Two weeks later, natremia decreased. Enalapril was discontinued. Three days later the serum sodium level rose to 140 mmol/L. Severe symptomatic hyponatremia induced by the syndrome of inappropriate secretion of antidiuretic hormone should be considered a rare but possible complication associated with ACE inhibitor therapy.
Pharmacokinetics and dosage adjustment of rifabutin in a haemodialysis patient.
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Lymphopenia in Wegener's granulomatosis. A new clinical activity index?
BACKGROUND: Significant lymphopenia is a prominent feature in systemic erythematous lupus, but has not been described in Wegener's granulomatosis (WG). We suggest from a retrospective analysis that lymphopenia may also be an index of WG disease activity. METHODS: Medical charts form 19 patients diagnosed with systemic active WG between 1990 and 2000 were reviewed retrospectively. All patients had crescentic glomerulonephritis and alveolar hemorrhage. Clinical and biological markers were reviewed at three different time points: diagnosis, time of relapse, and during remission. RESULTS: Average lymphocyte count was significantly lower at diagnosis and relapse than during remission times (p < 0.008 and p < 0.000002, respectively). During disease activity either at diagnosis and during relapses, ANCA titers were highly positive (> or =50 IU/ml) in 27.5% of patients (8/29). The corresponding lymphocyte counts were below normal (1,500/min(3)) in 28 of 29 patients (96.5%). In patients with either negative or weakly positive ANCA, mean lymphocyte count was 728.5, 744.2 and 2,551/ml at diagnosis, during relapse and remission times, respectively. There was a clear negative correlation between the lymphocyte count and disease activity. CONCLUSION: Lymphopenia appears to be a good marker of WG activity. This index might be useful in all patients including those with negative ANCA.